TAG: "Cancer"

Link identified between stem cell regulation, development of lung cancer

UCLA findings could lead to new personalized treatments for lung cancer.

UCLA researchers led by Dr. Brigitte Gomperts have discovered the inner workings of the process thought to be the first stage in the development of lung cancer. Their study explains how factors that regulate the growth of adult stem cells that repair tissue in the lungs can lead to the formation of precancerous lesions.

Findings from the three-year study could eventually lead to new personalized treatments for lung cancer, which is responsible for an estimated 29 percent of U.S. cancer deaths, making it the deadliest form of the disease.

The study was published online today (June 19) in the journal Stem Cell. Gomperts, a member of the UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research and the UCLA Jonsson Comprehensive Cancer Center, collaborated with Manash Paul and Bharti Bisht, postdoctoral scholars and co-lead authors of the study.

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off

Targeting a key driver of cancer

UCSF hosting two-day symposium, Targeting RAS Now for Future Cancer Therapy.

In the epic fight against cancer, a protein called Ras has been one of the arch-villains.

First identified in human cancers in the 1980s, this protein is responsible for roughly one-third of all cases, as well as some of the deadliest, including lung, colon and pancreatic cancers.

Ras is a key switch in a multistep cascade of molecular interactions that take place within cells. Mutations in Ras proteins can result in excessive signals for cells to proliferate and cause them to ignore cues for programmed cell death, leading to unchecked growth and tumor formation.

The key to curing many cancers could be to disrupt this cell signaling and dependence on Ras.

Decades of research have proven unsuccessful in developing a drug that can target the mutant Ras proteins found in cancer, yet the potential remains huge – so huge that the National Cancer Institute (NCI) last year announced a $10 million effort, dubbed the RAS Program, aimed at developing new ideas for targeting the protein. Frank McCormick, Ph.D., FRS, a leader in Ras research, recently stepped down as director of the UCSF Helen Diller Comprehensive Cancer Center to lead the new NCI project.

“A lot of people got into the drug discovery for Ras very early on and failed,” McCormick explained. “The clinical need [for a Ras drug] is the same or perhaps even better recognized than it was 30 years ago, but technology has advanced to the point where it’s worth having another shot at it.”

McCormick and other experts around the world will share their knowledge this week at a two-day symposium hosted by UC San Francisco called “Targeting RAS Now for Future Cancer Therapy.”

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off

Groundbreaking lung cancer trial launched

UC Davis expert David Gandara a key architect of national effort.

David Gandara, UC Davis

UC Davis Comprehensive Cancer Center patients will soon be part of an unprecedented clinical trial designed to improve access to promising therapies and speed development of effective treatments for an advanced form of lung cancer, the leading cancer killer of both men and women.

The approach, known as Lung-MAP (Lung Cancer Master Protocol), or S1400, is the product a unique public-private collaboration among the National Cancer Institute (NCI), SWOG Cancer Research, Friends of Cancer Research, the Foundation for the National Institutes of Health (FNIH) and five pharmaceutical companies. It is the first of several planned large, genomically driven trials that will be conducted by the NCI’s newly formed National Clinical Trials Network.

Lung-MAP’s strategy uses cutting-edge genomic profiling to match patients with late-stage squamous cell carcinoma to investigational treatments that target the molecular drivers of their individual tumors.

David Gandara, an internationally renowned oncologist and lung cancer expert and director of the UC Davis Thoracic Oncology Program, is a lead architect of the effort and serves as one of three leaders of the national trial.

“This is an entirely new way of looking at the development of cancer drugs,” said Gandara. “This is no longer business as usual. This approach changes the paradigm.”

Frustrated with the slow pace of lung cancer clinical trials of experimental therapies and their high failure rate, he talked to NCI officials more than 10 years ago about a more innovative approach.

“If you think about both the monetary investment and also the patient resources, hundreds of millions of dollars and clinical trials enrolling many tens of thousands of patients are wasted because we have an ineffective way of developing new anti-cancer drugs,” he said.

Lung-MAP aims to establish a model of clinical testing that more efficiently meets the needs of patients, clinical investigators and drug developers. Instead of having to undergo multiple diagnostic tests to determine eligibility for many different studies, enrollees are tested just once according to a “master protocol” and assigned to one of five different trial arms, each testing a different drug from a different developer. The approach is cost-effective for researchers because it gives them easier access to relevant enrollees based on their genomic profiles, and ensures patients better access to promising drugs.

