Monthly Archives: May 2017

Here’s Why Editas Medicine Fell as Much as 15.7% Today – Madison.com

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Shares of gene editing pioneer Editas Medicine (NASDAQ: EDIT) dropped nearly 16% today after a new study published in Nature Methods drew attention to unintended effects of using the highly touted genetic engineering tool known as CRISPR. Shares of genome-editing peers CRISPR Therapeutics (NASDAQ: CRSP) and Intellia Therapeutics (NASDAQ: NTLA) were down as much as 6.9% and 14.9%, respectively, on the news.

The study, conducted by a team from Columbia University Medical Center, provided data showing that the technology can "introduce hundreds of unintended mutations into the genome," according to Genetic Engineering & Biotechnology News. That contradicts one of the better-known characteristics of CRISPR: precision.

Simply put, it's not sitting well with investors, who are (in knee-jerk fashion) adjusting the value placed on early-stage platforms, especially Editas Medicine, which will be the first of the group to enter clinical trials. As of 3:31 p.m. EDT, the stock had settled to a 11.3% loss.

Image source: Getty Images.

The study is among the first to quantify the specificity of CRISPR tools, which work by delivering gene editing enzymes to specific parts of the genome through the use of synthetic guide RNAs. Or that's how they're supposed to work. The authors of the study show that although intended edits can be made with respectable efficiency, such as correcting a mutation in a gene that causes blindness in mice, there are also unintended secondary edits made to the genome.

This may seem like a bombshell report, but it's a matter of optics. Researchers have never shied away from the reality that CRISPR gene editing tools can stray off target and make unintended edits to genomes in mammalian cells (i.e., humans). Many labs -- including Editas Medicine, CRISPR Therapeutics, and Intellia Therapeutics -- are working on increasing the efficiency and specificity of the technology. This is how science works. By quantifying these off-target mutations, which the paper attempted to do, researchers can begin to better understand how to improve the technology.

Investors and traders did not take the same cool-headed approach to the news, instead giving into a knee-jerk reaction to adjust the value of each pre-clinical technology platform. While off-target edits could prove troublesome for a CRISPR therapeutic used in humans, it's important to remember that there are currently no clinical trials underway in the United States. Editas Medicine will become the first to initiate a clinical trial later this year.

The sharp contrasts in reactions from researchers and investors is likely driven by how CRISPR is perceived by the media. Unfortunately, there is a generous amount of hyped-up science journalism that sticks to simple narratives -- "CRISPR has arrived and will cure all diseases!" -- instead of more nuanced takes that give equal weight to each current obstacles and future potential facing an emerging technology. Just remember: Biology is never quite so simple.

The results from the study don't really change anything, except for bringing more attention to the already existent clinical risk inherent to the development of early-stage CRISPR therapeutics. There is still plenty of work and new technology left to be developed before gene editing fulfills its promise in treating and curing human diseases. Hopefully, this can be a long-term positive for investors in CRISPR stocks by forcing them to listen to the fundamental hurdles for the technology. Hopefully.

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Here's Why Editas Medicine Fell as Much as 15.7% Today - Madison.com

Researchers make breakthrough discovery in fight against bowel cancer – Medical Xpress

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May 31, 2017 Professor Mark Lawler, Queen's University Belfast. Credit: Queen's University Belfast

New research led by Queen's University Belfast has discovered how a genomic approach to understanding bowel (colorectal) cancer could improve the prognosis and quality of life for patients.

For clinicians, treating patients with bowel cancer can be particularly challenging. Professor Mark Lawler, Chair in Translational Genomics, Centre for Cancer Research and Cell Biology at Queen's and joint Senior Author on the study explains: "Currently patients with colorectal cancer are offered chemotherapy treatment. While this treatment may be successful for some patients, for others it will have no effect on fighting the cancer, though the patients may suffer debilitating side effects such as nerve damage that can result in a loss of sensation or movement in a part of the body. A 'one size fits all' approach isn't a viable option if we are to effectively tackle this disease."

Researchers at Queen's, in collaboration with the University of Oxford and the University of Leeds have made a significant advance in the treatment of bowel cancer. The study, which has been published in the high impact journal Nature Communications, has shown how defining precise gene signatures within bowel cancer cells can allow us to develop novel prognostic and predictive markers for bowel cancer and help to drive personalised medicine approaches.

Dr Philip Dunne, Senior Research Fellow at Queen's said: "Through analysing the molecular and genetic data generated from patient tissue samples, we have discovered that there are different subtypes of bowel cancer. This research unequivocally identifies robust gene signatures that can be used to inform patient management. It will allow us to identify particular gene signatures that indicate sensitivity or resistance to specific therapies. Thus, we can tailor treatment to the individual patient, maximising its effectiveness while minimising potential side effects."

Dr Catherine Pickworth, science information officer at Cancer Research UK, a funder of the study, added: "Personalised medicine aims to give the best treatment to each patient, sparing people unnecessary therapy if it won't help.

"This study is a step forward in achieving this, giving us genetic signatures to look out for in bowel cancer patients. The next steps will be to find out which treatment works best for each genetic signatures so that cancer treatments can be tailored to each patient, so they have the best chance of beating cancer."

Bowel cancer is the fourth most common cancer in the UK, with 41,200 people newly diagnosed each year. A number of treatment options are available but mortality rates remain high, with bowel cancer the second most common cause of cancer death in the UK.

This research was performed as part of Stratified Medicine in Colorectal Cancer (S:CORT), an MRC-Cancer Research UK funded stratified medicine consortium, bringing together the best of UK science and clinical care in bowel cancer to develop personalised medicine treatment approaches in this common malignancy.

S:CORT involves key partnerships with patients and patient advocacy groups. Ed Goodall, a survivor of bowel cancer and a member of S:CORT explains: "In the past, a tumour was a tumour. Patients are offered chemotherapy and this may not be effective or necessary depending on the patient yet they will still endure all the horrors this treatment can cause including nausea and hair loss.

"If the oncologist knows more about the subtype of bowel cancer, they will know whether the treatment will be necessary or effective. From a patient point of view, discovering the subtypes of this cancer is really ground breaking work because it will have massive implications for patient care and treatment."

Professor Tim Maughan, Professor of Clinical Oncology at the University of Oxford and Principal Lead of the S:CORT Consortium said: "This research emphasises how a collaborative approach can give significant insight into bowel cancer disease biology, but also to begin to translate this knowledge into clinically-relevant applications. As part of the work of the S:CORT consortium, we will now focus on making sure that the research is put into practice so that it can become part of the standard of care for patients."

