Category Archives: Transhuman News

February 11, 2021 -A team from Cleveland Clinic has developed a precision medicine platform designed to accelerate cancer gene therapies and genome-informed drug discovery.

In a study published in Nature Genetics, researchers describe the My Personal Mutanome (MPM) platform. The platform features an interactive database that offers insight into the role of somatic mutations in cancer acquired mutations that cant be passed to offspring and prioritizes mutations that may be responsive to drug therapy.

Although advances in sequencing technology have bestowed a wealth of cancer genomic data, the capabilities to bridge the translational gap between large-scale genomic studies and clinical decision making were lacking, said Feixiong Cheng, PhD, assistant staff in theGenomic Medicine Institute, and the studys lead author.

MPM is a powerful tool that will aid in the identification of novel functional mutations/genes, drug targets and biomarkers for cancer, thus accelerating the progress towards cancer precision medicine.

The team used clinical data to integrate nearly 500,000 mutations from over 10,800 tumor exomes the protein-coding part of the genome across 33 cancer types into the platform. The team then systematically mapped the mutations to over 94,500 protein-protein interactions (PPIs) and over 311,000 functional protein sites where proteins physically bind with one another. Researchers then incorporated patient survival and drug response data.

The platform analyzes the relationships between genetic mutations, proteins, PPIs, protein functional sites, and drugs to help users easily search for clinically actionable mutations. The MPM database includes three interactive visualization tools that offer two- and three-dimensional views of somatic mutations and their associated survival and drug responses.

According to the researchers, previous studies have linked disease pathogenesis and progression to mutations and variations that disturb the human interactome, the complex network of proteins and PPIs that impact cellular function. Mutations can disrupt the network by directly changing the normal function of a protein, known as nodetic effect, or by altering PPIs, known as edgetic effect.

Additionally, in a separate, previous study, a team of researchers found that somatic mutations were highly enriched where PPIs occurred. The group also demonstrated that PPI-perturbing mutations were significantly correlated with drug sensitivity or resistance as well as poor survival rate in cancer patients.

The results from another study published inNature Genetics, which was a collaboration between Cleveland Clinic and several other institutions, motivated us to develop the mutanome platform, said Cheng.

OurNature Geneticsfindings, along with previous research, provide proof-of-concept of both nodetic and edgetic effects of somatic mutations in cancer. What we learned from that study inspired us to develop a systems biology tool that, by mapping mutations to PPI interfaces and protein functional sites and integrating survival and drug response data, identifies cancer-driving and actionable mutations to guide personalized treatment and drug discovery.

Researchers expect that MPM will lead to a better understanding of mutations at the human interactome network level. This could lead to new insights in cancer genomics and treatments, ultimately achieving the goal of cancer precision medicine.

The team will continue to update MPM annually in order to provide researchers and physicians with the most comprehensive, complete data available. Researchers also plan to apply advanced analytics technologies to their insights to improve treatment development for other conditions.

OurNature Geneticsstudy also demonstrates the nodetic and edgetic effects of mutations/variations in other diseases, said Cheng.

As a next step, we are developing new artificial intelligence algorithms to translate these genomic medicine findings into human genome-informed drug target identification and precision medicine drug discovery (i.e., protein-protein inhibitors) for other complex diseases, including heart disease and Alzheimers disease.

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Precision Medicine Platform Aims to Advance Cancer Gene Therapies - HealthITAnalytics.com

Misfolded proteins (orange) in the endoplasmic reticulum may play a role in Wolfram syndromes many symptoms.

By Mitch LeslieFeb. 11, 2021 , 2:00 PM

Maureen Marshall-Doss says the first sign that her vision was deteriorating came when she misidentified the color of a dress. At a backyard get-together about 20 years ago, the Indianapolis resident pointed out an attractive yellow dress another woman was wearing. You see that as yellow? Shes wearing a pink dress, Marshall-Doss recalls her husband responding.

Today, Marshall-Doss is virtually blind. With help from custom made eyeglasses that magnify objects 500 times, I can see shapes, she says. But she can no longer drive and had to quit the job she loved as a school librarian. Along with her dimming vision, she has type 1 diabetes and has lost her sense of taste and smell.

