A man showing early signs of a heart attack detected by a bot tracking his heart activity from a sensor on his wrist is picked up by a self-driving car that checks his vital signs on the way to the hospital. There, his doctors video-conference with a specialist, who assesses his symptoms through a Skype-like screen and recommends a treatment plan.

The scenario, inconceivable a generation ago, is closer than you might think. Technological advancements are ushering in a new era of health care, eroding the long-held model of hospitals and doctors offices as the physical center of the health system. The change is unfolding on many fronts, and experts say we are on the cusp of a revolution that could come within the next decade.

The growth of telemedicine (video chats with your doctor) and tools to track chronic diseases (wearable glucose-monitoring devices for diabetics) is inching us toward a time when medical care and diagnoses can be accessed from afar, and often without having to see a physician in person.

The explosion of relatively inexpensive direct-to-consumer genetic tests is allowing millions of people to learn potentially life-changing medical information about themselves without ever stepping foot in a doctors office.

And cutting-edge research in gene therapy is opening the door to the possibility of people with genetic diseases being treated much earlier in life, and being cured for longer periods of time potentially improving the quality of life for millions.

This rapidly changing landscape raises the question: Will there come a day when we wont need to go to the doctors office anymore? Will we be able to navigate the health system without coming into contact with a medical professional? And would that be good or bad?

Unit coordinator Ricky Ng does prep work for recently admitted patients and supports patient information for critical care nurses at California Pacific Medical Center's eICU hub.

Unit coordinator Ricky Ng does prep work for recently admitted...

Developers of self-driving cars are already considering including some basic inward-facing sensors that can be used for medical applications such as those that can measure temperature or cameras that can visually assess the health of a passenger to aid the elderly and people with disabilities, according to Nidhi Kalra, senior information scientist at the think tank Rand Corp. who researches autonomous car policy.

Unit coordinator Ricky Ng (left) talks with critical care nurse Clark Wurth at California Pacific Medical Centers eICU hub, where off-site ICU patients are monitored on computers.

Unit coordinator Ricky Ng (left) talks with critical care nurse...

Some people may have health complaints or challenges that the car needs to be aware of as its taking them to the mall, she said.

Kaiser Permanente, one of the largest health systems in Northern California, recently set up a futuristic mock exam room where patients can sit in front of a computer screen to talk to a doctor remotely while using a stethoscope, digital thermometer and otoscope to check their own symptoms under the guidance of the physician. Kaiser CEO Bernard Tyson has personally participated in the experiment.

That is the future being able to provide a great health care service without someone having to get up and go all the way across town for that kind of medical visit, Tyson said. All these things represent the moving away from the hospital being the centerpiece of health care.

Critical care nurse Karen Laberge monitors vitals of present ICU patients at California Pacific Medical Center's eICU hub.

Critical care nurse Karen Laberge monitors vitals of present ICU...

Last year, 70 million interactions between Kaiser patients and their primary care doctor were done by secure email, video conference and other remote tools.

Worldwide revenue for telehealth devices and services is expected to hit $4.5 billion next year, compared to $441 million in 2013, according to the business analytics firm IHS Technology. During the same period, the number of people using telehealth services each year is projected to grow from 350,000 to 7 million.

I dont think well get to a point where well never see a doctor, but a large percentage (of doctors) will be seeing patients remotely in the future, said Dr. David Tong, director of the telestroke program at California Pacific Medical Center in San Francisco. His program connects his vascular neurology practice with 20 other hospitals from the Oregon border to Visalia, so hospital physicians can seek his help in treating a stroke patient. Tong does a visual assessment of the patients using technology similar to Skype.

Tong has led the program since its inception a decade ago, when just two hospitals were in the telestroke network, and the concept of talking to a doctor through a screen seemed foreign to many patients. Today, its commonplace People think, If I do this all the time with my friends, Ill do it with my doctors too. Whats the difference? Tong said.

Despite the promise of remote medical care, though, many traditional barriers to health care remain. Wealth, geography and access to insurance are privileges that no app or technological advancement can replace.

The major stumbling block right now is financial, said Tong. Right now, most insurance doesnt pay for telemedicine in a very efficient way. That blocks some people from doing it.

Medicare and Medi-Cal, for example, limit their reimbursement for telemedicine services to psychiatry and to patients who live in rural areas, Tong said.

There may also be drawbacks to receiving care remotely, which reduces the need for physical interaction. Studies have shown that human touch reduces stress, helps premature babies grow faster and improves the lives of nursing home residents.

A patient's chest x-rays shown on a monitor at California Pacific Medical Center's eICU hub.

A patient's chest x-rays shown on a monitor at California Pacific...

But in another promising development, medicine is also moving in the direction of preventing diseases before they even cause any symptoms. Efforts by genetic testing firms to screen large populations coupled with research in gene therapy and gene editing will give people more information than ever before on their genetic makeup.

As soon as five years from now, everyone who wants to be sequenced will have been sequenced, said Dr. Jill Hagenkord, chief medical officer at Color Genomics, a Burlingame company that sells a $249 test that analyzes 30 genes associated with common hereditary cancers including breast, ovarian and pancreatic cancer. People can buy the test directly from Color or on Amazon, but they must submit their health information and have a physician review it and order the test before Color will analyze the sample.

Whether thats newborn screening in the hospital system or in a research setting ... sequencing data will just exist, Hagenkord said.

Color is already taking steps toward population screening, working with 40 large self-insured employers including Visa and Salesforce which collectively cover tens of thousands of people that subsidize or pay for the test for employees and spouses.

Using gene testing as a preventive tool doesnt take the medical professional out of the equation, but maybe youll just have a conversation earlier with your doctor, about getting a colonoscopy sooner or making choices that may reduce your risk of certain cancers, Hagenkord said.

Meanwhile, researchers are working to bring gene therapy from the clinical trial stage to the real world to treat retinal disease and hemophilia though treatments are not yet available commercially, said Dr. Chris Haskell, who leads Bayer Corp.s West Coast Innovation Center. Bayer has a joint venture with CRISPR Therapeutics which uses the gene-editing tool known as CRISPR to develop and market therapeutics for blood disorders, blindness and congenital heart disease.

With gene therapies, the industry is moving ahead very rapidly in clinical development toward bringing these to patients very soon, Haskell said. Gene editing is still a number of years away behind gene therapy, but has promise for being able to treat many more diseases.

Gene editing is considered a subset of gene therapy. Gene therapy consists of adding a missing part of a persons DNA, typically through an injection of an engineered virus that carries the replacement gene. With the blood-clotting disorder hemophilia A, patients are missing a blood-clotting protein called factor VIII. This protein is injected and, over the course of the next several days or weeks, the cells start producing the clotting factor and allow the circulatory system to clot normally.

The trailblazing is happening with hemophilia because we understand the disease, Haskell said. But theres a huge promise for bringing therapies to patients around the world, especially kids with metabolic disorders who have no good therapy.

Gene editing makes it possible to modify the genetic code and the applications seem limitless.

This opens up a whole new realm of ways to treat diseases in that we can turn things on and off, take things out, Haskell said. With gene therapy, we have the hammer. Now we have the whole toolbox. However, were still learning how to use all these tools.

And the workshop for those tools? It will be anywhere but your old, familiar doctors office.

Catherine Ho is a San Francisco Chronicle staff writer. Email: cho@sfchronicle.com Twitter: @Cat__Ho

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Why doctors' offices could become obsolete - San Francisco Chronicle

Intermountain Healthcare on Monday announced that its stepping closer to bringing a version of its precision medicine tool for cancer to the open market.

The health system, in fact, is pumping an additional $15 million into its spin-out Navican Genomics, which makes the TheraMap technology for matching patients with prioritized treatment options or appropriate clinical trials.

[Also:Promise of precision medicine depends on overcoming big obstacles] While precision medicine has great potential to positively impact cancer patients, its use is currently fragmented at best, Navican CEO Ingo Chakravarty said in a statement. TheraMap will provide precision care for all cancer patients, not just a few.

Navican employs sequencing tests developed at Intermountain to determine exactly which gene mutations are causing the cancer. From there, TheraMap provides testing and treatment options for the greatest number of actionable gene mutations, the startup said.

Intermountains Innovations division launched Navican Genomics in October 2016.

Twitter: @Bernie_HITN Email the writer: bernie.monegain@himssmedia.com

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Intermountain preps precision medicine tool for commercialization - Healthcare IT News

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The randomized controlled trial has long been held up as the gold standard for testing new drugs. But the nations top drug evaluator, Janet Woodcock, believes they arent necessary for all new experimental treatments. Randomized trials are long, expensive to run, and ultimately produce limited answers, she said at a medical conference last week.

The ability to use genetic information to classify patients and match them to potential therapies opens up new possibilities for evaluating drugs. As these capabilities increase, Woodcock says, the FDA should adjust its approach to reviewing drugs.

People have been very happy with the use of the traditional standard randomized controlled trial, Woodcock said last Thursday at the Precision Medicine World Conference at Duke University. People know how to interpret that evidence. Yet that may not be appropriate for some of these diseases.

The FDA has shown such flexibility with two recent approvals based on better genetic insights. Last week, the FDA approved Mercks (NYSE: MRK) cancer drug pembrolizumab (Keytruda) for all solid tumors with a specific genetic signature, regardless of where in the body the cancer started. That decision came days after the regulator expanded use of Vertex Pharmaceuticals (NASDAQ: VRTX) cystic fibrosis drug, ivacaftor (Kalydeco), so more patients with a particular genetic mutations could get treatment. The additional approvals for both drugs did not require the companies to conduct more randomized controlled trials. Woodcock described the approvals as landmarks for precision medicine.

Pembrolizumab was already approved to treat cancers of the skin, lung, and bladder, among others. The data supporting the latest approval for the Kenilworth, NJ-based companys drug came from open-label basket trials that simultaneously tested pembrolizumab on a variety of tumors that all share a specific genetic alteration. Patients were selected for the studies based on genetic tests that identified that signature, a predictor of whether they would respond to the Merck therapy. The FDAs ruling was an accelerated approval, meaning Merck must gather additional evidence to confirm the earlier studies. Woodcock said that this type of flexible approach is particularly important for diseases that have no treatment alternatives.

Genetic information has also played a role in the development and approval of Vertexs cystic fibrosis drug, ivacaftor. The drug was initially approved to treat patients who have specific mutations that indicate they would respond to the drug. On May 17, the FDA expanded the approval from 10 mutations to 33. Woodcock said the FDA based this decision on several factors, but the main evidence was a laboratory test that showed the drug could also help CF patients with more gene mutations. Woodcock said that this decision opens a pathway for drugs in cystic fibrosis and other diseases that have similar signs and symptoms. After a drug is first approved, a drugmaker could get additional approvals for additional patient subsets by using the lab test, rather than conducting a randomized clinical trial for each group.

The FDA and drug companies have been talking about adding new approaches to clinical trials for years, and that effort is now getting a nudge forward under federal law. Among the provisions of the wide-ranging 21st Century Cures Act, signed into law last year, are requirements that the FDA hold public hearings and issue guidance to help drug companies use new clinical trial designs to test their drugs. The law also calls on the FDA to use real-world evidence to support applications for new uses of already approved drugs. (Regulatory Affairs has a good breakdown of what the new federal law means for the FDA.)

Woodcock didnt reference the Cures Act in her remarks. But she said that for some drugs, different trial designs are warranted. Platform trials might be useful to evaluate multiple drugs and drug combinations simultaneously, with the ability to adjust the studies on the fly by adding or dropping arms. This flexibility allows Next Page

Frank Vinluan is editor of Xconomy Raleigh-Durham, based in Research Triangle Park. You can reach him at fvinluan [at] xconomy.com

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Woodcock: New Approvals Show FDA Is Adapting to Precision Medicine - Xconomy

Joselin Linder and members of the DeMoe family of North Dakota both lost genetic lotteries: They carry harmful inherited mutations that will impair, and likely curtail, their lives.

But the respective protagonists of "The Family Gene" and "The Inheritance" are far more than victims. At some sacrifice to their time, comfort and even health, they have become contributors to cutting-edge genomic medicine a field whose inevitable advances will benefit future generations.

Linder's mutation is exceedingly rare. In fact, it exists only in her family. Its marker is a heart murmur, often barely detectable. Its pre-eminent symptom is leakage of lymphatic fluid into the lungs and other body cavities, resulting in swollen limbs, damaged organs, breathing problems and eventual starvation. The gene, located on an X chromosome, expresses less virulently in women because they carry a second, nonlethal X chromosome that may temper its effects.

RELATED: TRENDING LIFE & STYLE NEWS THIS HOUR

The DeMoes of North Dakota are plagued by early-onset Alzheimer's disease a rare variation of the growing health scourge. Alzheimer's affects as many as 36 million people worldwide and about 5.3 million in the United States, but early-onset Alzheimer's represents just 1 percent of cases. It arises from three genetic mutations and typically presents between ages 30 and 50.

In rural Colombia, one extended family wrestling with this highly heritable dementia calls it "the curse." But for Alzheimer's researchers, the malady represents a scientific windfall an opportunity to test preventive drugs on a population known to be headed for illness.