Deborah Alsina MBE, Chief Executive of Bowel Cancer UK, the UK's leading bowel cancer research charity and a partner in S:CORT said: "This important study highlights how increasing our understanding of what makes normal cells go wrong is key to developing new approaches that can improve outcomes for patients. With nearly 16,000 people dying from bowel cancer each year, it is essential that we increase our understanding of what drives the disease and then improve and extend the range of treatment options available. The results of this study take us a step closer to achieving this."

Explore further: Researcher finds key to drug resistant bowel cancer

More information: Nature Communications (2017). DOI: 10.1038/NCOMMS15657

Blocking a molecule could bypass bowel cancer's defence against the drug cetuximab, according to new research presented at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool.

A new test could help patients with advanced bowel cancer get the best treatment for their disease, according to a Cancer Research UK clinical trial published today in JAMA Oncology.

A new study that combines genetic information on bowel cancer with NHS patient outcome data has found a link between family history of the disease and a better chance of survival, published in the British Journal of Cancer.

Researchers at Queen's University have made a significant breakthrough that may benefit patients with bowel cancer.

Manchester researchers have provided early evidence to suggest that a blood test could be used to identify bowel cancer patients that may benefit from more intensive chemotherapy.

Up to a quarter of patients with bowel cancer who have a family history of the disease could have the causes of their cancer identified through gene testing, a new study reports.

New research led by Queen's University Belfast has discovered how a genomic approach to understanding bowel (colorectal) cancer could improve the prognosis and quality of life for patients.

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Researchers make breakthrough discovery in fight against bowel cancer - Medical Xpress

CRISPR gene editing can cause hundreds of unintended mutations – Phys.Org

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May 29, 2017 CRISPR-associated protein Cas9 (white) from Staphylococcus aureus based on Protein Database ID 5AXW. Credit: Thomas Splettstoesser (Wikipedia, CC BY-SA 4.0)

As CRISPR-Cas9 starts to move into clinical trials, a new study published in Nature Methods has found that the gene-editing technology can introduce hundreds of unintended mutations into the genome.

"We feel it's critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR, including single nucleotide mutations and mutations in non-coding regions of the genome," says co-author Stephen Tsang, MD, PhD, the Laszlo T. Bito Associate Professor of Ophthalmology and associate professor of pathology and cell biology at Columbia University Medical Center and in Columbia's Institute of Genomic Medicine and the Institute of Human Nutrition.

CRISPR-Cas9 editing technologyby virtue of its speed and unprecedented precisionhas been a boon for scientists trying to understand the role of genes in disease. The technique has also raised hope for more powerful gene therapies that can delete or repair flawed genes, not just add new genes.

The first clinical trial to deploy CRISPR is now underway in China, and a U.S. trial is slated to start next year. But even though CRISPR can precisely target specific stretches of DNA, it sometimes hits other parts of the genome. Most studies that search for these off-target mutations use computer algorithms to identify areas most likely to be affected and then examine those areas for deletions and insertions.

"These predictive algorithms seem to do a good job when CRISPR is performed in cells or tissues in a dish, but whole genome sequencing has not been employed to look for all off-target effects in living animals," says co-author Alexander Bassuk, MD, PhD, professor of pediatrics at the University of Iowa.

In the new study, the researchers sequenced the entire genome of mice that had undergone CRISPR gene editing in the team's previous study and looked for all mutations, including those that only altered a single nucleotide.

The researchers determined that CRISPR had successfully corrected a gene that causes blindness, but Kellie Schaefer, a PhD student in the lab of Vinit Mahajan, MD, PhD, associate professor of ophthalmology at Stanford University, and co-author of the study, found that the genomes of two independent gene therapy recipients had sustained more than 1,500 single-nucleotide mutations and more than 100 larger deletions and insertions. None of these DNA mutations were predicted by computer algorithms that are widely used by researchers to look for off-target effects.

"Researchers who aren't using whole genome sequencing to find off-target effects may be missing potentially important mutations," Dr. Tsang says. "Even a single nucleotide change can have a huge impact."

Dr. Bassuk says the researchers didn't notice anything obviously wrong with their animals. "We're still upbeat about CRISPR," says Dr. Mahajan. "We're physicians, and we know that every new therapy has some potential side effectsbut we need to be aware of what they are."

Researchers are currently working to improve the components of the CRISPR systemits gene-cutting enzyme and the RNA that guides the enzyme to the right geneto increase the efficiency of editing.

"We hope our findings will encourage others to use whole-genome sequencing as a method to determine all the off-target effects of their CRISPR techniques and study different versions for the safest, most accurate editing," Dr. Tsang says.

The paper is titled, "Unexpected mutations after CRISPR-Cas9 editing in vivo." Additional authors are Kellie A. Schafer (Stanford University), Wen-Hsuan Wu (Columbia University Medical Center), and Diana G. Colgan (Iowa).

Explore further: Accurate DNA misspelling correction method

More information: Unexpected mutations after CRISPR-Cas9 editing in vivo, Nature Methods (2017).

Researchers at the Institute of Basic Science (IBS) proved the accuracy of a recently developed gene editing method. This works as "DNA scissors" designed to identify and substitute just one nucleotide among the 3 billion. ...

A team from the Center for Genome Engineering, within the Institute for Basic Research (IBS), succeeded in editing two genes that contribute to the fat contents of soybean oil using the new CRISPR-Cpf1 technology: an alternative ...

Researchers from Memorial Sloan Kettering Cancer Center (MSK) have harnessed the power of CRISPR/Cas9 to create more-potent chimeric antigen receptor (CAR) T cells that enhance tumor rejection in mice. The unexpected findings, ...

The IBS research team (Center for Genome Engineering) has successfully confirmed that CRISPR-Cas9 has accurate on-target effects in human cells, through joint research with the Seoul National University College of Medicine ...

A team of researchers at Western University is playing with molecular-Lego by adding an engineered enzyme to the revolutionary new gene-editing tool, CRISPR/Cas9. Their study, published today in the Proceedings of the National ...

Using the new gene-editing enzyme CRISPR-Cpf1, researchers at UT Southwestern Medical Center have successfully corrected Duchenne muscular dystrophy in human cells and mice in the lab.

An ancient sea creature, discovered off the coast of Scotland in 2011, has shed new light on how evolution formed the modern brain.

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Biologists have always been fascinated by the diversity and changeability of life on Earth and have attempted to answer a fundamental question: How do new species originate?

With prices down and weather patterns unpredictable, these are tough times for America's cotton farmers, but new research led by Z. Jeffrey Chen at The University of Texas at Austin might offer a break for the industry. He ...