Marshall-Doss is one of 15,000 to 30,000 people around the world with Wolfram syndrome, a genetic disease. For decades, the condition remained enigmatic, untreatable, and fatal. But in the past few years, insights into its mechanism have begun to pay off, leading to the first clinical trials of drugs that might slow the illness and sparking hopes that gene therapy and the CRISPR DNA-editing tool might rectify the underlying genetic flaws. Here is a rare disease that the basic science is telling us how to treat, says physiologist Barbara Ehrlich of the Yale School of Medicine.

The research could also aid more than the relatively few patients with Wolfram syndrome. Driving the diseases many symptoms is a malfunction of the endoplasmic reticulum (ER), the multichambered organelle that serves as a finishing school for many cellular proteins. Known as ER stress, the same problem helps propel far more common illnesses, including type 2 diabetes, amyotrophic lateral sclerosis (ALS), Parkinsons disease, and Alzheimers disease. Wolfram syndrome is the prototype of an endoplasmic reticulum disorder, says medical geneticist Fumihiko Fumi Urano of Washington University School of Medicine in St. Louis. Because Wolfram syndrome is simpler, says Scott Oakes, a cell biologist and pathologist at the University of Chicago, researchers think it could illuminate the mechanisms of other ER-disrupting diseases, which affect hundreds of millions of people worldwide.

In the late 1930s,four children with diabetes were going blind, and doctors were stumped. Like many other people in the United States struggling through the Great Depression, the siblings ate a paltry diet, subsisting on potatoes, bread, oatmeal, and a little milk. But after examining three of the children, Donald Wolfram, a physician at the Mayo Clinic in Rochester, Minnesota, and an ophthalmologist colleague ruled out malnutrition as the cause of their puzzling condition. Lead poisoning and syphilisthough common enoughwerent to blame, either. When Wolfram and his partner wrote up the cases in 1938, they concluded that the symptoms could be manifestations of an hereditary or acquired cerebral lesion.

The physicians were right that the syndrome eventually named for Wolfram is hereditary. Recessive mutations in the gene for a protein called wolframin are responsible for most cases, with glitches in a second gene causing most of the rest. However, the pair was wrong to think the defect lies only in the brain. Instead, the symptoms stem from widespread cell death. Its definitely a disease that affects the whole body, Marshall-Doss says.

The first sign of the illness, appearing when patients are children, is usually diabetes mellitus, or faulty sugar metabolism, sparked by the demise of insulin-secreting beta cells in the pancreas. Most patients also develop the unrelated condition diabetes insipidus, in which the pituitary gland doesnt dole out enough of a hormone that helps control the bodys fluid balance, causing the kidneys to produce huge amounts of urine.

Mutations in the gene for wolframin disrupt the endoplasmic reticulum and lead to cell death throughout the body, causing a range of symptoms.

V. Altounian/Science

Ellie White, 19, of Centennial, Colorado, who was diagnosed with Wolfram syndrome 12 years ago, says she hasnt had a full night of sleep since she was 3 years old. She gets up again and again to use the bathroom and monitor her blood sugar.

Yet she and other patients say that as disruptive as those problems are, they are not the diseases most dismaying consequence. The biggest symptom of Wolfram syndrome that affects me the most is my vision, White says. Because neurons in the optic nerve perish, patients usually go blind within 10 years of their first visual symptoms.

Other neurons die as well. As the disease progresses, brain cells expire, and walking, breathing, and swallowing become difficult. Most people with Wolfram syndrome die before age 40, often because they can no longer breathe. At 57, Marshall-Doss is one of the oldest patients; one of her mutated genes may yield a partly functional version of wolframin, triggering a milder form of the disease, Urano says.

Two advanceshave made it possible to begin to tackle those symptoms. The first was Uranos discovery nearly 20 years ago that linked Wolfram syndrome to ER stress. The ER is where about one-third of a cells newly made proteins fold into the correct shapes and undergo fine-tuning. Cells can develop ER stress whenever they are under duress, such as when they dont have enough oxygen or when misfolded proteins begin to pile up inside the organelle.

In test tube experiments, Urano and his colleagues were measuring the activity of genes to pinpoint which ones help alleviate ER stress. One gene that popped up encodes wolframin, which scientists had shown in 1998 was mutated in patients with Wolfram syndrome. Following up on that finding, Urano and his team determined that wolframin takes part in whats known as the unfolded protein response, which is a mechanism for coping with ER stress in which cells take steps including dialing back protein production.