"The Family Gene" and "The Inheritance," while concerned with explicating the relevant science, also share an unusual emotional intimacy. That intimacy takes different forms. Linder's memoir is a personal tale of loss, illness, ethical dilemmas and emotional fallout. Some of the details are harrowing. But Linder tells her story in a smart, wry voice devoid of self-pity.

"The Inheritance" is more straightforward in style, but ultimately no less involving. A model of immersion journalism, it is especially notable for its specificity and author Niki Kapsambelis' empathy. The DeMoes laid bare their lives, and Kapsambelis repays their candor with a warts-and-all portrait softened by fondness and respect.

"The Family Gene" begins with Linder's discovery of the severity of her father's illness. Dr. William I. Linder was himself a physician. But he would spend years, baffled and increasingly terrified, in a struggle with a nameless disease that could be neither diagnosed nor successfully treated.

At one point, the widow of William Linder's uncle notes that her husband had suffered similar symptoms on his way to a horrific death. Joselin Linder's great-grandmother, Mae, though longer-lived, had also experienced the disease's characteristic swelling. The family history pointed to a genetic link.

Linder uses gentle humor to distance herself, and the reader, from the grim reality of her father's condition. "We were not a family who routinely dealt with catastrophe," she writes. "We lived in Ohio." Recounting a story of a neighbor's disaster, she writes: "It's where we excelled: watching lightning strike other people's houses."

Eventually, the family makes a fortunate connection with Dr. Christine "Kricket" Seidman, a Boston-area genetic researcher with a specialty in cardiology. She recommends screening every family member for the telltale heart murmur. Out of 41 of Mae's descendants, 13 apparently have the murmur, forecasting health troubles ahead. Linder is one of them.

During her father's illness, she tries to maintain "a semblance of normalcy," attending Tufts University, finding her first serious boyfriend. But she soon swerves off course, abandoning her studies, acting out with drugs and men. "The idea of tempering my emotions, seeking any kind of balance at all, just seemed incomprehensible," she writes.

Then her medical and insurance woes begin. Months after her father's death, Linder discovers that her platelets are "alarmingly low," a condition that Seidman diagnoses as anemia. Meanwhile, her family doctor apparently has reported her heart murmur to a medical database, saddling Linder with a pre-existing condition. For a decade, in those pre-Obamacare years, she is unable to buy health insurance a problem solved only by marriage to a man with employer-based insurance.

Meanwhile, more relatives are stricken, the men succumbing "faster and in more devastating ways" than the women. One day, Linder's ankles swell up. Later, she discovers that she has a blocked portal vein, another symptom. Procedures to clear it ultimately fail.

But there are breakthroughs to cheer: A postdoctoral fellow in the Seidman lab maps the variant gene. Technology can now detect it and keep it from being passed to the next generation. Seidman develops a hypothesis about the disease mechanism, which implicates an improperly functioning liver. There is as yet no cure nor even a name for the disease. But Linder, while postponing childbearing, resolves to enjoy her life as best she can.

Like "The Family Gene," "The Inheritance" is partly about the impact a genetic disease has on entire families even relatives who are not afflicted. At the center of Kapsambelis' narrative are two remarkably courageous women: Gail DeMoe and her daughter Karla.

Gail's husband, Galen "Moe" DeMoe, is "a hard drinker, a harder worker, and one of the best-liked men in the oil fields" of Tioga, N.D. Gail, with her "ribald sense of humor," is an even more popular figure. The couple has six children and a household filled with noise and laughter.

But, by 1973, Moe's forgetfulness and confusion are sufficiently worrisome that Gail takes him to a neurologist, who makes the Alzheimer's diagnosis. Over time, his temper turns violent; his children fear him and regard him as abusive. Gail blames his rages on the disease, saying she remembers a different man. But as his belligerence worsens, she finally sends him to a state mental hospital. He dies in a nursing home.

Carrying a gene associated with early-onset Alzheimer's is a guarantee of disaster: Everyone who has it will develop the disease, and so will approximately half that person's offspring. Moe's family, however, is particularly unfortunate: Of his six children, only Karla has been spared.

Kapsambelis tells the extended family's story in pointillist detail, perhaps too much so for some readers. A DeMoe family tree helps keep the relationships straight, while a generous array of photographs underlines the poignancy of their fate.

"The Inheritance" is equally concerned with the history of Alzheimer's research. Dr. Francisco Lopera, who spent years traveling the dangerous back roads of Colombia to investigate the disease, emerges as an especially sympathetic figure. Kapsambelis is also a fan of the University of Pittsburgh's Dr. Bill Klunk, a pioneer of brain imaging.

The case of Dr. Pearson "Trey" Sunderland III, chief of geriatric psychiatry at the National Institute of Mental Health, is more complicated. For all his brilliance and personal charm, Sunderland was compromised by a consulting relationship with the pharmaceutical company Pfizer, manufacturer of Aricept. Sunderland promoted the Alzheimer's drug without disclosing the extent of his financial ties to Pfizer, and eventually pleaded guilty to a criminal conflict of interest.

Kapsambelis carefully lays out the somewhat arcane internecine disputes within the field between, for instance, those who attribute Alzheimer's primarily to amyloid plaques and those who fault tau tangles.

She notes that early intervention is the holy grail of Alzheimer's research which is why families like the DeMoes, who carry an autosomal dominant gene mutation, are so important. The DeMoes, who worked with both NIMH and Pitt, are now part of the Dominantly Inherited Alzheimer's Network, a major international study aimed at finding drugs to prevent or halt the disease.

Most won't benefit directly from the study, and traveling to Pittsburgh for batteries of tests has at times strained their health. But the DeMoes remain highly motivated. "If their bodies could help science ferret out an answer," Kapsambelis writes, "they might save their children."

The younger DeMoes Gail's grandchildren and their cousins have faced difficult decisions about whether to submit to genetic testing, and whether to have children. Relatives already diagnosed have lost not just memory and jobs, but all but their most steadfast friends. Their caregivers sometimes have had to resort to deception to move them to nursing homes. "No matter what decisions you make, you never feel good about them," Karla says.

To both the Linders and the DeMoes, medical genetics offers the possibility of a reprieve. "We now understand the gene and its impact on our bodies," Linder writes. "For us, this means hope, and the chance to change our fate."

The DeMoes, too, are waiting, as clinical trials of potential Alzheimer's drugs proceed. "Tragedy would intertwine with their blessings," Kapsambelis writes, "until they found the thread that would lead them out of the labyrinth."

Julia M. Klein was a finalist for the 2016 National Book Critics Circle's Nona Balakian Citation for Excellence in Reviewing.

'The Family Gene' | By Joselin Linder, Ecco, 261 pages, $28.99

'The Inheritance' | By Niki Kapsambelis, Simon & Schuster, 344 pages, $26

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'For us, this means hope': Exploring the promise of genomic medicine - Chicago Tribune

March 14, 2017 by Heather Lindsey Prostate organoids from genetically engineered mouse models. Credit: Mirjam Blattner and Dennis Huang

A newly discovered genetic mutation that is found in a subtype of prostate cancer is integral to the disease's development and growth, according to research from Weill Cornell Medicine scientists. Their findings could pave the way for new targeted treatment approaches.

A mutation of the gene Speckle Type BTB/POZ Protein, or SPOP, occurs in about 10 percent of men with prostate cancer. Roughly 20,000 men per year in the United States will be diagnosed with prostate cancers harboring SPOP mutations. But until now, SPOP's role in driving cancer was largely unknown. In a study published March 13 in Cancer Cell, researchers found in mice that the SPOP mutation leads to prostate cancer that grows in a distinctively different way from other common subtypes.

"This is important because now we have to think about SPOP cancers differently," said co-senior author Dr. Mark Rubin, director of the Caryl and Israel Englander Institute for Precision Medicine and the Homer T. Hirst III Professor of Oncology in Pathology at Weill Cornell Medicine. "This may have implications for how people respond to treatment and how amendable they are to certain drugs."

Prostate cancer containing the SPOP mutation was first discovered in 2011 by Weill Cornell Medicine researchers, who found that the malignancy has unique molecular features that characterize it as a distinct subtype.

"The key is we discovered these mutations several years ago, but because there are many mutations in cancer, knowing which ones are causing the disease and changing the biology of cells requires scientists to do some additional experiments," said co-senior author Dr. Christopher Barbieri, an assistant professor of urology at Weill Cornell Medicine.

In the new study, the research team, which included doctoral student and first author Mirjam Blattner, showed that the SPOP mutation drives prostate cancer formation in genetically engineered mice. This is a critical step in understanding the importance of mutations found in human cancers, Barbieri said. Additionally, they demonstrated that the SPOP mutation activates two major pathways in prostate cancer androgen receptor signaling and phosphoinositide 3-kinase (PI3K) signaling which are both important to cell survival and growth, and are processes that contribute to malignancy.

The androgen receptor is one of the main signaling pathways that underlies the growth of the prostate and prostate cancer, said Barbieri, who is a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine and a urologic surgeon at NewYork-Presbyterian/Weill Cornell Medical Center. Consequently, it is a main therapeutic target for men who have the disease. In recent years, researchers have shown that the androgen receptor works with the enzyme PI3K to promote prostate cancer cell survival.

Typically, these two pathways balance each other out, meaning the activation of one keeps the other in check and prevents cells from growing too out of control. "So, the fact that SPOP activates both pathways breaks the normal balance between the two, allowing cells to grow in an uncontrolled fashion," Barbieri said.

Now that scientists have a better understanding of the signaling pathways that are activated in this prostate cancer subtype, "we could potentially design therapies for it or use combinations of therapies that already exist to successfully target the cancer," Barbieri said.

The researchers are evaluating clinical trial data of patients being treated with androgen receptor antagonists and PI3K inhibitors to see whether they have SPOP mutations and how well they are responding to treatment. They're also investigating new agents to directly target SPOP cancers, pursuing a precision medical approach to treatment.

"This is a significant advancement for precision oncology," said Dr. Howard R. Soule, executive vice president and chief science officer of the Prostate Cancer Foundation, which helped fund the study through three research awards to Rubin and Barbieri. "Dr. Barbieri, Dr. Rubin, Blattner and team have identified the molecular mechanisms by which SPOP gene mutations, which define one of the most frequently occurring prostate cancer subtypes, drive prostate cancer. This provides a roadmap for developing precision treatment strategies for patients with this tumor type, which may shift towards improved outcomes."

Explore further: Gene mutation can allow proteins to gather, spark tumor growth

More information: http://www.cell.com/cancer-cell/fulltext/S1535-6108(17)30047-8

Journal reference: Cancer Cell

Provided by: Cornell University

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Gene mutation found to drive prostate cancer subtype - Medical Xpress

March 9, 2017 In the Department of Genomics at the Life & Brain research center: Dr. Andreas Forstner (seated at the front), associate professor (Privatdozent) Dr. Rupert Conrad and psychologist Stefanie Rambau. Credit: Katharina Wislsperger/UKB-Ukom

People with social anxiety avoid situations in which they are exposed to judgment by others. Those affected also lead a withdrawn life and maintain contact above all on the Internet. Around one in ten people is affected by this anxiety disorder over the course of their life. Researchers at the University of Bonn have now found evidence for a gene that is believed to be linked to the illness. It encodes a serotonin transporter in the brain. Interestingly, this messenger suppresses feelings of anxiety and depressiveness. The scientists want to investigate this cause more precisely and are thus looking for more study participants. The results will be published in the journal Psychiatric Genetics.

Heart palpitations, trembling and shortness of breath: those who suffer from social phobia avoid larger groups. Verbal tests or everyday arrangements are filled with fear - after all, other people could make a negative judgement. Those affected often avoid such situations for this reason. Contact is often easier over social media or anonymously over the Internet. Social phobias are among the psychiatric disorders that are triggered simultaneously by genetic and environmental factors. "There is still a great deal to be done in terms of researching the genetic causes of this illness," says Dr. Andreas Forstner from the Institute of Human Genetics at the University of Bonn. "Until now, only a few candidate genes have been known that could be linked to this."

Individual base pairs can vary in the DNA

Together with the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy at the University Hospital Bonn, Dr. Forstner is conducting a study into the genetic causes of social phobia. The research team investigated the DNA of a total of 321 patients and compared it with 804 control individuals. The focus of the scientists lay on what are known as single nucleotide polymorphisms (SNPs). "There are variable positions in the DNA that can exist to various degrees in different people," explains Dr. Forstner.

The cause of genetic illnesses often lies in the SNPs. It is estimated that more than thirteen million such changes exist in the human DNA. The scientists investigated a total of 24 SNPs that are suspected in the widest sense of being the cause of social phobias and other mental disorders. "This is the largest association study so far into social phobia," says associate professor (Privatdozent) Johannes Schumacher from the Institute of Human Genetics at the University of Bonn.