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off

UC Davis faculty share cancer research innovation with partners in Spain

Workshop in Madrid runs June 12-14.

Ralph de Vere White, UC Davis

UC Davis Comprehensive Cancer Center researchers take center stage this week in Madrid during the second in a series of workshops designed to enhance cultural, academic, scientific and business relations between UC Davis and Madrid.

Cancer center Director Ralph de Vere White will share the podium with Primo Lara, Julie Sutcliffe and Luis Carvajal in presentations on cancer imaging and diagnosis and improving patient outcomes in oncology through clinical and translational research initiatives. The Cancer and Regenerative Medicine Life Sciences Workshop runs June 12-14.

The global partnership was organized by the UC Davis School of Education and Office of Research with the Madrid Network, comprising more than 750 businesses, research centers and universities. The network, focused on innovation, represents the Madrid region’s government, Comunidad de Madrid, in the agreement with UC Davis.

De Vere White, a distinguished professor of urology, will give an overview on the comprehensive cancer center and its role in improving survival rates in patients with advanced disease. Specifically, he said, he will focus on the center’s partnership with Jackson Laboratories (JAX West), an National Cancer Institute-designated cancer research facility, to find more targeted treatments for bladder cancer using a mouse model capable of growing human tumors.

De Vere White said he hopes to interest counterparts in Spain to cooperate in research that can advance and quicken the pace of development and clinical use of more precise cancer therapies. He likened the potential of the collaboration to the international approach to finding drugs to control the virus that causes AIDS.

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off

Longer telomeres linked to risk of brain cancer

Gene variants may promote overall health while increasing risk of gliomas.

New genomic research led by UC San Francisco scientists reveals that two common gene variants that lead to longer telomeres, the caps on chromosome ends thought by many scientists to confer health by protecting cells from aging, also significantly increase the risk of developing the deadly brain cancers known as gliomas.

The genetic variants, in two telomere-related genes known as TERT and TERC, are respectively carried by 51 percent and 72 percent of the general population. Because it is somewhat unusual for such risk-conferring variants to be carried by a majority of people, the researchers propose that in these carriers the overall cellular robustness afforded by longer telomeres trumps the increased risk of high-grade gliomas, which are invariably fatal but relatively rare cancers.

The research was published online in Nature Genetics today (June 8).

“There are clearly high barriers to developing gliomas, perhaps because the brain has special protection,” said Margaret Wrensch, M.P.H., Ph.D., the Stanley D. Lewis and Virginia S. Lewis Endowed Chair in Brain Tumor Research at UCSF and senior author of the new study. “It’s not uncommon for people diagnosed with glioma to comment, ‘I’ve never been sick in my life.’”

In a possible example of this genetic balancing act between risks and benefits of telomere length, in one dataset employed in the current study — a massive genomic analysis of telomere length in nearly 40,000 individuals conducted at the University of Leicester in the United Kingdom — shorter telomeres were associated with a significantly increased risk of cardiovascular disease.

“Though longer telomeres might be good for you as a whole person, reducing many health risks and slowing aging, they might also cause some cells to live longer than they’re supposed to, which is one of the hallmarks of cancer,” said lead author Kyle M. Walsh, Ph.D., assistant professor of neurological surgery and a member of the Program in Cancer Genetics at UCSF’s Helen Diller Family Comprehensive Cancer Center.

In the first phase of the new study, researchers at UCSF and The Mayo Clinic College of Medicine analyzed genome-wide data from 1,644 glioma patients and 7,736 healthy control individuals, including some who took part in The Cancer Genome Atlas project sponsored by the National Cancer Institute and National Human Genome Research Institute. This work confirmed a link between TERT and gliomas that had been made in previous UCSF research, and also identified TERC as a glioma risk factor for the first time.

Since both genes have known roles in regulating the action of telomerase, the enzyme that maintains telomere length, the research team combed the University of Leicester data, and they found that the same TERT and TERC variants associated with glioma risk were also associated with greater telomere length.

UCSF’s Elizabeth Blackburn, Ph.D., shared the 2009 Nobel Prize in Physiology or Medicine for her pioneering work on telomeres and telomerase, an area of research she began in the mid-1970s. In the ensuing decades, untangling the relationships between telomere length and disease has proved to be complex.