Scientists think wolframin plays a key role in the unfolded protein response, though they havent nailed down exactly how. When wolframin is impaired, cells become vulnerable to ER stress. And if they cant relieve that stress, they often self-destruct, which could explain why so many neurons and beta cells die in the disease.

Defective wolframin may harm cells in other ways. The ER tends the cells supply of calcium, continually releasing and absorbing the ion to control the amount in the cytoplasm. Changes in calcium levels promote certain cellular activities, including the contraction of heart muscle cells and the release of neurotransmitters by neurons. And wolframin affects calcium regulation.

Beta cells genetically engineered to lack functional wolframin brim with calcium, Ehrlich and colleagues reported in July 2020 in theProceedings of the National Academy of Sciences. When exposed to lots of sugar, the altered cells release less insulin and are more likely to die than healthy beta cells, the team found. The cells share that vulnerability with beta cells from patients with Wolfram syndrome. We think that excess calcium is leading to excess cell death, Ehrlich says.

ER malfunctions could hamstring other organelles as well. The ER donates calcium to the mitochondria, the cells power plants, helping them generate energy. In 2018, a team led by molecular biologist Ccile Delettre and molecular and cellular biologist Benjamin Delprat, both of the French biomedical research agency INSERM, discovered that in cells from patients with Wolfram syndrome, mitochondria receive less calcium from the ER and produce less energy. Those underpowered mitochondria could spur the death of optic nerve cells, the researchers speculate.

Fumihiko Urano holds dantrolene, a muscle relaxant drug he helped test as a treatment for Wolfram syndrome.

The link between ER stress and Wolfram syndrome has been crucial for identifying potential treatments because otherwise we would have nothing to target, Urano says. But a second development was also key, he says: the advocacy and support of patient organizations, such as the Snow Foundation and the Ellie White Foundation, headed by its namesakes mother. The foundations have stepped up with money for lab research and clinical trials when other sources, including government agencies, didnt come through.

Scientists, patients, and their advocates say Urano also deserves much of the credit. Besides treating patients, he heads the international registry of cases and has taken the lead in organizing clinical trials, screening compounds for possible use as treatments, and devising potential therapies. Fumi is clearly the driving force, says Stephanie Snow Gebel, co-founder of the Snow Foundation, who about 10 years ago helped persuade him to forgo a plum job as department chair at a Japanese university and take over the Wolfram program at Washington University.

Patients could soonstart to reap the benefits. In 2016, Urano and colleagues started the worlds first clinical trial for the disease: a phase 1/2 study of dantrolene, an approved muscle relaxant. The molecule was a top performer when they screened 73 potential treatments for their ability to save cells with terminal ER stress. Dantrolene didnt improve vision in the 22 participants, including White, the scientists reported in an October 2020 preprint. But in some patients, beta cells appeared to be working better and releasing more insulin. The drug is safe, but Urano says it will need to be chemically tweaked to target its effects before future trials are warranted.

Researchers are pursuing other possible treatments targeting ER stress or calcium levels. In 2018, U.K. scientists launched a trial that will include 70 patients to evaluate sodium valproate, a therapy for bipolar disorder and epilepsy that, in the lab, prevents cells with faulty wolframin from dying. Last year, another compound that emerged from Uranos screens, the diabetes drug liraglutide, entered a clinical trial. Also last year, an experimental drug developed by Amylyx Pharmaceuticals for Alzheimers disease and ALS received orphan drug designation from the U.S. Food and Drug Administration for Wolfram syndrome because it curbs ER stress. That designation offers tax breaks and other incentives, and it will get trials started sooner, Urano says.

Ehrlich and her team have a candidate of their own that they have begun to test in rodents: the drug ibudilast, which is approved in Japan to treat asthma. The researchers found it reduces calcium levels in beta cells lacking wolframin and boosts their survival and insulin output. New screening projects may reveal still more candidates.

But Urano knows that even if a treatment receives approval, it would be only a Band-Aid for Wolfram syndrome. Hoping to develop a genetic cure, he and colleagues are introducing replacement genes into cells from patients and from mice engineered to replicate the disease. The researchers are endowing the cells with healthy copies of the gene for wolframin or the gene for a protein that reduces ER stress to determine whether they restore cellular function and reduce cell death. At INSERM, Delettre and colleagues are also evaluating whether directing a working gene into optic nerve cells can curtail vision loss in mice with faulty wolframin. The scientists are still gathering data, but early results suggest the treatment can halt the deterioration.