From Charles Darwin's famous finches to a new study that takes a rare look at a common order of birdswaterfowlevolution has a tendency to reveals itself through bird beaks.

Researchers have identified key genes associated with flowering time in the pigeon pea, a finding that could lead to more productive plants for this important source of protein.

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If a person has 3 months to live and they use crispr/cas9 to cure the cancer, and it works, what is the worst than can happen to him?

I'm not a biologist, so no idea how conceivable or absurd that idea might be. But then there's the whole thing with the Tasmanian devils. Anyway, you asked about worst cases, and that is one possible thing that people who are against this might be thinking.

Open a door, find 12 new doors. Like the knowledge that carbon nanos caused cancer but the powers-that-be decided we should use it any way because it was so convenient.

We are so screwed! This is worse than the advent of nuclear weapons.

this might cause regulated interests to think twice before deploying this for profit. It will not help us at all against weaponized CRISPR, though...

Crispr is the only way the human race will survive. Without it the machines rule. With crispr the human race increases everyone's IQ 10 fold. The vary smartest of us say "be very afraid of AI". Musk likened AI to a devil in a bottle. It's the 2nd level of our most brilliant people that can't see the danger AI poses. Raise everyone's IQ by 10X and we will make much better decisions and solve the current world's problems overnight.

Meatbrains are passe which is why we are so intent on replacing them.

Watch Forbidden Planet to see what happens when you mix intelligence with the need to survive to procreate.

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

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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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A Fresno staffer finds his way from business to high school chemistry teacher – EdSource

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Patrick Jensen happily teachers high school chemistry after a 20 year career in business.

Patrick Jensen happily teachers high school chemistry after a 20 year career in business.

Patrick Jensen, 41, took a 50 percent pay cut to teachchemistry and web development in the Fresno Unified School District.

After working for 20 years as a fiscal analyst, mutual fund accountant and school district business chief, he decided a great career isnt always about money.

In my old job, I felt like I was pushing a lot of paperwork around but not making much of a difference. He said. I wanted to do something more directly connected to kids, have more of an impact on my community.

Last year, Jensen quit his job and enrolled in a teacher intern credential program at Fresno State. After taking an intense summer course, he started at Patino High School, a newly-opened, business-themed school in Fresno. Weekends and nights he takes teacher preparation classes, and works closely with colleagues and mentor teachers.

He had never volunteered in a classroom, and his mastery of chemistry dated from his years as an undergraduate. But overall, his first months in the classroom went very smoothly, thanks to colleagues support. He has no regrets.

The toughest part, he said, was getting used to teenagers. Until he started teaching, most of his experience with kids was from raising his own. Understanding teenagers and keeping them engaged was a little more challenging than he expected.

If youre not used to teenagers, its hard to know how much freedom to give them, where to draw the line, when are you being too strict, he said. You can have a great career and be an expert in something, but you might not know how to teach. You have to have the humility and openness to ask for help.

He encourages other mid-career professionals in science and math to consider teaching if theyre looking for a change, have the support of their families and dont mind a few years of sacrifice in exchange for long-term job stability, summers off and the rewards of educating young people.

When youre teaching, you see these moments of growth with the kids, when they suddenly grasp a concept they previously didnt understand . Those moments make it all worth it, he said. And if it turns out you dont like teaching, you can always go back to that boring office job. Those jobs will always be there.

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A Fresno staffer finds his way from business to high school chemistry teacher - EdSource

Public donations sought for career returners’ chemistry fellowship – Chemistry World (subscription)

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The University of Oxford is asking the public for donations to support a new chemistry fellowship that will be awarded to someone returning to research after a career break.

The Dorothy Hodgkin fellowship named after the x-ray crystallographer and chemistry Nobel laureate who was the first woman at the university to receive maternity pay aims to help address the leaky pipeline of women leaving academia. The initial goal is to fund a five-year research post in the universitys chemistry department as well as a stipendiary lecturer to cover teaching.

The crowdfunding campaign is a joint enterprise between the universitys chemistry department and Somerville College, where Hodgkin was a fellow.

So far it has raised more than 162,000 of the 500,000 target. When the total reaches 196,500 it will be matched by a group of four anonymous donors. Eventually, the project hopes to raise enough money to ensure a continuous stream of fellows returning to chemistry.

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Public donations sought for career returners' chemistry fellowship - Chemistry World (subscription)

Miami Dolphins safeties Reshad Jones, Nate Allen aim for ‘beautiful thing’ called chemistry – Palm Beach Post (blog)

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Dolphins S Reshad Jones played only six games before injuring his shoulder last season. (Allen Eyestone/The Post)

DAVIE The chemistry with fellow safety Reshad Jones isnt what it needs to be, but its coming along, Nate Allen was saying. There was no panic in his voice because, after all, this is only May.

This is what OTAs are for, said Allen, who joined the Dolphins in free agency from Oakland.

Only a few minutes earlier Tuesday, Jones addressed the media and was equally calm about one of the more pressing matters concerning the Dolphins defense, but for one other reason: He has been through this before.

If its the offseason, theres a good chance the Dolphins are sorting out wholl be lining up alongside Jones at safety. Except for a brief spell of continuity with Chris Clemons early in his career, Jones has been on an endless quest to develop chemistry with safeties ranging from Louis Delmas to Jimmy Wilson to Michael Thomas, to name a few.

I know I had a lot, Jones said. But I didnt know it was eight.

Dolphins safety Nate Allen listens to a question during a news conference during OTAs on Tuesday. (AP Photo/Wilfredo Lee)

Injuries have played a huge role, wiping out both Jones and Isa Abdul-Quddus last year and ending Abdul-Quddus career.

That left an opening. In stepped Allen, who was taken 126 spots earlier than Jones in the 2010 draft, which is a blessing of sorts for the Dolphins. Playing the same position and having entered the league at the same time, theyve kept tabs on one another from afar.

We came out together, so I kind of knew him, Jones said. He knows ball.

Allen also knows Jones.

His play speaks for itself, Allen said. Hes who he is for a reason and hes the guy. He makes a lot of plays. Hes just a great playmaker. I could see it early and Ive watched him through the years. As Ive been in other places, Ive always watched him on tape. He stands out.

Jones made the Pro Bowl in 2015 and stood a good chance of repeating last season before a shoulder injury ended his season. From the sidelines, he watched his team qualify for the playoffs for the first time since he arrived.

It was kind of brutal for me, but I was happy for my guys, he said.

Having recently gained full medical clearance, Jones is confident hell regain top form.