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off

Researchers report double dose of promising lung cancer findings

New drugs shown to increase survival time, fewer toxic side effects than standard treatments.

Researchers with UCLA’s Jonsson Comprehensive Cancer Center report that two new experimental drugs have shown great promise in the treatment of patients with non–small-cell lung cancer, which accounts for about 85 percent of all lung cancers. Lung cancer is the leading cause of cancer death in the United States.

The drugs — ramucirumab and CO-1868 — were shown in separate clinical trials to increase survival times with fewer toxic side effects than standard treatments. The findings were presented this week at the American Society of Clinical Oncology annual meeting in Chicago.

Ramucirumab: A new second-line defense

The standard therapy for patients with non–small-cell lung cancer after initial therapy, or when their disease worsens, is chemotherapy with a single drug. Overall, survival time among these patients is generally about 6 to 9 months. Less than 10 percent of patients respond to therapy, and even then, responses are usually of short duration.

Dr. Edward Garon, an assistant professor of hematology–oncology and member of the Jonsson Cancer Center, conducted an extensive multiyear Phase 3 clinical trial testing the investigational drug ramucirumab in a population of 1,253 patients with non–small-cell lung cancer whose cancer had progressed during or after first-line chemotherapy treatment.

Ramucirumab, which is being developed by Eli Lilly and Co., is an antibody that targets VEGFR-2, an extracellular protein that is important in the formation of the blood vessels that support cancer cells. Patients were given ramucirumab in combination with docetexal, a clinically approved chemotherapy drug considered the cornerstone of second-line treatment in advanced non–small-cell lung cancer.

Response to ramucirumab — that is, individuals whose tumors shrank — was 23 percent at the time the study was analyzed. The drug is the first new therapy for previously treated non–small-cell lung cancer pateints to improve overall survival, with findings showing a progression-free survival rate of 4.5 months and median overall survival of 10.5 months.

“We are excited to have a drug that lengthens survival time in lung cancer patients, who often have few options,” Garon said. “Although adverse effects were experienced by patients, most commonly neutropenia, fatigue and hypertension, toxicities were largely manageable with appropriate dose reductions and supportive care, and without substantial reduction in planned dose intensity.”

The research appears in the June edition of The Lancet.

Combating the T790M mutation with CO-1686

A major advance in understanding lung cancer has been the identification of specific mutations that drive the disease and which are presumed to be the initial genetic event that triggers cells to become cancerous. The Jonsson Cancer Center was one of a group of leading institutions that participated in the Lung Cancer Mutation Consortium, showed that personalized therapies could be directed at a large percentage of non–small-cell lung patients. (The cosortium’s findings were published last month in the Journal of the American Medical Association.)

One example of targetable mutations in lung cancer involved the identification of the EGFR (epidermal growth factor recepator) mutation. The discovery has resulted in a new class of targeted therapeutic agents called EGFR tyrosine kinase inhibitors. And while these inhibitors have delivered promising results, the duration of benefit to patients still remains relatively short, with progressive disease generally occurring about a year after the beginning of treatment. Tyrosine kinase inhibitor treatment is also complicated by side effects such as diarrhea and skin rash.

Recent studies have shown that when a patient develops resistance to EGFR inhibitors, more than half the time it is due to the emergence of a new “gatekeeper” mutation, called T790M. Currently, there are no targeted therapies approved for the treatment of this mutation.

CO-1686 is an oral investigational drug discovered being developed by Clovis Oncology to selectively target both the initial EGFR mutations and the T790M resistance mutation.

Dr. Jonathan Goldman, an assistant professor of hematology–oncology and member of the Jonsson Cancer Center, was one of the leaders of a study of 88 patients with advanced non–small-cell lung cancer who had previously been treated with an EGFR inhibitor and had developed resistantance. In a Phase 1 trial, CO-1686 was administered continuously to the patients in 21-day cycles.

Response to the drug was seen in 58 percent of the patients. The benefit has been durable, with more than 75 percent of patients still on the drug at the time the study was analyzed. Treatment-related side effects, including elevated blood sugar levels, were for the most part mild and manageable.

“The results we’ve seen with CO-1686 are very promising,” Goldman said. “Many of these responses are very dramatic, and the result is that patients can feel better and live longer, often with fewer side effects than chemotherapy.”

View original article

CATEGORY: NewsComments Off

UCLA scientists take brakes off immune system to fight deadly cancers

Experimental drug shows promising results in patients with skin and lung cancers.