Patients provided information about their symptoms

Over the course of the study, scientists at the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy at the University Hospital Bonn will ask the patients about their symptoms and the severity of their social phobia. Their DNA is also examined using a blood sample. Whether there is a link between the signs of the illness and the genes is being investigated by the scientists using statistical methods. The evaluation of the previously collected data indicated that an SNP in the serotonin transporter gene SLC6A4 is involved in the development of social phobia.

This gene encodes a mechanism in the brain that is involved in transporting the important messenger serotonin. This substance suppresses, among other things, feelings of fear and depressive moods. "The result substantiates indications from previous studies that serotonin plays an important role in social phobia," says associate professor (Privatdozent) Dr. Rupert Conrad from the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy. Medications that block serotonin reuptake and increase the concentration of the messenger in the tissue fluid in the brain have already long been used to treat anxiety disorders and depression.

Subjects can participate in expanded study

The scientists now want to investigate more closely what the links are between the DNA and social phobia. "In order to achieve this goal, we need many more study participants who suffer from social anxiety," says the psychologist and study coordinator Stefanie Rambau from the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy at University Hospital Bonn. Information about the study is available at http://www.SocialPhobiaResearch.de. "Those who take part will help to research social phobia. This is the basis of better diagnosis and treatment procedures in the future," says Stefanie Rambau.

Explore further: Psychotherapy normalizes the brain in social phobia

More information: Andreas J. Forstner et al, Further evidence for genetic variation at the serotonin transporter gene SLC6A4 contributing toward anxiety, Psychiatric Genetics (2017). DOI: 10.1097/YPG.0000000000000171

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Social phobia: Indication of a genetic cause - Medical Xpress

In 2008, Congress passed the Genetic Information Nondiscrimination Act to prevent employers and insurance companies from discriminating against Americans based on their medical records.

Now a House committee is taking steps to remove GINAs protections.

On March 8, the House Committee on Education and the Workforce narrowly approved HR 1313, which could allow employers to require genetic testing as part of a workplace wellness program. Employees could face financial penalties if they refused.

The idea behind this is to make employees healthier and reduce health care costs for companies. But medical ethicists argue that this is not only unethical, its scientifically incoherent. Simply put, an employer wouldnt be able to glean anything particularly useful from commercially available genetic testing.

Theres this notion that somehow we could give you a genetic test and find out your risk factors and control them or monitor them,Arthur Caplan, the founding director of New York Universitys Division of Medical Ethics told The Huffington Post.Thats science that isnt here yet.

Dr. Lainie Ross, professor of clinical medical ethics at the University of Chicago Medicine, said,Were advancing in our understanding of genetics, but were nowhere near being able to say, Because you have this gene, you definitely should take this medicine or not.

Even Dr. Tom Price, the former orthopedic surgeon and Affordable Care Act opponent who now heads the Department of Health and Human Services, expressed reservations about HR 1313.

Im not familiar with the bill, but it sounds like there would be some significant concerns about it, Price said Sunday on Meet the Press. If the departments asked to evaluate it, or if its coming through the department, well be glad to take a look at it.

In 2015, the Food and Drug Administration cautioned that some laboratory tests could harm patients because they led to false diagnoses and unnecessary treatments (the agency later withdrew its regulatory proposalsand left lab test regulation up to President Donald Trumps FDA commissioner and Congress).

In fact, in a study in which researchers gave nine labs a genetic variant and asked them to analyze it, the labs gave different answers 22 percent of the time.

Even if everyone agrees that a genetic variant can cause disease, the actual risk to an individual of developing that disease is not that clear, Heidi Rehm of Brigham and Womens Hospital told the STAT health news site. That risk depends on environmental factors as well as other genetic ones, but truthfully we dont know what those factors are.

Forced genetic testing could push highly personal, sensitive and potentially inaccurate informationon individuals who may not want to know if they have specific health risks, particularly if they carry genetic mutations for serious or incurable conditions.

Genetics is based on probabilities, not certainties. So, although a test may find that you have an increased risk of breast cancer, to use one example, that does not mean you are certain to get the disease.

It maypush people into seeking out untested treatments or treatments that they really dont need because they come from a low-risk family, Ross said. Its not good medical practice.

Then theres the possibility that employers and insurance companies could use genetic information (which might not even accurately represent disease risk) to discriminate against employees and customers. Insurance companies could potentially charge people who show a risk for certain genetic conditions higher premiums, and unscrupulous employers would have the ability to make hiring and firing decisions based on employee health.

Theres also the dicey question of which genes employers and insurance companies might choose to look at.

Cherry-picking who gets insurance could potentially stigmatize one group of people.

We all have health risks. Were all going to die, Ross said. This is all about risk, and we want to share the risk.

Workplace wellness programs are popular (about half of U.S. companies with 50 or more employees had workplace wellness programs in place, according to a 2013 report from the nonpartisan Rand Corp. think tank), but theres not much evidence that such programs improve employee health.

Most of the studies that do exist fail to prove causation, show only short-term effects or are written by the wellness industry,according to The New York Times. The more rigorous studies are more likely to show that wellness programs neither save money nor improve employee health.

Thats not to say health and wellness shouldnt be employer priorities. But workplace wellness programs that incentivize and penalize employees based on their health are fundamentally unethical, according to Caplan.

The notion that your boss is in the best position to monitor your health is morally tenuous, he said. For example, your boss doesnt care if your job is stressing you out. Theyre not going to fix that. Theyre just going to tell you to lose weight.

If your boss really cares about your health, then they can build a gym and incentivize you to go down there when they give you that extra 30-minute break.

This reporting is brought to you by HuffPosts health and science platform, The Scope. Like us onFacebookandTwitterand tell us your story:scopestories@huffingtonpost.com.

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Workplace Genetic Testing Isn't Just Unethical, It's Scientifically Unsound - Huffington Post

March 8, 2017 Colonies of mouse embryonic stem cells, where cell nuclei are stained in blue. The DNA from the nuclei is sequenced to infer the relative positions of genes and their switches. Credit: C. Ferrai, MDC

Cells face a daunting task. They have to neatly pack a several meter-long thread of genetic material into a nucleus that measures only five micrometers across. This origami creates spatial interactions between genes and their switches, which can affect human health and disease. Now, an international team of scientists has devised a powerful new technique that 'maps' this three-dimensional geography of the entire genome. Their paper is published in Nature.

Genes are activated to produce RNA and proteins, then switched off again when the molecules are no longer needed. Both the gene and its switches are DNA sequences, and they may lie far apart on the linear genome. This presents a challenge for the cell, because these regions usually have to be brought into contact to activate the gene.

It also creates a problem for scientists trying to understand one of the central questions in biology: how do cells decide which genes should be activated, and when? The answer will partly depend on matching every gene to its control sequences. But DNA strands are too thin to be tracked under the microscope, and even if that were possible, you'd have the vast amount of DNA in the nucleus to contend with. Imagine examining a tangle of yarn the size of the Earth in hopes of observing an encounter between individual strands.

A new technique called Genome Architecture Mapping, or GAM, now helps to identify these contacts. It involves flash-freezing tissue or cells, then cutting thin slices of individual nuclei. The tiny amount of DNA within each slice of the nucleus is then sequenced, and the team deploys a mathematical model, named SLICE, to identify 'hotspots' of increased interaction between strands. The model looks at the frequency with which different genomic regions appear in the slice to infer information about the relative positions of genes and regions called enhancers that activate them.

"An analogy might be this; if you want to understand how school children interact you might take occasional photographs of where they sit in the canteen or appear together in the playground", explains joint-lead author Ana Pombo, who began the project whilst working at the MRC London Institute of Medical Sciences (LMS) and is now based at the Berlin Institute for Medical Systems Biology, Max Delbrck Center for Molecular Medicine in the Helmholtz Association (MDC) and the Berlin Institute of Health (BIH). "If you do that many times over a month, you will begin to see a pattern in those who often sit next to each other, or who run around together while playing. These random snapshots might tell you about their social interactions."

"This is made possible by filtering out random encounters from real interactions using mathematical methods," says the joint-lead author Mario Nicodemi at the Universit di Napoli Federico II, who conceived such mathematical models and, aided by his PhD student Antonio Scialdone, developed them.

Paul Edwards, of the Hutchison/MRC Research Centre and Department of Pathology at the University of Cambridge, and Ana Pombo had the initial idea before the techniques necessary to do the experiment were available. "My research team optimised the approach, and as new technical steps came along we added them to our method," she says.

The study, which appears today in Nature, applies the method to mouse embryonic stem cells and the authors hope it will help shed light on many genes whose activity is disturbed in some very serious diseases. In some diseases, the problem lies within the sequence of a gene, but defects in regulatory regions found elsewhere in the genome can be equally dangerous and much harder to understand. The new data provides a long list of new suspects that can now be scrutinized by researchers.

Whilst previous studies have identified two-way contacts, this information does not reveal how often such contacts take place and by implication how important they might be, Pombo says: "They can spot that you and I are friends, but not how strong this friendship is relative to everyone else."

"People have been measuring two-way contacts for a long time," says Robert Beagrie, joint first author on the paper, who was a PhD student with Ana Pombo at the LMS when he collected the data for the study and is now based at the University of Oxford. "Those studies have often shown that you can have a set of different DNA elements that interact with each other in pairs. With this new approach we are able to generate a genome-wide catalogue of all the regions that we are confident interact in groups." Now, the researchers are able to reliably detect and quantify so-called 'three-way contacts' in regions of the genome that are vigorously expressed.

But perhaps the most notable advance of through GAM is that experiments are based on single cells - whether common or scarce in a tissue - and track their positions relative to each other within the tissue. Existing methods require lots of cells of the same type, which has made it difficult to study the biology and diseases of rare types. "There is huge potential for applying this in human tissue samples to catalogue contacts between regulatory regions and their target genes, and to use that to understand genetic variation and how it might alter aspects of nuclear biology," Pombo says.

Some researchers are starting to show interest in using the technique to explore what happens when retroviruses insert their DNA into the genome of a host. Cancer scientists are also keen to create DNA maps of particular areas of a tumor. "By exploiting the unique nature of GAM data, mathematical models can reliably derive such information, opening the way to identify multiple, group interactions that could play a key role in the regulation of genes," explains Nicodemi. "We can now ask whether a gene is contacted at the same time by all of its enhancers, or by each enhancer one at a time?", Beagrie says. "We know that many genes that are important for early development have multiple enhancers. But how and why they are acting to regulate genes remain unanswered questions."

Explore further: Study finds recurrent changes in DNA activate genes, promote tumor growth

More information: Robert A. Beagrie et al, Complex multi-enhancer contacts captured by genome architecture mapping, Nature (2017). DOI: 10.1038/nature21411

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A three-dimensional map of the genome - Medical Xpress

WEDNESDAY, March 1, 2017 (HealthDay News) -- Researchers are reporting early success using gene therapy to treat, or even potentially cure, sickle cell anemia.

The findings come from just one patient, a teenage boy in France. But more than 15 months after receiving the treatment, he remained free of symptoms and his usual medications.

That's a big change from his situation before the gene therapy, according to his doctors at Necker Children's Hospital in Paris.

For years, the boy had been suffering bouts of severe pain, as well as other sickle cell complications that affected his lungs, bones and spleen.

Medical experts stressed, however, that much more research lies ahead before gene therapy can become an option for sickle cell anemia.

It's not clear how long the benefits will last, they said. And the approach obviously has to be tested in more patients.

"This is not right around the corner," said Dr. George Buchanan, a professor emeritus of pediatrics at the University of Texas Southwestern Medical Center in Dallas.

That said, Buchanan called the results a "breakthrough" against a disease that can be debilitating and difficult to treat.

Buchanan, who wasn't involved in the research, helped craft the current treatment guidelines for sickle cell.

"This is what people have been wanting and waiting for," he said. "So it's exciting."

Sickle cell anemia is an inherited disease that mainly affects people of African, South American or Mediterranean descent. In the United States, about 1 in 365 black children is born with the condition, according to the U.S. National Heart, Lung, and Blood Institute.

It arises when a person inherits two copies of an abnormal hemoglobin gene -- one from each parent. Hemoglobin is an oxygen-carrying protein in the body's red blood cells.

When red blood cells contain "sickle" hemoglobin, they become crescent-shaped, rather than disc-shaped. Those abnormal cells tend to be sticky and can block blood flow -- causing symptoms such pain, fatigue and shortness of breath. Over time, the disease can damage organs throughout the body.

There are treatments for sickle cell, such as some cancer drugs, Buchanan pointed out, but they can be difficult to manage and have side effects.

There is one potential cure for sickle cell, Buchanan said: a bone marrow transplant.

In that procedure, doctors use chemotherapy drugs to wipe out the patient's existing bone marrow stem cells -- which are producing the faulty red blood cells. They are then replaced with bone marrow cells from a healthy donor.

A major problem, Buchanan said, is that the donor typically has to be a sibling who is genetically compatible -- and free of sickle cell disease.

"We've known for a long time that bone marrow transplants can work," Buchanan said. "But most patients don't have a donor."

That's where gene therapy could fit in. Essentially, the aim is to genetically alter patients' own blood stem cells so they don't produce abnormal hemoglobin.