I always felt like I was one of the best safeties in the league and I still feel that way, Jones said. Numbers dont lie. My numbers are top of the line of all of them.

Allen, who signed a one-year, $3.4 million deal, also believes hes 100 percent after suffering an MCL injury early in 2015 and serving as a backup with the Raiders last season. Allen said he feels comfortable, whether its at strong safety or free safety, in coverage or run support. Its largely a matter of developing an understanding with Jones.

I think were making good progress, Allen said. And its not just me and Reshad. Its the entire DB group. This is the first time Ive played with these guys and the first time a lot of us have played together, so everybodys just kind of feeling each other out.

Because once you get that chemistry in the back end, you can make it a beautiful thing.

The question is, how long will this tandem last? The Dolphins also added safety T.J. McDonald from the Rams, but hell miss the first half of the season for violating the leagues substance abuse policy.

I think we can be special, Jones said. Weve got the ball rolling in the right direction. We just have to continue to put the work in and make it happen.

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Royal Bank of Canada Boosts Puma Biotechnology Inc (PBYI) Price Target to $60.00 – The Cerbat Gem

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Chaffey Breeze
Royal Bank of Canada Boosts Puma Biotechnology Inc (PBYI) Price Target to $60.00
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Puma Biotechnology Inc logo Puma Biotechnology Inc (NYSE:PBYI) had its price objective lifted by Royal Bank of Canada from $40.00 to $60.00 in a report published on Thursday. The brokerage currently has a sector perform rating on the biopharmaceutical ...
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Royal Bank of Canada Boosts Puma Biotechnology Inc (PBYI) Price Target to $60.00 - The Cerbat Gem

Form 8-K PUMA BIOTECHNOLOGY, INC. For: May 24 – StreetInsider.com

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UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, DC 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section13 or 15(d)

of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): May30, 2017 (May 24, 2017)

PUMA BIOTECHNOLOGY, INC.

(Exact Name of Registrant as Specified in its Charter)

10880 Wilshire Boulevard, Suite 2150

Los Angeles, California 90024

(Address of principal executive offices) (Zip Code)

(424) 248-6500

(Registrants telephone number, including area code)

N/A

(Former name or former address, if changed since last report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (240.12b-2 of this chapter).

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.

On May24, 2017, Puma Biotechnology, Inc. (the Company) announced that the U.S. Food and Drug Administrations (FDA) Oncologic Drugs Advisory Committee (ODAC) voted 12 to 4 to recommend approval of PB272 (neratinib) for the extended adjuvant treatment of HER2-positive early stage breast cancer based on finding that the risk-benefit profile of neratinib is favorable. Neratinib is an investigational therapy for the extended adjuvant treatment of early stage HER2-positive breast cancer that has previously been treated with a trastuzumab containing regimen.

ODAC is an independent panel of experts that evaluates data concerning the efficacy and safety of marketed and investigational products for use in the treatment of cancer and makes appropriate recommendations to the FDA. Although the FDA will consider the recommendation of the panel, the final decision regarding the approval of the product is made by the FDA solely, and the recommendations by the panel are non-binding.

SIGNATURE

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

/s/ Alan H. Auerbach

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Form 8-K PUMA BIOTECHNOLOGY, INC. For: May 24 - StreetInsider.com

Everything from pirate games to bioengineering – Shanghai Daily (subscription)

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I applied for the trip because I thought it sounded enjoyable and exciting and I would be able to learn about new things. I most enjoyed Pirate Training, where we got to make cannons, take part in fencing and archery and play capture the flag in an ice rink.

These are things I never thought I would do. Meeting the other students from NAE was great because they all seemed very similar to me and that made me feel a lot more confident about myself. It was also good fun to make new friends from around the world who I can continue to connect with through Nord Anglias Global Classroom.

MIT was a huge university, if I went there Id worry about getting lost but it looked like a nice place to live and learn. The same can be said for Harvard, which we also really enjoyed spending time at and learning about. If youre lucky enough to be picked next year, be prepared to take part in a range of activities which will make you work hard both physically and mentally, and pack some comfortable shoes as the MIT and Harvard sites are big and we did a lot of walking in order to visit the different facilities!

Iwan Jones, Year 7 student

When I first saw the STEAM (science, technology, engineering, art and maths) festival being offered by BISS Puxi I thought it would be an awesome opportunity to see how MIT use their research to apply science to the real world, and I was excited about these subjects. I knew it would be a great chance to work with other students who shared similar interests and to speak to students studying at MIT.

The activity I enjoyed the most was Biobuilder. In this session we learnt about how, in the future, we will be able to take parts of cells, which perform a certain function, and build it to make a new cell.

The most interesting aspect is these cells can be designed so they can be controlled to complete certain tasks. We used different shapes and colors to represent these different functions, and built a cell that would kill only cancer cells. This is a lot harder in real life, as you would need to take the cell and find what the function is before fusing the different parts together.

It was really fun working with schools from around the world, and we all felt like one big school. It was very easy to make friends with everyone and we were very upset to leave each other on Friday.

This experience has inspired me to go to a school like MIT because of all the different fields in science and technology I can have the chance to experience if I studied there. Some advice Id give to a student who plans to go next year is to really throw yourself into every activity and to make the most of this experience.

Alison Ohene-Djan, Year 7 student

When I heard about the chance to go to MIT I was really excited and applied to attend as I was sure I would learn a lot and I might not get the chance to attend something like this again.

Once we arrived we met with the students from all of the other Nord Anglia schools; I enjoyed working with different people from different places because they all had other stories and ideas to share. The fun really started once we got to start on the STEAM activities, I cant single out one particular activity because each one was a unique experience and fun in their own way, although I did enjoy being a pirate. This trip has inspired me to continue to work on areas of STEAM, Ive had the interest of going to universities like MIT before, but this trip just made me even more motivated to work hard and be accepted into a place like MIT. The one piece of advice I would give to students who plan to attend next years trip is to not worry so much about remembering everything that will be taught to you, if you enjoy and focus on the activity, you will pick it up along the way.

Liam Chan, Year 7 student

I applied for the trip because it is a once in a lifetime experience at one of the best universities in the world. Also, we would meet students from Nord Anglia schools around the world.

My favorite part was the 2.009 workshop, where in groups of ten we designed, and actually created, carnival games which could be used in real carnivals. Working with Professor David Wallace was a real highlight. I enjoyed collaborating with other schools because people from all across the globe worked together and came up with so many ideas to try and give the best possible answer.