Antoni Ribas, UCLA

Researchers at UCLA’s Jonsson Comprehensive Cancer Center are reporting promising treatment milestones for patients with deadly skin and lung cancers who are being treated with an experimental drug called MK-3475.

The drug is an antibody that targets a protein known as PD-1, which is expressed by immune cells. In the body, PD-1 acts as an immune checkpoint, tamping down the activity of T cells, which would otherwise attack cancer cells. MK-3475 takes the brakes off, allowing T cells to identify and attack cancer cells.

In May 2013, MK-3475 received a “breakthrough therapy” designation under the U.S. Food and Drug Administration’s accelerated approval program for the treatment of melanoma that has metastasized or is not removable through surgery.

In clinical trials at UCLA, doctors are seeing major treatment successes with MK-3475 in two types of cancer with historically low survival rates: metastatic melanoma, a malignant skin cancer that spreads aggressively to vital organs such as the brain, lungs and liver, and lung cancer, which causes the highest number of cancer deaths in the U.S. annually.

The findings were presented this week at the American Society of Clinical Oncology conference in Chicago.

Metastatic melanoma

Dr. Antoni Ribas, a professor of hematology–oncology and member of the Jonsson Cancer Center, led one of the largest Phase 1 studies in cancer, with 411 patients who had metastatic melanoma, which has an average five-year survival rate of less than 5 percent. The one-year overall survival rate was 69 percent for all patient subgroups.

Response to MK-3475 — that is, individuals whose tumors shrank — was continuing in 88 percent of patients at the time the study was analyzed, generally at 12-month follow-up. Tumors responded in patients on various dose regimens and in various subgroups, including those whose cancers had worsened on the drug ipilimumab; there are currently no treatment options with proven activity for these patients.

“We are seeing unprecedented durable responses with this drug,” Ribas said. “MK-3475 is working in patients who had not been treated, as well as those who had been given ipilimumab and other therapies. These are early data, but response rates of this magnitude in such a large sample, with only 4 percent of patients discontinuing because of drug-related side effects, indicate the importance of moving forward quickly with this drug.”

Overall, 34 percent of patients had responses to MK-3475, including 40 percent who had not been treated with ipilimumab and 28 percent whose cancer worsened despite ipilimumab treatment. Treatment-related side effects were generally mild and reversible; 8 percent of patients had serious side effects.

Non–small-sell lung cancer

Dr. Edward Garon, an assistant professor of hematology–oncology and member of the Jonsson Cancer Center, led a cohort of 217 patients with metastatic non–small-cell lung cancer whose disease worsened during or after at least one prior therapy. This MK-3475 research was the largest report of lung cancer patients being treated with this approach of inhibiting PD-1.

The standard therapy for patients in this situation is chemotherapy with a single drug. After one prior therapy, overall survival is generally about six to nine months. Less than 10 percent of patients respond to therapy, and even then, the responses are usually of short duration. Outcomes are typically worse in patients who have received two or more therapies, as was often the case in this study.

Among lung cancer patients whose tumors expressed PD-L1, a target of PD-1 — who accounted for a majority of the study participants — 23 percent had a response to the MK-3475 therapy, and the responses were often durable.

“We are very excited about the preliminary results we are seeing with MK-3475 in these advanced lung cancer patients,” Garon said. “It is a very well tolerated drug, so the benefits are enhanced by the fact that it generally has very little negative effect on patient quality of life. We are conducting additional trials with MK-3475, and based on our work, we hope the drug will soon be available to patients throughout the world.”

View original article

CATEGORY: NewsComments Off

Cancer survivors, families, caregivers celebrate National Cancer Survivor Day

UC San Diego Moores Cancer Center’s Survivor Beach brings community together June 15.

Andre Niemeyer navigates the waves at last year’s Survivor Beach. (Photo by Tom English)

The UC San Diego Moores Cancer Center will host the 8th annual Survivor Beach on Sunday, June 15, from 8 a.m. to 3 p.m., at the Catamaran Resort Hotel and Spa in Mission Bay. The event will culminate Cancer Survivor Week, a weeklong series of annual special events hosted by Moores Cancer Center. Survivor Beach will feature a beach festival, barbeque, live music, stand-up paddleboard (SUP) competitions for all skill levels and ages, and a paddle out for cancer survivors. Hundreds of community members are expected to gather for the day-long event in solidarity with and celebration of survivors and their caregivers.