Urano and his collaborators have also turned to the genome editor CRISPR, deploying it to correct the gene defect in patients stem cells and then growing them into beta cells. When the researchers transplanted the revamped cells into mice with diabetes, the animals blood sugar returned to healthy levels, the team reported in April 2020 inScience Translational Medicine.

Stem cell biologist Catherine Verfaillie of KU Leuven is collaborating on the CRISPR research. But she notes that because the faulty wolframin gene affects so many tissues, researchers will have to figure out how to deliver the CRISPR components to most cells in large organs such as the brain and livera prospect she calls pretty daunting. Urano agrees, predicting that CRISPR-based Wolfram therapies might take 10 to 20 years to develop. The alternative approach, gene therapy, could reach clinical trials more quickly, in 3 to 10 years, he says, because researchers have more experience with gene therapy and have created several treatments that have already been approved for other illnesses.

Because it stems from a single genetic glitch, Wolfram syndrome could also help scientists tease out the role of the ER in more complex diseases, including neurological conditions, type 2 diabetes, and cancer. The ER also falters in those diseases, causing cells to die, but the mechanism is harder to discern because they stem from myriad genetic and environmental factors. In Alzheimers disease, for instance, neurons develop ER stress as misfolded proteins accumulate inside and outside the cells.

Besides deepening researchers understanding of other conditions, the research on Wolfram syndrome might even deliver candidate treatments. Everyone would be very excited if we can make advances in targeting ER stress in Wolfram syndrome, Oakes says. It would open up the whole field to doing this in other degenerative diseases.

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The race to treat a rare, fatal syndrome may help others with common disorders like diabetes - Science Magazine

How often a person takes daytime naps, if at all, is partly regulated by their genes, according to new research led by investigators at Harvard-affiliated Massachusetts General Hospital (MGH) and published inNature Communications.

In this study, the largest of its kind ever conducted, the MGH team collaborated with colleagues at the University of Murcia in Spain and several other institutions to identify dozens of gene regions that govern the tendency to take naps during the day. They also uncovered preliminary evidence linking napping habits to cardiometabolic health.

Napping is somewhat controversial, says Hassan Saeed Dashti of the MGH Center for Genomic Medicine, co-lead author of the report with Iyas Daghlas, a medical student at Harvard Medical School (HMS). Dashti notes that some countries where daytime naps have long been part of the culture (such as Spain) now discourage the habit. Meanwhile, some companies in the United States now promote napping as a way to boost productivity. It was important to try to disentangle the biological pathways that contribute to why we nap, says Dashti.

Previously, co-senior author Richa Saxena, principal investigator at the Saxena Lab at MGH, and her colleagues used massive databases of genetic and lifestyle information to study other aspects of sleep. Notably, the team has identified genes associated with sleep duration, insomnia, and the tendency to be an early riser or night owl. To gain a better understanding of the genetics of napping, Saxenas team and co-senior author Marta Garaulet of the department of physiology at the University of Murcia, performed a genome-wide association study (GWAS), which involves rapid scanning of complete sets of DNA, or genomes, of a large number of people. The goal of a GWAS is to identify genetic variations that are associated with a specific disease or, in this case, habit.

For this study, the MGH researchers and their colleagues used data from the UK Biobank, which includes genetic information from 452,633 people. All participants were asked whether they nap during the day never/rarely, sometimes or usually. The GWAS identified 123 regions in the human genome that are associated with daytime napping. A subset of participants wore activity monitors called accelerometers, which provide data about daytime sedentary behavior, which can be an indicator of napping. This objective data indicated that the self-reports about napping were accurate. That gave an extra layer of confidence that what we found is real and not an artifact, says Dashti.

Several other features of the study bolster its results. For example, the researchers independently replicated their findings in an analysis of the genomes of 541,333 people collected by 23andMe, the consumer genetic-testing company. Also, a significant number of the genes near or at regions identified by the GWAS are already known to play a role in sleep. One example isKSR2, a gene that the MGH team and collaborators had previously found plays a role in sleep regulation.

Digging deeper into the data, the team identified at least three potential mechanisms that promote napping:

This tells us that daytime napping is biologically driven and not just an environmental or behavioral choice, says Dashti.