The trip has definitely inspired me to attend MIT or universities like MIT because they have really good facilities and the professors teach lessons in a very exciting and interesting way. Advice that I would give students going next year would be: when stuck on a problem, look at things from a different perspective. The answer is usually there, it just needs more thought to reach it.

Emma Tang, Year 7 student

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Peek into your genes: NASA one-year mission investigators identify links to vision problems – Phys.Org

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May 31, 2017 by Amy Blanchett Astronaut Scott Kelly opens a bag of assorted fruit (oranges, lemons, grapefruits) in the Node 2 module after being unpacked from the Kounotori H-II Transfer Vehicle 5 (HTV-5). Astronauts are pleased to discover fresh fruit and vegetables in cargo shipments to the International Space Station because sometimes due to delivery schedules, weight factors and accessibility of refrigeration on the station these type of foods are not always readily available. It is important for astronauts to consume vitamins and minerals in space to maintain their health. Credit: NASA

Healthy Vision Month, NASA's One-Year Mission investigators are peering into their new findings to help address astronaut vision issues. While the One-Year Mission has concluded for retired astronaut Scott Kelly, NASA's Human Research Program is focusing on comparing previous six-month mission findings to One-Year Mission preliminary findings.

Nutritional Biochemistry Lab lead Scott M. Smith, Ph.D., takes a broad look at biochemistry. He studies the astronaut diets along with protein, vitamin, mineral, and other chemicals in blood and urine to look for indicators of disease or other physiological changes. His team discovered that astronauts with vision issues had biochemical differences before ever leaving Earth as compared to astronauts without vision issues, and subsequently documented that this was evidence of a genetic predisposition for some astronauts to develop vision and eye issues. He thinks his team is on the path to help resolve vision issues for astronauts. This is an important finding as NASA prepares for a human journey to Mars.

Typically, physiologists and scientists study one system at a time, but nutrition is a cross-cutting science with impacts across systems biology. Smith emphasizes the importance of studying the human body holistically, which is why his team has led the effort to create a biochemical database making it more efficient to interface with other researchers, such as the 22 other One-Year Mission investigators.

Another investigator who works with Smith at NASA's Johnson Space Center is Michael Stenger, Ph.D. He is the Cardiovascular and Vision Lab lead and principal investigator for the Fluid Shifts investigation, which is an international experiment designed to determine the relationship between headward fluid shifts and ocular structural changes. Spaceflight Associated Neuro-ocular Syndrome, or SANS, is hypothesized to be caused by blood flow toward the head due to lack of gravity, resulting in changes to eye structure and possibly vision changes. This headward fluid shift may be responsible for vision changes, flattening of the eyeball and swelling of some tissues in the back of the eye and engorgement of the optic nerve sheath seen in approximately one out of three International Space Station astronauts.

The One-Year Mission was a great opportunity to see if vision changes occurring during six-month missions continued and worsened when the mission is extended to a year. Stenger could also see if astronauts who did not have vision issues at the six-month mark, developed them when extended to one year in space. The preliminary findings are a bit of both. One subject developed SANS early in the mission and had some symptoms worsen as the mission lengthened while another did not. The subject who did not experience SANS symptoms during the first six months of flight did start to show some changes near the end of his year in space, suggesting that length of time in space may impact the eye.

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Both Smith and Stenger are working together to solve eye and vision problems for astronauts. They agree their investigations are just scratching the surface and there is a lot of work that still needs to be done on the ground and in space to validate theories. While Scott Kelly returned to Earth in a healthy state, NASA continues to keep its vision focused on sending humans safely and effectively on a three-year journey to Mars.

Explore further: The 'eyes' have it: Astronaut vision and ophthalmologic problems explained

More information: Sara R. Zwart et al, Astronaut ophthalmic syndrome, The FASEB Journal (2017). DOI: 10.1096/fj.201700294

Journal reference: FASEB Journal

Provided by: NASA

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Everything We Know About Grey’s Anatomy Season 14 So Far … – TV Guide (blog)

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Now Playing Grey's Anatomy Season 14: Everything We Know So Far

We don't blame you if you're still recovering from the Grey's Anatomy Season 13 finale, but here at TVGuide.com, we've already got our eye on Season 14.

We know a few things about Season 14 for sure so far. First, Edwards (Jerrika Hinton) is gone for good given that Hinton has joined Alan Ball's upcoming HBO drama. Edwards' new lease on life unfortunately means an end to her life at Grey Sloan Memorial. We'll also almost certainly get a first look at the Grey's Anatomy firefighter spinoff before the new show launches in 2018.

As far as speculation goes, we're of the mind that we might be kissing Meredith (Ellen Pompeo) and Riggs' (Martin Henderson) relationship goodbye. Now that Owen's (Kevin McKidd) sister is back in the picture, we're getting serious deja vu from Season 2, when McDreamy (Patrick Dempsey) chose Meredith over his ex-wife Addison (Kate Walsh). It's a bit of a stretch to think she'll manage to pull that off again, no matter how great her relationship with Riggs is.

There's also a chance that Maggie's (Kelly McCreary) love life might take a "messy" turn according to TV Line. We're not sure how we'd feel about inserting Maggie into a love triangle with Jackson (Jesse Williams) and April (Sarah Drew) though, mostly because she deserves a win in the relationship department eventually.

Grey's Anatomy returns in the fall, and will air Thursdays at 8/7c on ABC.

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Grey’s Anatomy Ellen Pompeo Hamptons House Tour – People – PEOPLE.com

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Grey's Anatomy Ellen Pompeo Hamptons House Tour - People
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Ellen Pompeo's operations are usually restricted to the OR on Grey's Anatomy. But the actress found herself performing a surgery of sorts on her modern barn ...
Ellen Pompeo's Hamptons House | POPSUGAR HomePOPSUGAR
Ellen Pompeo's Sag Harbor Home Is a Modern Take on a Classic BarnArchitectural Digest

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Are These Two Of The New Characters In ‘Grey’s Anatomy’ Firefighter Spinoff? – moviepilot.com

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A few weeks ago, Grey's Anatomy fans were overjoyed to hear that Shonda Rhimes is expanding the Grey's universe with a spinoff series focusing on the personal and professional lives of Seattle's firefighters.

The yet-to-be-titled series is the second spinoff from Grey's Anatomy Private Practice ran from 2007 until 2013 and will be executive produced by both Rhimes and Betsy Beers. Long time #GreysAnatomy writer and producer, Stacy McKee, will act as showrunner.

But while we've been given details about the crew of what will no doubt become a popular series, the information about the characters of the series has been less forthcoming. However, one hint we have been given came during the Grey's Anatomy Season 13 finale, when the hospital required evacuation during the explosion.