“Survivor Beach gives us, as a community, the opportunity to celebrate the lives of those battling cancer and the families who support them while enjoying the natural beauty San Diego offers,” said Scott M. Lippman, M.D., director of UC San Diego Moores Cancer Center. “The generous support from Celgene, our lead sponsor, helps us to further our mission of translating promising scientific discoveries into new options for the care of our patients.”

Survivor Beach honors those who have fought cancer, as well as their families, friends and caregivers. For the second year in a row, Survivor Beach will feature paddleboarding races and activities including SUP clinics and vendors, an open paddle, an open race and a technical race for both stand-up and prone paddlers. The event will also feature a kid’s race.

In honor of National Cancer Survivor Day which was on June 1, Moores Cancer Center’s Cancer Survivor Week of events runs from June 9 through the Survivor Beach event on Sunday, June 15. For a full listing of activities, visit: cancer.ucsd.edu/survivor.

This year, Survivor Beach is sponsored by Celgene Corp., a global biopharmaceutical company that seeks to deliver innovative and life-changing treatments to patients with cancer and other severe immune and inflammatory conditions. “Celgene is proud to partner with Moores Cancer Center to celebrate cancer survivors and their caregivers,” said Jonathan Usuka, director of global partnerships at Celgene. “This event reflects Celgene’s unwavering support for patients and our commitment to researching new therapies with the potential to transform cancer treatment.”

“Survivor Beach offers a unique and moving way for anyone who has been affected by cancer to come together to support and inspire each other,” said Greg Gorgas, of MAST Therapeutics and the chair of the organizing committee. “We are excited to host a family-friendly paddleboard event at Mission Bay for everyone, including first-time paddlers, spectators, recreational competitors and some of the top athletes in the sport.”

The event is a warm-up to the 21st annual Luau and Legends of Surfing Invitational (formally the Luau and Longboard Invitational) on Aug. 17 at Scripps Pier, which, since its establishment in 1993, has raised more than $6 million to advance research at UC San Diego Moores Cancer Center, the region’s only National Cancer Institute-designated comprehensive cancer center.

Survivor Beach will begin at 8 a.m. and continue until 3 p.m., at the Catamaran Resort Hotel and Spa in Mission Bay. The beach festival and paddle out are free and open to the public. Race registration is $40 and the barbeque lunch is $25, with all net proceeds supporting UC San Diego Moores Cancer Center. For more information and to register, please visit survivorbeachsup.org.

View original article

CATEGORY: NewsComments Off

National study shows notable progress against colorectal cancer

Ten-year investigation clarifies standard of care.

Alan Venook, UC San Francisco

Research led by a UC San Francisco investigator establishes a new benchmark in the treatment of patients with metastatic colorectal cancer and sets a new expectation for how long patients can live with the particularly lethal disease.

The research, which spanned a decade, was unveiled at a plenary presentation today (June 1) at the 2014 Annual Meeting of the American Society of Clinical Oncology (ASCO) in Chicago. The plenary session spotlights research deemed to have the highest scientific merit and greatest impact on cancer research and care. The colorectal cancer study was selected from among more than 5,000 abstracts to be shared at the meeting.

The study was led by UCSF medical oncologist Alan P. Venook, M.D.

In the phase III study, researchers determined that cetuximab plus chemotherapy is similarly effective as bevacizumab plus chemotherapy for patients.

Median survival rate during the trial was approximately 29 months under either approach – seven months longer than the expectations 10 years ago and nearly triple the survival span of 20 years ago. About 10 percent of the patients lived more than five years, an extremely encouraging amount of time compared to two decades ago.

The results answer long-standing questions about the relative effectiveness of four common treatments, and provide patients and physicians important new information as they grapple with treatment choices. Moreover, the study, which began in 2004, reflects the evolution of the highly lethal cancer, the second leading cause of cancer deaths in the United States and the third most common malignant neoplasm in the world, according to the National Cancer Institute (NCI).

“Our investigation has clarified the standard of care and given us a deeper understanding of metastatic colorectal cancer,” said Venook, principal investigator and lead author of the study. He is a professor of clinical medicine and chief of gastrointestinal oncology at UCSF.

“Today, patients with this form of cancer have real choices, more ways to personalize their treatment,” he said. “Treatment should reflect their preferences and concerns for potential side effects without compromising its effectiveness.”