Some of these subtypes were linked to cardiometabolic health concerns, such as large waist circumference and elevated blood pressure, though more research on those associations is needed.

Future work may help to develop personalized recommendations for siesta, says Garaulet.

Furthermore, several gene variants linked to napping were already associated with signaling by a neuropeptide called orexin, which plays a role in wakefulness. This pathway is known to be involved in rare sleep disorders like narcolepsy, but our findings show that smaller perturbations in the pathway can explain why some people nap more than others, says Daghlas.

Saxena is the Phyllis and Jerome Lyle Rappaport MGH Research Scholar at the Center for Genomic Medicine and an associate professor of anesthesia at HMS.

The work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Heart, Lung, and Blood Institute, MGH Research Scholar Fund, Spanish Government of Investigation, Development and Innovation, the Autonomous Community of the Region of Murcia through the Seneca Foundation, Academy of Finland, Instrumentarium Science Foundation, Yrj Jahnsson Foundation, and Medical Research Council.

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The science behind those afternoon naps Harvard Gazette - Harvard Gazette

PROVIDENCE, R.I.[Brown University] New research provides insights into the treatment of Christianson syndrome (CS), an X-linked genetic disease characterized by reduced brain growth after birth, intellectual disability, epilepsy and difficulties with balance and speech.

One of the major challenges in developing treatments for human brain disorders, like CS, is developing an experimental system for testing potential therapeutics on human neurons, said study senior author Dr. Eric Morrow, an associate professor of molecular biology, neuroscience and psychiatry at Brown University. In recent years, advanced stem cell therapies that use tissues from patients have provided powerful new approaches for engineering human neurons from the patients themselves, who may undergo the treatment in the future.

For the study, published in Science Translational Medicine on Feb. 10, 2021, Morrow and his colleagues obtained blood samples from five CS patients and the patients unaffected brothers. They then reprogrammed these blood cells into stem cells, and these stem cells were converted into neurons in a petri dish. As a result, they obtained neurons that were representative of those from CS patients, and they used these neurons to test treatments.

Morrow who directs the Center for Translational Neuroscience at the Carney Institute for Brain Science and the Brown Institute for Translational Science said the team also used a new gene-editing approach that employs CRISPR-Cas9 technologies to correct patient mutations back to a healthy gene sequence.

CS is caused by a mutation in a gene encoding for NHE6, a protein that helps regulate acid levels within cell structures called endosomes. Past research suggests that the loss of NHE6 causes endosomes to become overly acidic, which disrupts the abilities of developing neurons to branch out and form connections in the growing brain.

Loss of this important protein can arise from a variety of gene mutations in patients. The majority of CS mutations are called nonsense mutations, which prevent NHE6 from being produced at all; four of the five CS patients involved in this study exhibited this class of mutation. However, some CS patients exhibit missense mutations. Individuals with missense mutations still have some NHE6, but it is produced in smaller amounts, and the protein fails to function as it should.

The research team tested two main forms of treatment on the stem-cell-derived neurons: first, gene transfer, which involves adding a healthy NHE6 gene into the cell; and second, administration of trophic factors, which are substances that promote neuron growth and encourage neurons to develop connections with other neurons. The researchers found that the neurons response to treatment depended on the class of mutation present.

The gene transfer studies, which may represent the first steps toward developing gene therapy, were successful in neurons with nonsense mutations. After the researchers inserted a functional NHE6 gene into nonsense-mutation CS neurons, the neurons branched out properly. In neurons with missense mutations, however, gene transfer failed completely. Further tests suggested that the abnormal NHE6 produced as a result of missense mutations may interfere with normal NHE6, thereby rendering gene transfer therapy ineffective in patient cells with these mutations.

In contrast, administration of trophic factors, such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1), successfully promoted proper branching in all the CS neurons studied, regardless of mutation type.

While these initial results are encouraging, Morrow hopes that future studies will examine these treatments in animal models.

Our results provide an initial proof-of-concept for these treatment strategies, indicating that they should be studied further, he said. However, we may ultimately need to pay close attention to the class of mutation that a patient has when we choose a specific treatment.

In addition to Morrow, the research team included scientists from Brown University, the University of South Carolina and the Icahn School of Medicine at Mount Sinai. The study was supported by multiple grants from the National Institutes of Health as well as a number of awards from foundations and academic institutions.