As fans will remember, part of the hospital exploded after Stephanie's plan to set the rapist on fire went awry. With the hospital quickly burning, firefighters were soon on the scene to battle the flames and help rescue patients and doctors. Given the news about the firefighter spinoff series was announced shortly before the finale aired, it was implied that some of the firefighters from the Season 13 finale will appear in new series. So who did we see in Episode 13 that might crop again? Take a look:

We were first introduced to firefighter Carroll while announcements were being made on how the hospital buildings will be evacuated. Carroll later accompanied Ben inside to find Stephanie, and we learned she was actually the fire captain when she was called on to inspect the body of the rapist killed in the blast.

Given that Shonda Rhimes' series are so often led by strong female characters, it would be no surprise to see actor Stephanie Czajkowski return as firefighter Carroll in the new spinoff in a major role. When asked about the possibility of her character return, Czajkowski was unable to give a definite answer, though remarked that it would "be a dream come true to have Firefighter Carroll be a part of the expansion of Shondaland."

We briefly met firefighter Ben as he came across Meredith, Riggs and nurse Bohkee while Riggs was part way through a lobectomy. After first ordering the group to evacuate, he eventually gave them 15 minutes to close up the patient, and assured Meredith that the firefighters were all keeping an eye out for the missing Erin.

The actor who played firefighter Ben is Nelson Grande, a man who is no stranger to hospital dramas having already starred in General Hospital, but what's even more interesting is that Grande apparently studied Fire Science in college before dropping out to pursue his acting dream. Talk about a perfect role!

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Antibody Fights Fat, Fires up Metabolism – Anti Aging News

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Two international research teams have determined an antibody decreases fat while simultaneously boosting metabolism. Their studies involved mice yet it is believed the findings will also apply to humans. It is hoped that this breakthrough will help treat osteoporosis, obesity and a number of other conditions.

About FSH

It is known that a specific antibody targets follicle-stimulating hormones (FSH). These hormones increase when menopause occurs. Menopause is tied to a number of different health problems in women like the loss of bone density and an increase in weight gain. FSH is generated by the pituitary gland in mammals of both sexes. It spurs the growth of ovarian follicles in females and also regulates several reproductive processes. The antibody in question heightens bone mass, increases metabolism and decreases body fat in mice. It is believed that blocking FSH to counteract menopause symptoms will help treat conditions like cardiovascular disease, obesity, cancer, and osteoporosis.

About the Study

The two international research teams were supervised by Clifford J. Rosen, Li Sun, and Mone Zaidi. The teams performed their work at the Maine Medical Center Research Institute and the Icahn School of Medicine at Mount Sinai. They used a synthetic mouse antibody to key in on a 13-amino-acid sequence of a single subunit of FSH. The antibody was tested on female mice whose ovaries were removed. The removal of the ovaries caused high levels of FSH. The antibody was also tested on female and male mice that were provided with high-fat foods.

The Findings

In both instances, treatment using the antibody spurred fat loss and a faster metabolism. The results have intrigued scientists and medical professionals around the world. More extensive studies will be performed in the near future to determine if the findings are relevant to human health.

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Wright State spinoff closes on $680K in funding – Dayton Business Journal

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Wright State spinoff closes on $680K in funding
Dayton Business Journal
The company has closed on a $680,000 Seed B convertible note, which brings the total amount of seed funding it has raised to $845,000. This comes on top of the $2 million in grants it landed as part of the Kno.e.sis center at Wright State, thanks to ...

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Wright State spinoff closes on $680K in funding - Dayton Business Journal

Behavioral neuroscience – Wikipedia

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Behavioral neuroscience, also known as biological psychology,[1]biopsychology, or psychobiology[2] is the application of the principles of biology to the study of physiological, genetic, and developmental mechanisms of behavior in humans and other animals. [3]

Behavioral neuroscience as a scientific discipline emerged from a variety of scientific and philosophical traditions in the 18th and 19th centuries. In philosophy, people like Ren Descartes proposed physical models to explain animal and human behavior. Descartes, for example, suggested that the pineal gland, a midline unpaired structure in the brain of many organisms, was the point of contact between mind and body. Descartes also elaborated on a theory in which the pneumatics of bodily fluids could explain reflexes and other motor behavior. This theory was inspired by moving statues in a garden in Paris.[4]

Other philosophers also helped give birth to psychology. One of the earliest textbooks in the new field, The Principles of Psychology by William James, argues that the scientific study of psychology should be grounded in an understanding of biology:

Bodily experiences, therefore, and more particularly brain-experiences, must take a place amongst those conditions of the mental life of which Psychology need take account. The spiritualist and the associationist must both be 'cerebralists,' to the extent at least of admitting that certain peculiarities in the way of working of their own favorite principles are explicable only by the fact that the brain laws are a codeterminant of their result.

Our first conclusion, then, is that a certain amount of brain-physiology must be presupposed or included in Psychology.[5]

The emergence of both psychology and behavioral neuroscience as legitimate sciences can be traced from the emergence of physiology from anatomy, particularly neuroanatomy. Physiologists conducted experiments on living organisms, a practice that was distrusted by the dominant anatomists of the 18th and 19th centuries.[6] The influential work of Claude Bernard, Charles Bell, and William Harvey helped to convince the scientific community that reliable data could be obtained from living subjects.

Even before the 18th and 19th century, behavioral neuroscience was beginning to take form as far back as 1700 B.C.[7] The question that seems to continually arise is what is the connection between the mind and body. The debate is formally referred to as the mind-body problem. There are two major schools of thought that attempt to resolve the mindbody problem; monism and dualism.[4]Plato and Aristotle are two of several philosophers who participated in this debate. Plato believed that the brain was where all mental thought and processes happened.[7] In contrast, Aristotle believed that the brain served the purpose of cooling down the emotions derived from the heart.[4] The mind-body problem was a stepping stone toward attempting to understand the connection between the mind and body.

Another debate arose about was localization of function or functional specialization versus equipotentiality which played a significant role in the development in behavioral neuroscience. As a result of localization of function research, many famous people found within psychology have come to various different conclusions. Wilder Penfield was able to develop a map of the cerebral cortex through studying epileptic patients along with Rassmussen.[4] Research on localization of function has led behavioral neuroscientist to a better understanding of which parts of the brain control behavior. This is best exemplified through the case study of Phineas Gage.