In this case, the French team, led by Dr. Marina Cavazzana, of Necker Children's Hospital's biotherapy department, focused on a gene called beta globin. In sickle cell anemia, beta globin is mutated.

First, the researchers extracted a stem cell supply from their teen patient's bone marrow, before using chemotherapy to wipe out the remaining stem cells.

Then they used a modified virus to deliver an "anti-sickling" version of the beta globin gene into the stem cells they'd removed pre-chemo. The modified stem cells were infused back into the patient.

Over the next few months, the boy showed a growing number of new blood cells bearing the mark of the anti-sickling gene. The result was that roughly half of his hemoglobin was no longer abnormal.

In essence, Buchanan explained, the therapy "converted" the patient to sickle-cell trait -- that is, a person who carries only one copy of the abnormal hemoglobin gene. Those individuals don't develop sickle cell disease.

"This is encouraging," said Dr. David Williams, president of the Dana-Farber/Boston Children's Cancer and Blood Disorders Center.

But, he cautioned, "the caveat is, this is one patient, and 15 months is a short follow-up."

Williams and his colleagues are studying a different approach to sickle cell gene therapy. It aims to restart the body's production of healthy fetal hemoglobin -- to replace the abnormal "adult" hemoglobin seen in sickle cell.

The hope, Williams said, is that gene therapy will ultimately offer a one-time treatment that cures sickle cell. But no one knows yet whether that will happen.

According to Williams, two key questions are: What's the long-term safety? And will the altered stem cells last for a patient's lifetime?

If gene therapy is proven to work, there will no doubt be practical obstacles to its widespread use, according to Buchanan. It's a high-tech treatment, and many sickle cell patients are low-income and far from a major medical center, he said.

But, Buchanan said, the new findings have now "opened a door."

The study was partly funded by Bluebird Bio, the company developing the therapy.

The results were published March 1 in the New England Journal of Medicine.

Continued here:
Gene Therapy: A Breakthrough for Sickle Cell Anemia? - Montana Standard

March 1, 2017 Representative images of kidney tissue from APOL1-G1 and APOL1-G2 mice, showing severe scarring of the kidney filter. Credit: Katalin Susztak, Perelman School of Medicine, University of Pennsylvania

African Americans have a heightened risk of developing chronic and end-stage kidney disease. This association has been attributed to two common genetic variants - named G1 and G2in APOL1, a gene that codes for a human-specific protein. However, direct evidence showing that these variants definitively cause kidney disease was lacking because APOL1 is widely expressed in different cell types but the gene is present in only some primates and humans. The challenge has been to create an animal model to prove this. Now, a team led by researchers from the Perelman School of Medicine at the University of Pennsylvania has engineered mice with these mutations that cause human-like kidney disease.

"The key missing piece has been whether these variants are true disease culprits," said senior author Katalin Susztak, MD, PhD, an associate professor of Medicine and Genetics, of the study published online in Nature Medicine. "Our study established that these mutations are definitely disease causing."

The G1 and G2 APOL1 gene variants, found almost exclusively in people of West African descent, have been shown to be associated with two-to-100-fold increased risk of kidney disease development, according to previous studies. Despite this highly significant risk, more than one third of African Americans carry the G1 and G2 variants. Biologists surmise that the reason these two mutations are so prevalent is that they emerged as a result of "positive selection" in people of African descent because the mutant proteins protect humans against the parasite that causes African sleeping sickness. Cells that express the G1 and G2 variants of the APOL1 protein are better able to kill these parasites.

To prove that expression of APOL1 with the G1 and G2 mutations causes kidney disease, the team made mice in which they could induce the expression of the non-mutated APOL1 gene as well as the G1 or G2 mutated APOL1 genes in different cell types. The team found that when the G1 and G2 variants are expressed in the filtering cells of the kidney the disease in the mouse model strongly resembled features of human kidney disease at the functional, structural, and molecular level. "These mutant proteins caused the kidney filter to become leaky and scarred, resulting in defective kidney function" Susztak said.

Kidney disease development was specific to the filtering cells of the kidney. The scientists found that G1 or G2 mutated APOL1 proteins interfere with the normal house-cleaning function of the cell, leading to an accumulation of jumbled proteins, inflammation, and eventually cell death. This trash removal system is especially important in kidney filtering cells, as these cells do not renew and losing them results in scarring of kidney tissue.

"Now that we know that the G1 and G2 mutated APOL1 proteins cause human-like kidney disease, we can start to look for ways to target them to reduce kidney disease risk among millions of people of African descent," Susztak said. "The good news is that in mice the disease development was experimentally reversible when the G1 and G2 genes were turned off, and in a related finding, disease severity also correlated with the amount of expression of G1 and G2 APOL1 variant proteins in patient samples."

Explore further: Gene variants in organ donors linked to shorter survival of transplanted kidneys

More information: Pazit Beckerman et al. Transgenic expression of human APOL1 risk variants in podocytes induces kidney disease in mice, Nature Medicine (2017). DOI: 10.1038/nm.4287

Transplanted kidneys may not function long-term if they come from donors with variants in a particular gene, according to a study that will be presented at ASN Kidney Week 2014 November 11-16 at the Pennsylvania Convention ...

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African Americans have a heightened risk of developing chronic and end-stage kidney disease. This association has been attributed to two common genetic variants - named G1 and G2in APOL1, a gene that codes for a human-specific ...

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Highly prevalent gene variants in minority populations cause kidney ... - Medical Xpress

Editorial Board | Published 8 hours ago

On Feb. 14, the National Academies of Sciences and the National Academy of Medicine released a report recommending that heritable gene-editing trials in human embryos be permitted to move forward given certain conditions.

The report is a scientific green light for humanity to start using new technology to address an intransigent subset of disease. Its also, albeit in a much more limited sense, a go-ahead for us to intentionally alter our own genetic book. Thats a story we should care about.

Our genes play an essential role in determining our health as well as almost everything else about who we are. They contain the DNA code that guides the development and daily function of our bodies. This code is passed down and reassorted from generation to generation.

Unfortunately, genes dont always encode what we would like them to encode. Genetic variants directly affecting only one gene product, as in cystic fibrosis, are enough to cause crippling illness and early death. Single-gene inheritable diseases like these affect 5 to 7 percent of the population.

Gene-editing, especially since the development of the CRISPR-Cas9 system in the last few years, holds the promise to cure such diseases. In some cases, this will not involve changing heritable genetic material.

For genetic diseases that affect multiple different systems in the body, though, the most effective treatments may involve altering the genetic make-up of all cells (which would mean affecting the genes that are passed on in reproduction as well as those in normal body cells).

The limited applications of germ-line editing the editing of genes that will be passed to the next generation recommended by the NAS promise clear benefit in treating awful diseases. Once the era of germ-line gene-editing begins in earnest, though, its easy to imagine a rise in the availability of heritable gene-editing for other purposes. People may seek to have their embryos genetic material altered not only to prevent genetic disease, but also in the hopes of increasing the athleticism, intelligence or beauty of their future children.

While making changes to personal appearance or fitness is widely accepted (we dont worry too much about the flaunting of the natural order when people dye their hair or exercise), editing heritable genetic material brings up a whole slew of questions about autonomy and social impact: Is making changes to embryos without their consent OK? What about if such changes will endure as part of the human gene pool?

Just as concerning are questions of access to gene-editing. Such access will almost certainly not be universal, and a gap one more stark even than our socioeconomic or racial divides might split our future society into those who have been gene-edited and those who have not been.

Andrew Niccols 1997 sci-fi film, "Gattaca," envisions such a development. Does such a gap bother us? And, if so, can we avoid it while still reaping the benefits of gene-editing?

We dont know the answers to many of the questions that accompany the coming world of gene-editing. However, we do know that now is the time to begin seeking them as a society. The contents of our genetic compendium and of history hang in the balance.

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Opinion: Gene-editing is here. How should it be used? - The Daily Tar Heel

In 2017, Sangamo is conducting a Phase 1/2 clinical trial evaluating SB-913 as an in vivo genome editing treatment for MPS II. Sangamo is also conducting Phase 1/2 studies this year evaluating in vivo genome editing treatments SB-318 for MPS I, another rare lysosomal storage disorder, and SB-FIX for hemophilia B, a rare blood disease. Data from these studies and from a clinical trial for a fourth lead program, SB-525, a gene therapy approach for hemophilia A, are expected in late 2017 or early 2018.

Sangamo's In Vivo Genome Editing Approach Sangamo's ZFN-mediated in vivo genome editing approach makes use of the endogenous albumin gene locus, a highly expressing and liver-specific site that can be edited with ZFNs to accept and express therapeutic genes. The approach is designed to enable the patient's liver to permanently produce circulating therapeutic levels of a corrective protein. The ability to permanently integrate the therapeutic gene in a highly specific, targeted fashion significantly differentiates Sangamo's in vivo genome editing approach from conventional AAV cDNA gene therapy. Ultimately, the target population for these programs will include pediatric patients, and it will be important in this population to be able to produce stable levels of therapeutic protein for the lifetime of the patient.

About Sangamo Therapeutics Sangamo Therapeutics, Inc. is focused on translating ground-breaking science into genomic therapies that transform patients' lives using the company's industry leading platform technologies in genome editing, gene therapy, gene regulation and cell therapy. The Company is advancing Phase 1/2 clinical programs in hemophilia A and hemophilia B, and lysosomal storage disorders MPS I and MPS II. Sangamo has a strategic collaboration with Bioverativ Inc. for hemoglobinopathies, including beta thalassemia and sickle cell disease, and with Shire International GmbH to develop therapeutics for Huntington's disease. In addition, it has established strategic partnerships with companies in non-therapeutic applications of its technology, including Sigma-Aldrich Corporation and Dow AgroSciences. For more information about Sangamo, visit the Company's website at http://www.sangamo.com.

Forward Looking Statements This press release may contain forward-looking statements based on Sangamo's current expectations. These forward-looking statements include, without limitation references relating to research and development of therapeutic applications of Sangamo's gene therapy and ZFP technology platforms, the potential of Sangamo's technology to treat hemophilia and lysosomal storage disorders, the expected timing of these clinical trials and the release of data from these trials, the impact of Sangamo's clinical trials on the field of genetic medicine and the benefit of orphan drug status. Actual results may differ materially from these forward-looking statements due to a number of factors, including uncertainties relating to substantial dependence on the clinical success of lead therapeutic programs, the initiation and completion of stages of our clinical trials, whether the clinical trials will validate and support the tolerability and efficacy of ZFNs, technological challenges, Sangamo's ability to develop commercially viable products and technological developments by our competitors. For a more detailed discussion of these and other risks, please see Sangamo's SEC filings, including the risk factors described in its Annual Report on Form 10-K and its most recent Quarterly Report on Form 10-Q. Sangamo Therapeutics, Inc. assumes no obligation to update the forward-looking information contained in this press release.

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/sangamo-therapeutics-receives-orphan-drug-designation-from-the-fda-for-sb-913-genome-editing-treatment-for-mps-ii-300415719.html

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Sangamo Therapeutics Receives Orphan Drug Designation from the ... - PR Newswire (press release)

BioWorld Online

Harvard and MIT Scientists Win Gene-Editing Patent Fight New York Times The Broad Institute in Cambridge, Mass., will retain potentially lucrative rights to a powerful gene-editing technique that could lead to major advances in medicine and agriculture, the federal Patent and Trademark Office ruled on Wednesday. The ... There's a fine red line between cures, enhancements using gene editing techBioWorld Online What the CRISPR Patent Decision Means for Gene EditingThe Atlantic A Patent Decision on Crispr Gene Editing Favors MITWIRED Phys.Org -NPR -Yahoo News all 116 news articles »

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Harvard and MIT Scientists Win Gene-Editing Patent Fight - New York Times

SAN DIEGO and PENNINGTON, N.J., March 17, 2020 /PRNewswire/ --OncoSec Medical Inc. Incorporated (NASDAQ:ONCS) (the "Company" or "OncoSec"), a company developing late-stage intratumoral cancer immunotherapies, today announced the publication of positive TAVO monotherapy data in patients with metastatic melanoma in the Annals of Oncology. The publication titled, "Intratumoral Delivery of Tavokinogene Telseplasmid Yields Systemic Immune Responses in Metastatic Melanoma Patients," features data previously highlighted at both American Association of Cancer Research (AACR) and the Melanoma Bridge annual meetings.Annals of Oncologyis the official publication of the European Society for Medical Oncology.

The complete publication in Annals of Oncology is linked here and available on OncoSec's website at https://oncosec.com/publications/.

The publication describes OncoSec's study of patients with Stage III/IV melanoma who were treated intratumorally with plasmid encoding IL-12 (tavokinogene telseplasmid or TAVO), followed by electroporation on days 1, 5, and 8 every 90 days in the main study with additional patients treated in two exploration cohorts with alternative schedules. Correlative analyses for programmed death-ligand 1 (PD-L1), flow cytometry to assess changes in immune cell subsets and analysis of intratumoral immune-related gene expression were carried out on pre-and post-treatment samples from study patients, as well as from additional patients treated during exploration of additional dosing schedules beyond the pre-specified protocol dosing schedule.Response was measured by study-specific criteria to maximize detection of latent and potentially transient immune responses in patients with multiple skin lesions.Toxicities were graded by the Common Terminology Criteria for Adverse Events version 4.0 (CTCAE v4.0).