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off

Melanoma of the eye caused by two gene mutations

Therapeutic target identified for treatment.

Researchers at the UC San Diego School of Medicine have identified a therapeutic target for treating the most common form of eye cancer in adults. They have also, in experiments with mice, been able to slow eye tumor growth with an existing FDA-approved drug.

The findings are published online in today’s (May 29) issue of the journal Cancer Cell.

“The beauty of our study is its simplicity,” said Kun-Liang Guan, Ph.D., professor of pharmacology at UC San Diego Moores Cancer Center and co-author of the study. “The genetics of this cancer are very simple and our results have clear implications for therapeutic treatments for the disease.”

The researchers looked specifically at uveal melanoma. Uveal collectively refers to parts of the eye, notably the iris, that contain pigment cells. As with melanoma skin cancer, uveal melanoma is a malignancy of these melanin-producing cells.

Approximately 2,000 people in the United States are diagnosed with uveal melanoma each year. If the cancer is restricted to just the eye, the standard treatment is radiation and surgical removal of the eye. But uveal melanoma often spreads to the liver, and determining the metastatic status of the disease can be difficult. In cases of uveal melanoma metastasis, patients typically succumb within two to eight months after diagnosis.

Scientists have long suspected a genetic association with uveal melanoma because one of two gene mutations is present in approximately 70 percent of all tumors. Until this study, however, they had not identified a mechanism that could explain why and how these mutations actually caused tumors.

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off

STD may heighten risk of prostate cancer

UCLA study explores connection between them.

The parasite's stringy appendages adhere to skin cells, shown in pink and red.

Could a common sexually transmitted infection boost a man’s risk for prostate cancer?

In a new study, Patricia Johnson, a professor of microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA, explored the connection between prostate cancer and the parasite that causes trichomoniasis, the most common non-viral sexually transmitted infection in men and women.

Johnson’s team discovered that the parasite, Trichomonas vaginalis, secretes a protein that stimulates the growth of prostate cells and also induces an inflammatory response, which the researchers suspect enhances the cells’ progression to tumor cells.

According to the Centers for Disease Control, an estimated 275 million people worldwide have the parasite, including about 3.7 million in the United States. Previous studies found that men who have trichomoniasis are more vulnerable to developing an aggressive form of prostate cancer, which strikes 1 in 7 American men.

“Trichomoniasis can be successfully treated with a single dose of antibiotics,” said Johnson. ”But more than 70 percent of cases in men are asymptomatic, so many people are unaware they have it and do not seek treatment.”

Johnson’s next step will be using clinical samples from men with prostate cancer to verify whether her laboratory studies accurately reflect what happens during human infection.

The UCLA findings were published May 19 in Proceedings of the National Academy of Sciences.

View original article


CATEGORY: NewsComments Off

Gene mutation found for aggressive form of pancreatic cancer

Discovery may prove useful in future diagnoses and in developing new therapies.

Miles Wilkinson, UC San Diego

Researchers at the UC San Diego School of Medicine have identified a mutated gene common to adenosquamous carcinoma (ASC) tumors – the first known unique molecular signature for this rare, but particularly virulent, form of pancreatic cancer.

The findings are published in today’s (May 25) advance online issue of Nature Medicine.

Pancreatic cancer is the fourth leading cause of cancer-related death in the United States, with roughly 45,220 new cases diagnosed and more than 38,400 deaths annually. Both numbers are rising. ASC cases are infrequent, but typically have a worse prognosis than more common types of pancreatic cancer.

“There has been little progress in understanding pancreatic ASC since these aggressive tumors were first described more than a century ago,” said co-senior author Miles F. Wilkinson, Ph.D., professor in the Department of Reproductive Medicine and a member of the UC San Diego Institute for Genomic Medicine. “One problem has been identifying mutations unique to this class of tumors.”

In their paper, Wilkinson, co-senior author Yanjun Lu, Ph.D., of Tongji University in China, and colleagues report that ASC pancreatic tumors have somatic or non-heritable mutations in the UPF1 gene, which is involved in a highly conserved RNA degradation pathway called nonsense-mediated RNA decay or NMD. It is the first known example of genetic alterations in an NMD gene in human tumors.

Read more

For more health news, visit UC Health, subscribe by email or follow us on Flipboard.

CATEGORY: NewsComments Off