The term "psychobiology" has been used in a variety of contexts, emphasizing the importance of biology, which is the discipline that studies organic, neural and cellular modifications in behavior, plasticity in neuroscience, and biological diseases in all aspects, in addition, biology focuses and analyzes behavior and all the subjects it is concerned about, from a scientific point of view. In this context, psychology helps as a complementary, but important discipline in the neurobiological sciences. The role of psychology in this questions is that of a social tool that backs up the main or strongest biological science. The term "psychobiology" was first used in its modern sense by Knight Dunlap in his book An Outline of Psychobiology (1914).[8] Dunlap also was the founder and editor-in-chief of the journal Psychobiology. In the announcement of that journal, Dunlap writes that the journal will publish research "...bearing on the interconnection of mental and physiological functions", which describes the field of behavioral neuroscience even in its modern sense.[8]

In many cases, humans may serve as experimental subjects in behavioral neuroscience experiments; however, a great deal of the experimental literature in behavioral neuroscience comes from the study of non-human species, most frequently rats, mice, and monkeys. As a result, a critical assumption in behavioral neuroscience is that organisms share biological and behavioral similarities, enough to permit extrapolations across species. This allies behavioral neuroscience closely with comparative psychology, evolutionary psychology, evolutionary biology, and neurobiology. Behavioral neuroscience also has paradigmatic and methodological similarities to neuropsychology, which relies heavily on the study of the behavior of humans with nervous system dysfunction (i.e., a non-experimentally based biological manipulation).

Synonyms for behavioral neuroscience include biopsychology, biological psychology, and psychobiology.[9]Physiological psychology is a subfield of behavioral neuroscience, with an appropriately narrower definition

The distinguishing characteristic of a behavioral neuroscience experiment is that either the independent variable of the experiment is biological, or some dependent variable is biological. In other words, the nervous system of the organism under study is permanently or temporarily altered, or some aspect of the nervous system is measured (usually to be related to a behavioral variable).

Different manipulations have advantages and limitations. Neural tissue destroyed as a primary consequence of a surgery, electric shock or neurotoxin can confound the results so that the physical trauma masks changes in the fundamental neurophysiological processes of interest. For example, when using an electrolytic probe to create a purposeful lesion in a distinct region of the rat brain, surrounding tissue can be affected: so, a change in behavior exhibited by the experimental group post-surgery is to some degree a result of damage to surrounding neural tissue, rather than by a lesion of a distinct brain region. [23][24] Most genetic manipulation techniques are also considered permanent.[24] Temporary lesions can be achieved with advanced in genetic manipulations, for example, certain genes can now be switched on and off with diet.[24] Pharmacological manipulations also allow blocking of certain neurotransmitters temporarily as the function returns to its previous state after the drug has been metabolized.[24]

In general, behavioral neuroscientists study similar themes and issues as academic psychologists, though limited by the need to use nonhuman animals. As a result, the bulk of literature in behavioral neuroscience deals with mental processes and behaviors that are shared across different animal models such as:

However, with increasing technical sophistication and with the development of more precise noninvas
ive methods that can be applied to human subjects, behavioral neuroscientists are beginning to contribute to other classical topic areas of psychology, philosophy, and linguistics, such as:

Behavioral neuroscience has also had a strong history of contributing to the understanding of medical disorders, including those that fall under the purview of clinical psychology and biological psychopathology (also known as abnormal psychology). Although animal models do not exist for all mental illnesses, the field has contributed important therapeutic data on a variety of conditions, including:

Nobel Laureates

The following Nobel Prize winners could reasonably be considered behavioral neuroscientists or neurobiologists. (This list omits winners who were almost exclusively neuroanatomists or neurophysiologists; i.e., those that did not measure behavioral or neurobiological variables.)

Kavli Prize in Neuroscience

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Surgery Is No Longer Your Only Option! – The Clermont News Leader

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Now That We Have Your Attention Did you know Orlando Spine and Joint offers regenerative therapy? When you hear of regenerative medicine, you may be thinking things such as anti-aging, hair restoration, and wrinkle reduction. While these things are technically classified as regenerative medicine, they are not at all that we do. In an effort to help your body heal itself, and regenerate lost or broken tissues, we employ 2 major techniques. One is PRP, which stands for Platelet Rich Plasma. By drawing some blood from your arm, then spinning it in a special centrifuge, we are able to gather just the platelets and some of the plasma. This is then used as an injection into the injured area of your body, acting like a boost or jump start to your natural healing ability. We also use stem cell type therapy. By partnering with the University of Miamis tissue bank, along with New Life Regenerative Medicine, we can offer the latest, most technically sound, and purest form of stem cell type therapy available to you today, called AlloGen. 100% natural, AlloGen contains components that enhance your bodys ability to heal and regenerate itself. Instead of simply managing pain, AlloGen may contribute to minimizing or eliminating pain all together. Both PRP and AlloGen are ideal choices for patients considering regenerative medicine therapy for conditions such as: sports injury, joint pain, arthritis, soft tissue tears, plantars faciitis, carpal tunnel, neck and back pain and many more. Call today for a free consultation with the doctor. 407-614-5900. Orlando Spine & Joint, 821 Oakley Seaver Drive, Clermont, FL 34711. http://www.OrlandoSpineAndJoint.com

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Column: How the chemistry of sunscreen is protecting your skin this Memorial Day – PBS NewsHour

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No matter where your complexion falls on the Fitzpatrick Skin Type scale, ultraviolet radiation (UV) from the sun or tanning beds will damage your skin. Photo by Robert Lemann/via Adobe

Not so long ago, people like my Aunt Muriel thought of sunburn as a necessary evil on the way to a good base tan. She used to slather on the baby oil while using a large reflector to bake away. Aunt Muriels mantra when the inevitable burn and peel appeared: Beauty has its price.

Was she ever right about that price but it was a lot higher than any of us at the time recognized. What sun addicts didnt know then was that we were setting our skin up for damage to its structural proteins and DNA. Hello, wrinkles, liver spots and cancers. No matter where your complexion falls on the Fitzpatrick Skin Type scale, ultraviolet radiation (UV) from the sun or tanning beds will damage your skin.

Today, recognition of the risks posed by UV rays has motivated scientists, myself included, to study whats going on in our cells when theyre in the sun and devise modern ways to ward off that damage.

UV light that affects our skin has a shorter wavelength than the parts of the electromagnetic spectrum we can see. Photo by Inductiveload/NASA

Sunlight is composed of packets of energy called photons. The visible colors we can see by eye are relatively harmless to our skin; its the suns ultraviolet (UV) light photons that can cause skin damage. UV light can be broken down into two categories: UVA (in the wavelength range 320-400 nanometers) and UVB (in the wavelength range 280320 nm).