The objective overall response rate (ORR) was 35.7% in the main study, with a complete response (CR) rate of 17.9%.The median progression-free survival in the main study was 3.7 months while the median overall survival was not reached at a median follow up of 29.7 months. A total of 46% of patients in all cohorts having both injected and uninjected lesions experienced regression of at least one of these uninjected lesions and 25% had a net regression of all untreated lesions. Transient procedural pain (n= 24, 80%) and injection site reactions were the most commonly experienced adverse events.

Transcriptomic and immunohistochemistry analysis showed that immune activation and co-stimulatory transcripts were up-regulated, with an increase of adaptive immune resistance.

The publication concluded that intratumoral TAVO was well-tolerated and led to systemic immune responses in advanced melanoma patients. While tumor regression and increased immune infiltration were observed in treated as well as untreated/distal lesions, adaptive immune resistance limited the response.

"TAVO treatment appears to drive a change in the immune microenvironment, which results in an immune response to melanoma with minimal systemic toxicity. These data demonstrate that thisin situtumor vaccination strategy may be a safe and effective approach to inducing multiple sustained, productive changes in the immune microenvironment that would be too toxic using similar systemic agents and drive significant clinical results," concluded study co-author Adil Daud, M.D., Department of Medicine, University of California, San Francisco."We look forward to continued evaluation of the TAVO approach as a monotherapy in future clinical trials."

TAVOis currently being evaluated as a combination therapy in multiple clinical trials, including KEYNOTE-695, a pivotal trial in late-stage anti-PD-1 checkpoint refractory metastatic melanoma, and two phase 2 trials, one for triple negative breast cancer (TNBC) and a second for head and neck cancer. TAVO enables the intratumoral delivery of DNA-based IL-12, a naturally occurring protein with immune-stimulating functions.OncoSec's technology, which employs electroporation, is designed to produce a controlled, localized expression of IL-12 in the tumor microenvironment, enabling the immune system to target and attack tumors throughout the body.Results from recently completed clinical studies of TAVOhave demonstrated a local immune response, and subsequently, a systemic effect as either a monotherapy or combination treatment approach.

"While our ongoing pivotal KEYNOTE-695 study is evaluating TAVO and KEYTRUDA combination therapy in late-stage checkpoint refractory metastatic melanoma patients and has begun to yield positive results, publication of monotherapy data with TAVO demonstrates its utility as a standalone treatment in this patient population," stated Christopher Twitty, Ph.D., OncoSec's Chief Science Officer and a co-author of the publication. "The increase in adaptive resistance observed in the tumor microenvironment, in particular PD-L1, makes TAVO a particularly well-suited partner with anti-PD-1 checkpoint therapies.We are encouraged to see such a high response rate and will continue to evaluate TAVO's utility as a monotherapy for metastatic melanoma."

Annals of Oncology is the latest among a presently growing volume of peer-reviewed journals to highlight the potential of TAVO as a novel immunotherapy. A recent publication in Cancer Immunology Research, linked here, also explored the mechanism of activation of systemic immunity in patients from the TAVO monotherapy study in metastatic melanoma patients. Additionally, Clinical Cancer Research featured TAVO monotherapy data in Merkel cell carcinoma on the cover of its February 2020 issue, linked here. You can find a list of all TAVO publications and scientific presentations at https://oncosec.com/publications/.

About OncoSec Medical IncorporatedOncoSec Medical Incorporated (the "Company," "OncoSec," "we" or "our") is a late-stage biotechnology company focused on developing cytokine-based intratumoral immunotherapies to stimulate the body's immune system to target and attack cancer. OncoSec's lead immunotherapy investigational product candidate TAVO (tavokinogene telseplasmid) enables the intratumoral delivery of DNA-based interleukin-12 (IL-12), a naturally occurring protein with immune-stimulating functions.The technology, which employs electroporation, is designed to produce a controlled, localized expression of IL-12 in the tumor microenvironment, enabling the immune system to target and attack tumors throughout the body. OncoSec has built a deep and diverse clinical pipeline utilizing TAVOas a potential treatment for multiple cancer indications either as a monotherapy or in combination with leading checkpoint inhibitors; with the latter potentially enabling OncoSec to address a great unmet medical need in oncology: anti-PD-1 non-responders.Results from recently completed clinical studies of TAVOhave demonstrated a local immune response, and subsequently, a systemic effect as either a monotherapy or combination treatment approach. In addition to TAVO, OncoSec is identifying and developing new DNA-encoded therapeutic candidates and tumor indications for use with its new Visceral Lesion Applicator (VLA), to target deep visceral lesions, such as liver, lung or pancreatic lesions. For more information, please visit http://www.oncosec.com.

TAVOis a trademark of OncoSec Medical Incorporated.

KEYTRUDAis a registered trademark of Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc.

Risk Factors and Forward-Looking Statements This release, as well as other information provided from time to time by the Company or its employees, may contain forward-looking statements that involve a number of risks and uncertainties that could cause actual results to differ materially from those anticipated in the forward-looking statements. Forward-looking statements provide the Company's current beliefs, expectations and intentions regarding future events and involve risks, uncertainties (some of which are beyond the Company's control) and assumptions. For those statements, we claim the protection of the safe harbor for forward-looking statements contained in the Private Securities Litigation Reform Act of 1995. You can identify forward-looking statements by the fact that they do not relate strictly to historical or current facts. These statements may include words such as "anticipate," "believe," "could," "estimate," "expect," "intend," "may," "plan," "potential," "should," "will" and "would" and similar expressions (including the negative of these terms). Although we believe that expectations reflected in the forward-looking statements are reasonable, we cannot guarantee future results, levels of activity, performance or achievements. The Company intends these forward-looking statements to speak only at the time they are published on or as otherwise specified, and does not undertake to update or revise these statements as more information becomes available, except as required under federal securities laws and the rules and regulations of the Securities Exchange Commission ("SEC"). In particular, you should be aware that the success and timing of our clinical trials, including safety and efficacy of our product candidates, patient accrual, unexpected or expected safety events, and the usability of data generated from our trials may differ and may not meet our estimated timelines. Please refer to the risk factors and other cautionary statements provided in the Company's Annual Report on Form 10-K for the fiscal year ended July 31, 2019 and subsequent periodic and current reports filed with the SEC (each of which can be found at the SEC's websitewww.sec.gov), as well as other factors described from time to time in the Company's filings with the SEC.

Company Contact:Gem HopkinsHead of Corporate Communications858-210-7334ghopkins@oncosec.com

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OncoSec Announces Publication of Positive TAVO Monotherapy Results in Metastatic Melanoma Patients in Annals of Oncology - BioSpace

Photo: Nurses singing We Need PPEs (personal protective equipment) in Oakland

Hospital healthcare professionals are dying many because they do not have adequate personal protective equipment (PPE) such as gloves, masks, gowns, shoe booties, etc.

Countless hospitals for years utilized costly public relations, touting that their facility provided the best care insurance could buy. Many of us in medicine recognized the hype.

Statistically with this crisis, I worry healthcare professionals on the front line who become infected are concealed from the public to protect the hospital reputation or cash flow.

Numbers coming from East Coast teaching hospitals reveal exposure problems, but I wonder at private and nonprofit hospitals if this data could be buried because whistleblowing doctors and nurses have been threatened and financially silenced? Add the guise of confidentiality and HIPAA rules, and self-serving administrators can easily hide serious and culpable information.

Hospital healthcare professionals must be protected, so public health departments, local governments and other regulatory authorities must undertake careful scrutiny and demand truthful statistics.

Ask: How many doctors, nurses and hospital employees have been exposed and are now positive? How many are in quarantine? What criteria were used in allowing them back to work? And so forth.

Hospitals should show us the numbers and not jeopardize indispensable front-liners who are saving lives.

Gene Uzawa Dorio, M.D., is a geriatric house-call physician who serves as president of the Los Angeles County Commission for Older Adults and Assemblyman to the California Senior Legislature. He has practiced in the Santa Clarita Valley for 32 years.

Originally posted here:
SCV News | Show Us the Real Numbers - SCVNEWS.com

In the 1986 horror classic The Fly, a scientist played by Jeff Goldblum manages, quite unintentionally, to mix his biology with that of a housefly with gruesome results.

But the real-world mutant fruit flies that scientists used to understand body patterning are almost as bizarre: Flies with legs on their brows instead of antennae. Flies with extra chest sections, complete with duplicate wings. Flies missing big chunks of their heads.

These freaky flies have something in common: Theyre mixing up their head-to-tail body plans. And they earned three scientists the Nobel Prize in Physiology or Medicine in 1995.

Two of the scientists, Eric Wieschaus and Christiane Nsslein-Volhard, conducted a now-famous genetic screen of fruit fly embryos in 1979 and 1980 while working at the European Molecular Biology Laboratory in Heidelberg, Germany. By feeding parent flies a powerful mutagen, they created a horde of larvae with genetic mistakes, including ones that affected how the fly embryo arranges bits of tissue, from head to tail, in sections a process called segmentation. (The pair tell the tale of this landmark experiment in the 2016 Annual Review of Cell and Developmental Biology.)

The other Nobel laureate, Edward Lewis of Caltech, discovered key players, later named Hox genes, that tell these fruit fly segments and other body parts what tissues and structures they should become.

Fruit flies, it turns out, have their own segmentation path, different from ours: They make a big chunk of tissue and then slice it up, like one would a loaf of bread. In contrast, vertebrates (including humans) churn out segments one by one, like a string of sausages, as they build the tissue. But many of the genes involved Hox and others found later are the same.

A landmark genetics screen by two scientists unearthed mutants with segmentation defects in the fruit fly Drosophila. On the left is the outer layer, or cuticle, of a normal early larva. To the right are ones of various mutants, with clear abnormalities.

CREDIT: E. WIESCHAUS & C. NSSLEIN-VOLHARD / AR CELL AND DEVELOPMENTAL BIOLOGY 2016

These commonalities extend to the need for a sort of ruler that guides segmentation and Hox actions by helping cells identify their position in the body. That ruler takes the form of a two-way gradient. Cells closest to the head end make lots of a chemical called retinoic acid, and those at the tail end make two other compounds, called FGF and Wnt. These diffuse along the body, such that different spots contain different amounts of the chemicals. So, for example, a cell thats closer to the head than the tail will know its position because its bathed in plenty of retinoic acid, but not so much Wnt or FGF.

Vertebrate segments arise from tissue called the mesoderm. Sandwiched between the cells that will make skin and those that will make most internal organs, the mesoderm will yield tissues such as bone and muscle.

As the embryo grows, part of the mesoderm tissue near the head begins to make its segments in the form of beads of tissue called somites, one on each side of the future spinal cord. They are squeezed out of that mesoderm like toothpaste from a tube, says Robb Krumlauf, a developmental biologist at the Stowers Institute for Medical Research in Kansas City, Missouri. These will turn into vertebrae and skeletal muscles. (Other body parts will develop from cells outside of the segments.)

If the segmentation process goes wrong, vertebrae can take the wrong shape: half-vertebrae, fused vertebrae or wedge-shaped ones, for example. In people, this causes a type of scoliosis, and also may affect the kidneys, heart and other body parts.

How does the embryo make just the right number of segments, all the right size? In the 1970s, English researchers came up with a model they called clock and wavefront. The embryos clock would tick to indicate each time a segment should be produced. The wavefront would consist of a maturation process traveling from head to tail, and cells at the crest of that maturation wave would be ready to segment. Whenever the clock ticked, they would spit out a new segment.

The developing mammalian embryo produces two somites, one each side of the future spinal canal, every time an internal clock ticks. The process is guided by a protein called FGF that is made by the tail end of the embryo and diffuses along its length, forming a gradient. Somite production occurs at a spot (the wave front) where the concentration of FGF is at just the right level when the clock makes a tick. The process repeats itself over and over, gradually building up segments, from which vertebrae and skeletal muscle are made. Two other molecules, Wnt and retinoic acid, also form gradients, and with FGF these are key to telling tissues where they are along an embryos length.

At that time, scientists had no idea what molecules would control either clock or wavefront, or if the theory was even correct. The first hard evidence for a clock came from experiments with chicken eggs, published in 1997.

Developmental biologist Olivier Pourqui, now at Harvard Medical School, was studying the chick version of a gene called hairy that is involved in segmentation in fruit flies. He and his colleagues saw the hairy gene turn on in a cyclical manner: starting out at the tail, and then closer to the head, every 90 minutes. And every 90 minutes, the embryo made a new segment.

That study confirmed that a ticking clock did underlie segmentation, says Michalis Averof, a comparative developmental biologist at CNRS in Lyon, France. In 2012, he reported a similar oscillator in beetles.