This news story was authored by contributing science writerKerry Benson.

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Neurons from patient blood cells enable researchers to test treatments for genetic brain disease - Brown University

A scanning electron micrograph of an oral squamous cancer cell (white) being attacked by two cytotoxic T cells (red), part of a natural immune response. Image by NIH

For all their importance as a breakthrough treatment, the cancer immunotherapies known as checkpoint inhibitors still only benefit a small minority of patients, perhaps 15 percent across different types of cancer. Moreover, doctors cannot accurately predict which of their patients will respond.

A new study finds that inherited genetic variation plays a role in who is likely to benefit from checkpoint inhibitors, which release the immune systems brakes so it can attack cancer. The study also points to potential new targets that could help even more patients unleash their immune systems natural power to fight off malignant cells.

People who respond best to immunotherapy tend to have inflamed tumors that have been infiltrated by immune cells that are capable of killing both viruses and cancer. This inflammation is also driven by the immune signaling molecule interferon.

There are some factors that are already associated with how well the immune system responds to tumors, said Elad Ziv, MD, professor of medicine at UCSF and co-senior author of the paper, published Feb. 9, 2021, by an international team in Immunity. But whats been less studied is how well your genetic background predicts your immune systems response to the cancer. Thats what is being filled in by this work: How much is the immune response to cancer affected by your inherited genetic variation?

The study suggests that, for a range of important immune functions, as much as 20 percent of the variation in how different peoples immune systems are able to attack cancer is due to the kind of genes they were born with, which are known as germline genetic variations.

That is a significant effect, similar to the size of the genetic contribution to traits like high blood sugar levels or obesity.

Rather than testing selected genes, we analyzed all the genetic variants we could detect across the entire genome. Among all of them, the ones with the greatest effect on the immune systems response to the tumor were related to interferon signaling. Some of these variants are known to affect our response to viruses and our risk of autoimmune disorders, said Davide Bedognetti, MD, PhD, director of the Cancer Program at the Sidra Medicine Research Branch in Doha, Qatar, and co-senior author of the paper. As observed with other diseases, we demonstrated that specific genes can also predispose someone to have a more effective anti-cancer immunity.

The team identified variants in 22 regions in the genome, or in individual genes, with significant effects including one gene, IFIH1, that is already well known for the role its variants play in autoimmune diseases as varied as type 1 diabetes, psoriasis, vitiligo, systemic lupus erythematosus, ulcerative colitis and Crohns disease.

The IFIH1 variants act on cancer immunity in different ways. For instance, people with the variant that confers risk of type 1 diabetes had a more inflamed tumor, which suggests they would respond better to cancer immunotherapy. But the researchers saw the opposite effect for patients with the variant associated with Crohns, indicating they might not benefit.

Another gene, STING1, was already thought to play a role in how patients respond to immunotherapy, and drug companies are looking for ways to boost its effects. But the team discovered that some people carry a variant that makes them less likely to respond, which may require further stratification of patients to know who could benefit most from those efforts.

The study required a huge amount of data that could only be found in a dataset as large as The Cancer Genome Atlas (TCGA), and from which they analyzed the genes and immune responses of 9,000 patients with 30 different kinds of cancer.

All told, the scientific team, which includes members from the United States, Qatar, Canada, and Europe, examined nearly 11 million gene variants to see how they matched with 139 immune parameters measured in patient tumor samples.

But the 22 regions or genes identified in the new study are just the tip of the iceberg, the researchers said, and they suspect many more germline genes likely play a role in how the immune system responds to cancer.

The next step, Ziv said, is to use the data to formulate polygenic approaches taking a large number of genes into account to predict which cancer patients will benefit from current therapies, and developing new drugs for those who will not.

Its further off, he said, but its a big part of what we hope will come out of this work.

The co-first authors are Rosalyn Sayaman, PhD, at UCSF and City of Hope and Mohamad Saad, PhD, of Qatar Computing Research Institute at Hamad Bin Khalifa University in Doha, Qatar. See the paper online for additional author, funding and disclosure information.

The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.UCSF Health, which serves as UCSFs primary academic medical center, includes top-ranked specialty hospitals and other clinical programs, and has affiliations throughout the Bay Area.

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Response to Cancer Immunotherapy May Be Affected by Genes We Carry from Birth - UCSF News Services