Our skin contains molecules that are perfectly structured to absorb the energy of UVA and UVB photons. This puts the molecule into an energetically excited state. And as the saying goes, what goes up must come down. In order to release their acquired energy, these molecules undergo chemical reactions and in the skin that means there are biological consequences.

Interestingly, some of these effects used to be considered helpful adaptations though we now recognize them as forms of damage. Tanning is due to the production of extra melanin pigment induced by UVA rays. Exposure to the sun also turns on the skins natural antioxidant network, which deactivates highly destructive reactive oxygen species (ROS) and free radicals; if left unchecked, these can cause cellular damage and oxidative stress within the skin.

We also know that UVA light penetrates deeper into the skin than UVB, destroying a structural protein called collagen. As collagen degrades, our skin loses its elasticity and smoothness, leading to wrinkles. UVA is responsible for many of the visible signs of aging, while UVB light is considered the primary source of sunburn. Think A for aging and B for burning.

DNA itself can absorb both UVA and UVB rays, causing mutations which, if unrepaired, can lead to non-melanoma (basal cell carcinoma, squamous cell carcinoma) or melanoma skin cancers. Other skin molecules pass absorbed UV energy on to those highly reactive ROS and free radicals. The resulting oxidative stress can overload the skins built-in antioxidant network and cause cellular damage. ROS can react with DNA, forming mutations, and with collagen, leading to wrinkles. They can also interrupt cell signaling pathways and gene expression.

The end result of all of these photoreactions is photodamage that accumulates over the course of a lifetime from repeated exposure. And this cannot be emphasized enough this applies to all skin types, from Type I (like Nicole Kidman) to Type VI (like Jennifer Hudson). Regardless of how much melanin we have in our skin, we can develop UV-induced skin cancers and we will all eventually see the signs of photo-induced aging in the mirror.

The good news, of course, is that the risk of skin cancer and the visible signs of aging can be minimized by preventing overexposure to UV radiation. When you cant avoid the sun altogether, todays sunscreens have got your back (and all the rest of your skin too).

Sunscreens employ UV filters: molecules specifically designed to help reduce the amount of UV rays that reach through the skin surface. A film of these molecules forms a protective barrier either absorbing (chemical filters) or reflecting (physical blockers) UV photons before they can be absorbed by our DNA and other reactive molecules deeper in the skin.

In the United States, the Food and Drug Administration regulates sunscreens as drugs. Because we were historically most concerned with protecting against sunburn, 14 molecules that block sunburn-inducing UVB rays are approved for use. That we have just two UVA-blocking molecules available in the United States avobenzone, a chemical filter; and zinc oxide, a physical blocker is a testament to our more recent understanding that UVA causes trouble, not just tans.

The FDA also has enacted strict labeling requirements most obviously about SPF (sun protection factor). On labels since 1971, SPF represents the relative time it takes for an individual to get sunburned by UVB radiation. For example, if it takes 10 minutes typically to burn, then, if used correctly, an SPF 30 sunscreen should provide 30 times that 300 minutes of protection before sunburn.

Used correctly is the key phrase. Research shows that it takes about one ounce, or basically a shot glass-sized amount of sunscreen, to cover the exposed areas of the average adult body, and a nickel-sized amount for the face and neck (more or less, depending on your body size). The majority of people apply between a quarter to a half of the recommended amounts, placing their skin at risk for sunburn and photodamage.

In addition, sunscreen efficacy decreases in the water or with sweating. To help consumers, FDA now requires sunscreens labeled water-resistant or very water-resistant to last up to 40 minutes or 80 minutes, respectively, in the water, and the American Academy of Dermatology and other medical professional groups recommend reapplication immediately after any water sports. The general rule of thumb is to reapply about every two hours and certainly after water sports or sweating.

In the U.S., the FDA regulates sunscreens available to consumers. Photo by Jeff Greenberg/UIG via Getty Images

To get high SPF values, multiple UVB UV filters are combined into a formulation based upon safety standards set by the FDA. However, the SPF doesnt account for UVA protection. For a sunscreen to make a claim as having UVA and UVB protection and be labeled Broad Spectrum, it must pass FDAs Broad Spectrum Test, where the sunscreen is hit with a large does of UVB and UVA light before its effectiveness is tested.

This pre-irradiation step was established in FDAs 2012 sunscreen labeling rules and acknowledges something significant about UV-filters: some can be photolabile, meaning they can degrade under UV irradiation. The most famous example may be PABA. This UVB-absorbing molecule is rarely used in sunscreens today because it forms photoproducts that elicit an allergic reaction in some people.

But the Broad Spectrum Test really came into effect only once the UVA-absorbing molecule avobenzone came onto the market. Avobenzone can interact with octinoxate, a strong and widely used UVB absorber, in a way that makes avobenzone less effective against UVA photons. The UVB filter octocrylene, on the other hand, helps stabilize avobenzone so it lasts longer in its UVA-absorbing form. Additionally, you may notice on some sunscreen labels the molecule ethylhexyl methoxycrylene. It helps stabilize avobenzone even in the presence of octinoxate, and provides us with longer-lasting protection against UVA rays.

Next up in sunscreen innovation is the broadening of their mission. Because even the highest SPF sunscreens dont block 100 percent of UV rays, the addition of antioxidants can supply a second line of protection when the skins natural antioxidant defenses are overloaded. Some antioxidant ingredients my colleagues and I have worked with include to
copheral acetate (Vitamin E), sodium ascorbyl phosophate (Vitamin C), and DESM. And sunscreen researchers are beginning to investigate if the absorption of other colors of light, like infrared, by skin molecules has a role to play in photodamage.

As research continues, one thing we know for certain is that protecting our DNA from UV damage, for people of every color, is synonymous with preventing skin cancers. The Skin Cancer Foundation, American Cancer Society and the American Academy of Dermatology all stress that research shows regular use of an SPF 15 or higher sunscreen prevents sunburn and reduces the risk of non-melanoma cancers by 40 percent and melanoma by 50 percent.

We can still enjoy being in the sun. Unlike my Aunt Muriel and us kids in the 1980s, we just need to use the resources available to us, from long sleeves to shade to sunscreens, in order to protect the molecules in our skin, especially our DNA, from UV damage.

Kerry Hanson is a research chemist at the University of California, Riverside. She has consulted for Bayer, J&J/Neutrogena and P&G. Her academic work has been funded by Hallstar and through a joint University of California Discovery Grant with Merck. She is a member of the American Chemical Society. This article was originally published on The Conversation. Read the original article here.

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Column: How the chemistry of sunscreen is protecting your skin this Memorial Day - PBS NewsHour