Scientists still dont know what sets that clocks pace, but they now know that a variety of other proteins, including two of those ruler proteins, Wnt and FGF (and another called Notch), turn on genes like hairy. The other part of the system the wavefront of maturation is characterized by concentrations of FGF. Since FGF is made at the tail end, levels of the protein will be highest there and lowest at the head. Cells that have a low enough level of FGF when the clock ticks will form a segment.

Changing the speed of the clock can have profound effects on the body plan, as Pourqui found in a 2008 study on snakes. Snakes have hundreds of vertebrae, compared to the few dozen in other vertebrates like chickens, mice and humans. How did this come to be? Compared with that of a mouse, their clock is accelerated, Pourqui found. The faster it ticks, the more segments get made, creating the snakes long spine. He doesnt yet know why the snake clock ticks faster, though.

The bone-and-muscle segments, and the rest of the embryos developing tissues, need instructions so that the ones near the front make shoulders and arms, the ones at the back end make hips and legs, and so on. This process, too, depends on the ruler laid down by retinoic acid, Wnt and FGF. The position of cells with respect to the ruler tells them which Hox genes to activate. The Hox genes then turn on other genes, to make the right size and shape of vertebrae, or a tail, arm, liver, etc.

Its complicated: Mammals have 39 different Hox genes, activated in different combinations along the body and with different parts to play. For example, mice usually grow a defined series of vertebrae, including 13 thoracic segments with ribs and six lumbar segments without. But when scientists bred mice to lack the Hox10 gene, the creatures grew little ribs on the lumbar segments. In rare cases in people, mutations in Hox genes cause diverse effects such as club foot, hair loss and extra fingers and toes.

Lewis, who worked with Hox mutant flies in the 1970s, also discovered a remarkable pattern to the Hox genes. In DNA, they are lined up in the same order in which they are produced, from head to tail, in the embryo. Genes at one end of the line spring into action in response to retinoic acid, with that signal emanating from the head; the other end responds to Wnt and FGF, signals from the rear.

A collection of genes called HOX are activated in different parts of an animals body plan, telling cells and tissues what to become. In the DNA, the genes line up in the same order as they are used in a developing embryo. There are remarkable similarities between the HOX genes of disparate creatures, such as fruit flies, mice and humans. In mammals, the HOX genes diversified so that there are four sets (HOX A, B, C and D) to the flys single set. Duplications also led to an expanded number of HOX genes in each set.

Much remains unknown about how bodies are arranged how the same set of Hox genes creates such different body plans in different animals, for example, and how the pace of the segmentation clock sets just right to make a spine to fit a snake or a mouse or a person. Studying such things in people, of course, is difficult. So Pourqui and colleagues recently turned to human stem cells in a dish.

Using genetic trickery, they engineered the cells to flash yellow every time a certain clock gene turned on. Watching for the yellow glow, the researchers detected a clock that had five hours between each tick. Pourqui now aims to figure out just what controls that five-hour timing.

Its astounding, Krumlauf says, how similar the parts of the body-plan system are across such a wide variety of organisms. Each animal uses many of the same genetic tools, in different ways, to create its own unique shape.

In that respect, then, its not so surprising that Jeff Goldblums character melded so completely with a fly. Wnt, FGF, Hox genes its how we apply them that makes us the creatures we are.

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How do bodies position arms, legs, wings and organs? - Knowable Magazine

CARLSBAD, Calif. and ROTTERDAM, Netherlands, Dec. 10, 2019 /PRNewswire/ -- Prescient Medicine Holdings, Inc. and the Department of Clinical Chemistry at Erasmus MC (CC-EMC), Rotterdam today announced a partnership for CC-EMC to study opioid addiction risk in The Netherlands.The partnership will center on Prescient Medicine's novel genetic testing technology designed to objectively assess an individual's risk of opioid addiction prior to opioid exposure. The clinical research will be conducted with patients in The Netherlands to confirm that the positive results from research completed in the United Statesare also found in the Dutch health care system.

According to a 2019 study, the overall number of prescription opioid users in the Netherlands has nearly doubled between 2008 and 2017, and the number of opioid-related hospital admissions has tripled.

"We have seen the devastation of opioid addiction in the United States, and we are worried that we are on a similar path in the Netherlands, given the increased rates of opioid use and addiction," said Professor Ron HN Van Schaik, Ph.D., Erasmus MC. "Evaluating the potential of Prescient Medicine's diagnostic technology is an important step in future efforts aimed to help address and minimize opioid addiction in The Netherlands. A test like this would give clinicians a tool to proactively determine the risk of opioid addiction for an individual before they are prescribed a medication. This will enable prescribers to make a choice which drug would serve their patients' needs best."

The genetic panel leverages the power of machine learning to assess a patient's genetic risk of opioid addiction. The test received Breakthrough Device Designation from the Federal Drug Administration (FDA) in the United States in February 2018. The work done through this collaboration will be the first time the test has been researched outside of the United States.

"A test like this is valuable to anyone prescribing opioids, not just in the United States," said Keri Donaldson, M.D., medical director and CEO of Prescient Medicine. "We are excited to expand the use of this test to The Netherlands and potentially help play a part in helping combat the opioid crisis that may be developing in The Netherlands and throughout the world."

About Prescient Medicine Holdings, Inc.Prescient Medicine is a privately held company focused on developing diagnostic tools that advance the precision healthcare movement. Prescient Medicine's mission is to accelerate the development, commercialization and deployment of advanced clinical diagnostics to address the most pressing public health issues in the U.S and around the world. Prescient Medicine builds powerful tests and analytic solutions to offer deep predictive insights so doctors and patients have the data they need to make better, more informed clinical decisions, and achieve the best possible patient outcomes. Prescient Medicine technologies include LifeKit Predict, an in vitro diagnostic test commercialized in partnership with its subsidiary AutoGenomics, used for the identification of patients who may be at risk for opioid addiction and LifeKit Prevent a diagnostic test designed to detect pre-cancerous polyps, as well as early-stage carcinomas. Prescient Medicine operates three CLIA-certified labs supporting ToxKit, an advanced drug screening tool, and LifeKitPreScript, an advanced pharmacogenomic test. Prescient has locations in California, Pennsylvania, Illinois and Kentucky.

About Department of Clinical Chemistry, Erasmus MC.The Erasmus MC University Medical Center (Erasmus MC), an organization with 17,000 employees in 2019, is committed to a healthy population and excellence in healthcare through research and education. It excels in various research fields, studying fundamental and clinical domains as well as public health and prevention. Research at Erasmus MC is at the heart of society, resulting in innovation, quality improvement and more effectiveness in patient care. The overall research aim of Erasmus MC is to translate bench discoveries to bed-side applications. Bibliometric indicators place Erasmus MC in the top 20 of clinical medicine worldwide. In addition to scientific research, patient care and education are core tasks of Erasmus MC. The complete spectrum of medicine is offered, from disease to health and from individual to public healthcare. Erasmus MC is also the largest medical school in the Netherlands, with ~3,100 medical students and has approximately 250 PhD graduations per year. It offers BSc, MSc and PhD programs to train the next generation of medical practitioners and researchers. Its annual research budget amounts to 139.7 million. The impact of Erasmus MC on the Dutch economy is substantial: in 2012, it contributed 3.8 billion gross value added (GVA) to the Dutch economy and it indirectly supports 40,556 jobs.

The Department of Clinical Chemistry contains the International Federation for Clinical Chemistry (IFCC) Expert Center for Pharmacogenetics, led by Prof Ron HN van Schaik, investigating the translation of genetic information in guiding individualized drug therapy.

SOURCE Prescient Medicine

http://www.prescientmedicine.com

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Prescient Medicine and Erasmus MC Partner to Study Opioid Addiction Risk - PRNewswire

If certain vegetables have always made you choke, you may be more than a picky eater. Instead, you may be what scientists call a super-taster, an individual with a genetic predisposition to taste food differently. Unfortunately, being a super-taster does not make everything taste good. It can do exactly the opposite. Super-tasters are exceptionally sensitive to bitterness, a common feature of many dark green, leafy veggies such as cauliflower, broccoli, Brussels sprouts, and cabbage, to name a few.

The individual who has that genetic propensity gets more of the sulfur flavor of, say, Brussels sprouts, especially if theyve been overcooked, as stated by Professor Valerie Duffy of the University of Connecticut, an expert in the study of food taste, consumption and preference. So that bitter vegetable is disliked, and because people oversimplify, soon all vegetables are disliked, Duffy further added. If you ask people, do you like vegetables? They dont usually say, Oh yes, I dont like this, but I like these others. People tend to either like vegetables, or they dont like it completely. People with the bitter gene are 2.5 times more prone to eating fewer vegetables than people who do not have that gene, as per recent research presented recently at the annual meeting of the American Heart Association. We wanted to know if genetics affected the capability of people who require to eat heart-healthy foods from eating them, as stated by study author Jennifer Smith, a registered nurse who is a postdoc in cardiovascular science at the University of Kentucky School of Medicine. While we didnt see any results in gene type for sodium, saturated fat or sugar, we did see a difference in vegetables, Smith said, adding that individuals with the gene tasted a ruin-your-day level of bitterness.

Food scientists are trying to develop ways to decrease the bitterness in veggies, in the hopes that we can keep another generation of super-tasters from rejecting vegetables. Theres been some level of success. In fact, the Brussels sprouts we eat today are much sweeter as compared to those our parents or grandparents ate. Dutch growers in the 90s searched their seed archives for older, less bitter varieties, and then cross-pollinated them with todays high-yielding varieties.

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Your hatred for heart-healthy veggies might be genetic - SellRegular

MONDAY, June 5, 2017 (HealthDay News) -- Genetically tuning a person's own immune cells to target cancer appears to provide long-lasting protection against a blood cancer called multiple myeloma, an early trial from China shows.

The treatment, called CAR T-cell therapy, caused 33 out of 35 patients with recurring multiple myeloma to either enter full remission or experience a significant reduction in their cancer.

The results are "impressive," said Dr. Len Lichtenfeld, deputy chief medical officer for the American Cancer Society.

"These are patients who have had prior treatment and had their disease return, and 100 percent of the patients are reported to have had some form of meaningful response to these cells that were administered," Lichtenfeld said.

The new therapy is custom-made for each patient. Doctors collect the patient's own T-cells -- one of the immune system's main cell types -- and genetically reprogram them to target and attack abnormal multiple myeloma cells.

Lead researcher Dr. Wanhong Zhao likened the process to fitting immune cells with a GPS that steers them to cancer cells -- making them into professional killers that never miss their target.

Zhao is associate director of hematology at the Second Affiliated Hospital of Xi'an Jiaotong University in Xi'an, China.

CAR T-cell therapy is promising because the genetically altered T-cells are expected to roost in a person's body, multiplying and providing long-term protection, Lichtenfeld said.

"The theory is they should attack the tumor and continue to grow to become a long-term monitoring and treatment system," Lichtenfeld said. "It's not a one-shot deal."

The technology represents the next step forward in immunotherapy for cancer, said Dr. Michael Sabel, chief of surgical oncology at the University of Michigan.

"Immunotherapy is now really providing hope to a lot of patients with cancers that were not really responding to our standard chemotherapies," Sabel said.

CAR T-cell therapy previously has been used to treat lymphoma and lymphocytic leukemia, Lichtenfeld said.

Zhao and his colleagues decided to try the therapy to treat multiple myeloma. They re-engineered the patients' T-cells and then reintroduced them to the body in three infusions performed within one week.

Multiple myeloma is a cancer that occurs in plasma cells, which are mainly found in bone marrow and produce antibodies to fight infections. About 30,300 people will likely be diagnosed with multiple myeloma this year in the United States, researchers said in background notes.

"Multiple myeloma is a disease that historically was fatal in the course of a couple of years," Lichtenfeld said. During the past two decades, new breakthroughs have extended survival out 10 to 15 years in some patients, he noted.

To date, 19 of the first 35 Chinese patients have been followed for more than four months, researchers report.

Fourteen of those 19 patients have reached the highest level of remission, researchers report. There hasn't been a relapse among any of these patients, including five followed for more than a year.

"That's as far as you can go in terms of driving down the amount of tumor that's in the body," Lichtenfeld said.

Out of the remaining five patients, one experienced a partial response and four a very good response, researchers said.

However, about 85 percent of the patients experienced cytokine release syndrome (CRS), a potentially dangerous side effect of CAR T-cell therapy.

Symptoms of cytokine release syndrome can include fever, low blood pressure, difficulty breathing, and impaired organ function, the researchers said. However, most of the patients experienced only transient symptoms, and "now we have drugs to treat it," Lichtenfeld said.

History suggests the therapy will cost a lot if it receives approval, Lichtenfeld said. However, prior to approval, much more research will be needed, he added.

The Chinese research team plans to enroll a total of 100 patients in this clinical trial at four hospitals in China. They also plan a similar clinical trial in the United States by 2018, Zhao said.

The study was funded by Nanjing Legend Biotech Co., the Chinese firm developing the technology.

The findings were presented Monday at the American Society of Clinical Oncology annual meeting, in Chicago. Data and conclusions presented at meetings are usually considered preliminary until published in a peer-reviewed medical journal.

Excerpt from:
Gene-Based Therapy May Thwart a Tough Blood Cancer - Sioux City Journal

Sessions/Tracks

Track 1:Molecular Biology

Molecular biologyis the study of molecular underpinnings of the processes ofreplication,transcription,translation, and cell function. Molecular biology concerns themolecularbasis ofbiologicalactivity between thebiomoleculesin various systems of acell,gene sequencingand this includes the interactions between theDNA,RNAand proteinsand theirbiosynthesis. Inmolecular biologythe researchers use specific techniques native to molecular biology, increasingly combine these techniques and ideas from thegeneticsandbiochemistry.

RelatedMolecular Biology Conferences| Genetics Conferences|Gene Therapy Conferences|Biotechnology Conferences| Immune Cell Therapy Conferences

2nd World Congress onHuman Genetics&Genetic Disorders, November 02-03, 2017 Toronto, Canada; 9th International Conference onGenomicsandPharmacogenomics, June 15-16, 2017 London, Uk; 6th International Conference and Exhibition onCellandGene Therapy, Mar 27-28, 2017 Madrid, Spain; Gordon Research Conference,Viruses&Cells, 14 - 19 May 2017, Lucca, Italy;Human Genome Meeting(HGM 2017), February 5-7 2017, Barcelona, Spain; Embl Conference:Mammalian GeneticsAndGenomics:From Molecular Mechanisms To Translational Applications, Heidelberg, Germany, October 24, 2017;GeneticandPhysiological Impacts of Transposable Elements, October 10, 2017, Heidelberg, Germany.

American Society for Cell Biology;The Society for Molecular Biology & Evolution;American Society for Biochemistry and Molecular Biology;The Nigerian Society of Biochemistry and Molecular Biology;Molecular Biology Association Search Form - CGAP.

Track 2:Gene Therapy and Genetic Engineering

Thegenetic engineeringis also called asgenetic modification. It is the direct manipulation of an organism'sofgenomeby usingbiotechnology. It is a set of technologies used to change the genetic makeup of the cell and including the transfer of genes across species boundaries to produce improved novelorganisms. Genesmay be removed, or "knocked out", using anuclease.Gene is targetinga different technique that useshomologousrecombinationto change anendogenous gene, and this can be used to delete a gene, removeexons, add a gene, or to introducegenetic mutations. There is an dna replacement therapy, Genetic engineering does not normally include traditional animal and plant breeding, gene sequencing, in vitro fertilization, induction of polyploidy,mutagenesisand cell fusion techniques that do not use recombinant nucleic acids or a genetically modified organism in the process,diseases treated with gene therapywas initially meant to introduce genes straight into human cells, focusing on diseases caused by single-gene defects, such as cystic fibrosis, hemophilia, muscular dystrophy and sickle cell anemia

RelatedMolecular Biology Conferences| Genetics Conferences|Gene Therapy Conferences|Biotechnology Conferences| Immune Cell Therapy Conferences

8thWorld Congress onMolecular Pathology, June 26-27, 2017 San Diego, USA; 11thInternational Conference onSurgical Pathology& Practice, March 27-28, 2017, MADRID, SPAIN; 13th EuropeanPathologyCongress, Aug 02-03, 2017, MILAN, ITALY; 28th Annual Meeting, Austrian Society ForHuman GeneticsAnd The Swiss Society OfMedical GeneticsCombined Meeting 2017 march 29, 2017 - March 31, 2017, bochum , Germany.

Association for Clinical Genetic Science;Genetics Society of America | GSA;Association of Genetic Technologists;Molecular Genetics - Human Genetics Society of Australasia;Genetic Engineering - Ecological Farming Association.

Track 3:Cell & Gene Therapy

Cell therapy is also calledcellular therapyorCyto therapy, in which cellular material is injected into patient this generally means intact, living cells. The first category iscell therapyin mainstream medicine. This is the subject of intense research and the basis of potential therapeutic benefit. Such research can be controversial when it involves human embryonic material. The second category is in alternative medicine, and perpetuates the practice of injecting animal materials in an attempt to cure disease.Gene therapyis the therapeutic delivery of nucleic acid polymers into a patient's cells as a drug to treat disease. Gene therapy is a way to fix agenetic problemat its source. The polymers are either translated into proteins, interfere with targetgene expression, or possibly correct genetic mutations. The most common form uses DNA that encodes a functional,therapeutic gene to replace a mutated gene. The polymer molecule is packaged within a "vector", which carries the molecule inside cells. Vectors used in gene therapy, the vector incorporates genes intochromosomes. The expressed nucleases then knock out and replace genes in the chromosome. The Center forCell and Gene Therapyconducts research into numerous diseases, including but not limited to PediatricCancer, HIV gliomaandCardiovascular disease.

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2nd World Congress onHuman Genetics&Genetic Disorders, November 02-03, 2017 Toronto, 27 Canada ; 7th International Conference onPlant Genomics, July 03-05, 2017, Bangkok, Thailand ; American Society ofGeneandCell Therapy(ASGCT) 20th Annual Meeting, 10 - 13 May 2017, Washington, DC;Genomic Medicine for Clinicians(course), January 25-27, 2017, Hinxton , Cambridge, UK; Embo Conference:ChromatinandEpigenetics, Heidelberg, Germany, May 3, 2017; 14th International Symposium on Variants in theGenomeSantiago de Compostela, Galicia, Spain, June 5 - 8, 2017;

Genetics and Molecular Medicine - American Medical Association;Genetics Society of America / Gsa;British Society for Genetic Medicine;British Society for Gene and Cell Therapy; Australasian Gene Therapy Society.

Track 4:Cell Cancer Immunotherapy

Immunologydeals with the biological and biochemical basis for the body's defense against germs such as bacteria, virus and mycosis (fungal infections) as well as foreign agents such asbiological toxinsand environmental pollutants, and failures and malfunctions of these defense mechanisms. Cancer immunotherapy is the use of the immune system to treat cancer. Immunotherapies can be categorized as active, passive or hybrid (active and passive). Antibodies are proteins produced by the immune system that bind to a target antigen on the cell surface. The immune system normally uses them to fight pathogens. A type of biological therapy that uses substances to stimulate or suppress the immune system to help the body fight cancer, infection, and other diseases. Some types of immunotherapy only target certain cells of the immune system. Others affect the immune system in a general way. Types of immunotherapy include cytokines, vaccines, bacillus Calmette-Guerin (BCG), and some monoclonal antibodies.

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9thAnnual Meeting onImmunologyandImmunologist, July 03-05, 2017 Kuala Lumpur, Malaysia; 8th MolecularImmunology&ImmunogeneticsCongress, March 20-21, 2017 Rome, Italy; 8th EuropeanImmunologyConference, June 29-July 01, 2017 Madrid, Spain; July 03-05, 2017; B Cells and T Follicular Helper Cells Controlling Long-Lived Immunity (D2), April 2017, 2327, Whistler, British Columbia, Canada; Mononuclear Phagocytes in Health,Immune Defense and Disease, 304 May, Austin, Texas, USA;Modeling Viral Infections and ImmunityMAY 2017, 14, Estes Park, Colorado, USA; IntegratingMetabolism and Immunity(E4)292 June, Dublin, Ireland.

The American Association of Immunologists;Clinical Immunology Society ; Indian Immunology Society;IUIS - International Union of Immunological Societies;American Society for Histocompatibility and Immunogenetics.

Track 5:Clinical Genetics

Clinical geneticsis the practice of clinical medicine with particular attention tothe hereditary disorders. Referrals are made togenetics clinicsfor the variety of reasons, includingbirth defects,developmental delay,autism,epilepsy, and many others. In the United States, physicians who practice clinical genetics are accredited by theAmerican Board of Medical Genetics and Genomics(ABMGG).In order to become a board-certified practitioner of a Clinical Genetics, a physician must complete minimum of 24 months of his training in a program accredited by the ABMGG. Individual seeking acceptance intoclinical geneticstraining programs and should hold an M.D. or D.O. degree (or their equivalent)and he/she have completed a minimum of 24 months of their training in ACGME-accredited residency program internal medicine, pediatrics and gynecology or other medical specialty.

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Belgian Society OfHuman GeneticsMeeting 2017 february 17, 2017, Belgium; American College Of Medical Genetics 2017 AnnualClinical GeneticsMeeting march 21-25 2017, phoenix , United States; German Society Of Human Genetics 28th Annual Meeting, Austrian Society ForHuman GeneticsAnd The Swiss Society OfMedical GeneticsCombined Meeting 2017 march 29, 2017 - March 31, 2017, bochum , Germany; Spanish Society OfHuman GeneticsCongress 2017april 25, 2017 - April 28, 2017 madrid , Spain;

Clinical Genetics Associates;Clinical Genetics Society(CGS);The genetic associate;International Conference on Clinical and Medical Genetics;Association for Clinical Genetic Science;The American Society of Human Genetics.

Track 6:Pharmacogenetics

Pharmacogeneticsis the study of inherited genetic differences in drug metabolic pathways which can affect individual responses towards the drugs, both in their terms of therapeutic effect as well as adverse effects. In oncology, Pharmacogenetics historically is the study ofgerm line mutations(e.g., single-nucleotide polymorphisms affecting genes coding forliver enzymesresponsible for drug deposition and pharmacokinetics), whereaspharmacogenomicsrefers tosomatic mutationsin tumoral DNA leading to alteration in drug response.

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Spanish Society OfHuman GeneticsCongress 2017april 25, 2017 - April 28, 2017, madrid , Spain; 8th World Congress onPharmacology, August 07-09, 2017 Paris, France; World Congress onBio therapeutics, May 22-23, 2017, Mexico City, Mexico; 8th World Congress OnPharmacologyAndToxicology, July 24-26, 2017, Melbourne, Australia; German Society Of Human Genetics 28th Annual Meeting, Austrian Society ForHuman GeneticsAnd The Swiss Society OfMedical GeneticsCombined Meeting 2017march 29, 2017 - March 31, 2017 bochum , Germany.

Pharmacogenomics - American Medical Association;Associate Principal Scientist Clinical Pharmacogenetics;European Society of Pharmacogenomics and Personalised Therapy;Genome-wide association studies in pharmacogenomics.

Track 7:Molecular Genetic Pathology

Molecular genetic pathologyis an emerging discipline withinthe pathologywhich is focused in the study and diagnosis of disease through examination of molecules within the organs, tissues or body fluids. A key consideration is more accurate diagnosis is possible when the diagnosis is based on both morphologic changes in tissuestraditional anatomic pathologyand onmolecular testing. Molecular Genetic Pathology is commonly used in diagnosis of cancer and infectious diseases. Integration of "molecular pathology" and "epidemiology" led tointerdisciplinaryfield, termed "molecular pathological epidemiology" (MPE),which representsintegrative molecular biologicand population health science.

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8th World Congress OnMolecular Pathology, June 26-27, 2017 San Diego, USA; 11th International Conference OnSurgical Pathology& Practice, March 27-28, 2017, Madrid, Spain; 13th EuropeanPathologyCongress, Aug 02-03, 2017, Milan, Italy; Embl Conference:Mammalian GeneticsAndGenomics, Heidelberg, Germany, October 24, 2017; Embo|Embl Symposium: TheMobile Genome: Genetic And Physiological Impacts Of Transposable Elements, Heidelberg, Germany, October 10, 2017.

Clinical Pathology Associates Molecular Pathology; Association mapping Wikipedia;Association for Molecular Pathology(AMP);Molecular Pathology - Association of Clinical Pathologists;SELECTBIO - Molecular Pathology Association of India.

Track 8:Gene Mapping

Genomemappingis to place a collection of molecular markers onto their respective positions ongenome.Molecular markerscome in all forms. Genes can be viewed as one special type of genetic markers in construction ofgenome maps, and the map is mapped the same way as any other markers. The quality ofgenetic mapsis largely dependent upon the two factors, the number of genetic markers on the map and the size of themapping population. The two factors are interlinked, and as larger mapping population could increase the "resolution" of the maps and prevent the map being "saturated". Researchers begin a genetic map by collecting samples of blood or tissue from family members that carry a prominent disease or trait and family members that don't. Scientists then isolate DNA from the samples and closely examine it, looking for unique patterns in the DNA of the family members who do carry the disease that the DNA of those who don't carry the disease don't have. These unique molecular patterns in the DNA are referred to as polymorphisms, or markers.

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3rd WorldBio Summit&Expo, Abu Dhabi, UAE, June 19-21, 2017; 9th International Conference onGenomicsandPharmacogenomicsJune 15-16, 2017 London, Uk; Keystone Symposium: Mononuclear Phagocytes in Health,Immune DefenseandDisease, 304 May 2017, Austin, Texas, USA;Molecular Neurodegeneration(course) Hinxton, Cambridge, UK, January 9-14, 2017;

Association for Clinical Genetic Science;Genome-wide association study Wikipedia;Gene mapping by linkage and association analysis NCBI;Gene mapping by linkage and association analysis | Springer Link.

Track 9:ComputationalGenomics

Computational genomics refers to the use of computational and statistical analysis to decipherbiologyfromgenome sequencesand related data, including DNA and RNA sequence as well as other "post-genomic" data. This computational genomics is also known asComputational Genetics. These, in combination with computational and statistical approaches to understanding the function of the genes and statistical association analysis, this field is also often referred to as Computational and Statistical Genetics/genomics. As such, computational genomics may be regarded as a subset of bioinformatics and computational biology, but with a focus on using whole genomes rather than individual genes to understand the principles of how the DNA of a species controls its biology at the molecular level and beyond. With the current abundance of massive biological datasets, computational studies have become one of the most important means to biological discovery.The field is defined and includes foundations in thecomputer sciences,applied mathematics, animation, biochemistry, chemistry, biophysics,molecular genetics,neuroscienceandvisualization. Computational biology is different from biological computation, which is a subfield of computer engineering using bioengineering and biology to build computers, but is similar tobioinformatics.

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Modeling Viral Infections and Immunity,10. MAY 2017, 14, Estes Park, Colorado, USA;Integrating Metabolism and Immunity(E4)292 June, Dublin, Ireland; EMBL Conference:Mammalian GeneticsandGenomics, Heidelberg, Germany, October 24, 2017; EMBO|EMBL Symposium: The Mobile Genome:GeneticandPhysiological Impacts of Transposable Elements, Heidelberg, Germany, October 10, 2017;

American Association of Bio analysts - Molecular/Genetic Testing;ISCB - International Society for Computational Biology;International Society for Computational Biology Wikipedia;Bioinformatics societies OMICtools;Towards an Australian Bioinformatics Society.

Track 10:Molecular Biotechnology

Molecular Biotechnologyis the use of living systems and organisms to develop or to make products, or "any technological application that uses the biological systems, living organisms or derivatives, to make or modify products or processes for specific use. Molecular biotechnology results from the convergence of many areas of research, such as molecular biology, microbiology, biochemistry, immunology, genetics and cell biology. It is an exciting field fueled by the ability to transfer genetic information between organisms with the goal of understanding important biological processes or creating a useful product. The completion of the human genome project has opened a myriad of opportunities to create new medicines and treatments, as well as approaches to improve existing medicines. Molecular biotechnology is a rapidly changing and dynamic field. As the pace of advances accelerates, its influence will increase. The importance and impact of molecular biotechnology is being felt across the nation. Depending on the tools and applications, it often overlaps with the related fields of bioengineering,biomedical engineering, bio manufacturing andmolecular engineering.Biotechnologyalso writes on the pure biological sciences animalcell culture, biochemistry,cell biology, embryology, genetics, microbiology, andmolecular biology.

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8th EuropeanImmunologyConference, June 29-July 01, 2017 Madrid, Spain; World Congress onBio therapeutics, May 22-23, 2017, Mexico City, Mexico;Human Genome Meeting(HGM 2017), February 5-7 2017, Barcelona, Spain;Integrating MetabolismandImmunity (E4), 292 June, Dublin, Ireland.

Biotech Associations - Stanford University;Indian Society of Genetics, Biotechnology Research & Development;Genetics and Molecular Medicine - American Medical Association;Genetics Society of America | GSA, British Society for Genetic Medicine;Heritability in the Era of Molecular Genetics - Association for Psychological science.

Track 11:Genetic Transformation

Genetic Transformationis the genetic alteration of cell resulting from the direct uptake and incorporation ofexogenous genetic materialfrom its surroundings through thecell membrane. Transformation is one of three processes for horizontal gene transfer, in which exogenous genetic material passes from bacterium to another, the other two being conjugation transfer of genetic material between two bacterial cells in direct contact andTransductioninjection offoreign DNAby a bacteriophage virus into thehost bacterium. And about 80 species of bacteria were known to be capable of transformation, in 2014, about evenly divided betweenGram-positiveandGram-negative Transformation" may also be used to describe the insertion of new genetic material into non-bacterial cells, including animal and plant cells.

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13th EuropeanPathologyCongress, Milan, Italy; Embl Conference:Mammalian GeneticsAndGenomics, Heidelberg, Germany, October 24, 2017; Embo|Embl Symposium: TheMobile Genome: Genetic And Physiological Impacts Of Transposable Elements, Heidelberg, Germany, October 10, 2017; 2nd World Congress onHuman Genetics&Genetic Disorders, November 02-03, 2017 Toronto, Canada; 9th International Conference onGenomicsandPharmacogenomics, June 15-16, 2017 London, Uk;

American Society of Gene & Cell Therapy: ASGCT;Gene Therapy Societies and Patient Organizations - Gene Therapy Net;European Society of Gene and Cell Therapy (ESGCT);British Society for Gene and Cell Therapy;Gene Therapy - American Medical Association.

Track 12:Genetic Screening

Genetic screenis an experimental technique used to identify and select the individuals who possess a phenotype of interest inmutagenized population. A genetic screen is a type ofphenotypic screen. Genetic screen can provide important information on gene function as well as the molecular events that underlie a biological process or pathway. While thegenome projectshave identified an extensive inventory of genes in many different organisms, genetic screens can provide valuable insight as to how thosegenes function.

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13th EuropeanPathologyCongress, Aug 02-03, 2017, Milan, Italy; 2nd World Congress onHuman Genetics&Genetic Disorders, November 02-03, 2017 Toronto, 27 Canada; 7th International Conference onPlant Genomics, July 03-05, 2017, Bangkok, Thailand; Embl Conference:Mammalian GeneticsAndGenomics, Heidelberg, Germany, October 24, 2017; Embo|Embl Symposium: TheMobile Genome: Genetic And Physiological Impacts Of Transposable Elements, Heidelberg, Germany, October 10, 2017, 10 - 13 May 2017, American Society ofGeneandCell Therapy(ASGCT) 20th Annual Meeting, Washington, DC;

Association for Clinical Genetic Science; Association for Molecular Pathology (AMP);Mapping heritability and molecular genetic associations with cortical;Genetics and Molecular Medicine - American Medical Association.

Track 13:Regulation of Gene Expression

Regulation of Gene expressionincludes a wide range of mechanisms that are used by cells to increase or decrease the production of specific gene products (protein or RNA), and is informally termed gene regulation. Sophisticated programs of gene expression are widely observed in biology, Virtually any step of gene expression can be modulated, fromtranscriptional initiation,RNA processing, and post-translational modificationof a protein. Often, one gene regulator controls another in a gene regulatory network. Any step of gene expression may be modulated, from theDNA-RNA transcriptionstep to post-translational modification of a protein.

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7th International Conference onPlant Genomics, July 03-05, 2017, Bangkok, Thailand; EMBO|EMBL Symposium: The Mobile Genome:GeneticandPhysiological Impacts of Transposable Elements, Heidelberg, Germany, October 10, 2017; 10. MAY 2017, 14, Estes Park, Colorado, USA,Modeling Viral Infections and Immunity; 292 June, Dublin, Ireland,Integrating Metabolism and Immunity(E4); MAY 2017, 14, Estes Park, Colorado, USA,Modeling Viral InfectionsandImmunity; 8th EuropeanImmunologyConference, June 29-July 01, 2017 Madrid, Spain; 9th International Conference onGenomicsandPharmacogenomics, June 15-16, 2017 London, Uk;

Gene Therapy Societies and Patient Organizations - Gene Therapy Net;European Society of Gene and Cell Therapy (ESGCT);British Society for Gene and Cell Therapy;Gene Therapy - American Medical Association

Track 14: Cancer Gene Therapy

Cancer is an abnormal growth of cells the proximate cause of which is an imbalance in cell proliferation and death breaking-through the normal physiological checks and balances system and the ultimate cause of which are one or more of a variety of gene alterations. These alterations can be structural, e.g., mutations, insertions, deletions, amplifications, fusions and translocations, or functional (heritable changes without changes in nucleotide sequence). No single genomic change is found in all cancers and multiple changes (heterogeneity) are commonly found in each cancer generally independent of histology. In healthy adults, the immune system may recognize and kill the cancer cells or allow non-detrimental host-cancer equilibrium; unfortunately, cancer cells can sometimes escape the immune system resulting in expansion and spread of these cancer cells leading to serious life threatening disease. Approaches to cancer gene therapy include three main strategies: the insertion of a normal gene into cancer cells to replace a mutated (or otherwise altered) gene, genetic modification to silence a mutated gene, and genetic approaches to directly kill the cancer cells. Pathway C represents immunotherapy using altered immune cells. Another unique immunotherapy strategy facilitated by gene therapy is to directly alter the patient's immune system in order to sensitize it to the cancer cells. One approach uses mononuclear circulating blood cells or bone marrow gathered from the patient.

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8th EuropeanImmunologyConference, June 29-July 01, 2017 Madrid, Spain; World Congress onBio therapeutics, May 22-23, 2017, Mexico City, Mexico;Human Genome Meeting(HGM 2017), February 5-7 2017, Barcelona, Spain;Integrating MetabolismandImmunity (E4), 292 June, Dublin, Ireland.

Biotech Associations - Stanford University;Indian Society of Genetics, Biotechnology Research & Development;Genetics and Molecular Medicine - American Medical Association;Genetics Society of America | GSA, British Society for Genetic Medicine;Heritability in the Era of Molecular Genetics - Association for Psychological science.

Track 15:Genetic Transplantation

Transplantation genetics is the field of biology and medicine relating to the genes that govern the acceptance or rejection of a transplant. The most important genes deciding the fate of a transplanted cell, tissue, or organ belong to what is termed the MHC (the major histocompatibility complex). Genetic Transplantation is the moving of an organ from one body to another or from a donor site to another location on the person's own body, to replace the recipient's damaged or absent organ. Organs and/or tissues that aretransplantedwithin the same person's body are calledauto grafts. Transplants that are recently performed between two subjects of the same species are calledallografts. Allografts can either be from a living or cadaveric source Organs that can be transplanted are the heart, kidneys, liver, lungs, pancreas, intestine, and thymus. The kidneys are the most commonlytransplanted organs, followed by the liver and then the heart. The main function of the MHC antigens is peptide presentation to the immune system to help distinguish self from non-self. These antigens are called HLA (human leukocyte antigens). They consists of three regions: class I (HLA-A,B,Cw), class II (HLA-DR,DQ,DP) and class III (no HLA genes)

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8th World Congress onPharmacology, August 07-09, 2017 Paris, France; International Conference onClinicalandMolecular Genetics, Las Vegas, USA, April 24-26, 2017; Aug 02-03, 2017, 13th EuropeanPathologyCongress, Milan, Italy; Embl Conference:Mammalian GeneticsAndGenomics, Heidelberg, Germany, October 24, 2017; 7th International Conference onPlant Genomics, July 03-05, 2017, Bangkok, Thailand.

American society of Transplantation;American Society of Transplant Surgeons: ASTS; Patient associations. Donation and transplantation;American Society of Gene & Cell Therapy ASGCT;Gene Therapy Societies and Patient Organizations - Gene Therapy Net.

Track 16:Cytogenetics

Cytogeneticsis a branch ofgeneticsthat is concerned withstudy of the structure and function of the cell, especially thechromosomes. It includes routine analysis of G-banded chromosomes, othercytogenetic banding techniques, as well as molecular Cytogenetics such as fluorescent in suitable hybridization FISH and comparativegenomic hybridization.

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9thAnnual Meeting onImmunologyandImmunologist, July 03-05, 2017 Kuala Lumpur, Malaysia; 8th MolecularImmunology&ImmunogeneticsCongress, March 20-21, 2017 Rome, Italy; 8th EuropeanImmunologyConference, June 29-July 01, 2017 Madrid, Spain; July 03-05, 2017; B Cells and T Follicular Helper Cells Controlling Long-Lived Immunity (D2), April 2017, 2327, Whistler, British Columbia, Canada.

European Cytogeneticists Association;Association of Genetic Technologists;Association for Clinical Genetic Science;Cytogenetics - Human Genetics Society of Australasia;European Cytogeneticists Association

Molecular Biology 2016

Molecular Biology 2016 Report

2ndWorld Bio Summit & Molecular Biology Expowas organized during October 10-12, 2016 at Dubai, UAE. The conference was marked with the attendance ofEditorial Board Members of supporting journals, Scientists, young and brilliant researchers, business delegates and talented student communities representing more than 25 countries, who made this conference fruitful and productive.

This conference was based on the theme Recent advances in Bio Science which included the following scientific tracks:

Molecular Biology

Microbiology

Analytical Molecular Biology

Bioinformatics

Biochemistry and Molecular Biology

Molecular Biology and Biotechnology

Cancer Molecular Biology

Computational Biology

Molecular Biology of the Cell

Molecular biology of the cardiovascular system

Molecular Biology in Cellular Pathology

Molecular Biology of Diabetes

Molecular Biology and Genetic Engineering

Enzymology and Molecular Biology

Molecular Biology of the Gene

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Molecular Genetics - Cell and Gene Therapy Conferences