TAG: "Cancer"

Depression associated with lower survival rates in men with prostate cancer


UCLA study finds patients are often diagnosed later, receive less effective therapies.

Jim Hu, UCLA

Depressed men with localized prostate cancer are more likely to be diagnosed with more aggressive cancer, receive less effective treatments and survive for shorter times than prostate cancer patients who are not depressed, a UCLA study has found.

The study’s lead author, UCLA professor Dr. Jim Hu, said the negative outcomes may be the result of several factors, including bias against people with mental illness, depression’s impact on cancer’s biological processes, the patient’s lack of investment in his general health and disinterest in more effective care, and missed opportunities by physicians to educate patients about prostate cancer screening and treatment.

The population-based observational study used data from the Surveillance, Epidemiology and End Results Medicare database. Researchers focused on 41,275 men diagnosed with localized prostate cancer between 2004 and 2007 and observed through 2009, of whom 1,894 had a depressive disorder that had been discovered in the two years before the cancer was diagnosed.

“Men with intermediate- or high-risk prostate cancer and a recent diagnosis of depression are less likely to undergo definitive treatment and experience worse overall survival,” said Hu, UCLA’s Henry E. Singleton Professor of Urology and director of robotic and minimally invasive surgery at the David Geffen School of Medicine at UCLA. “The effect of depressive disorders on prostate cancer treatment and survivorship warrants further study, because both conditions are relatively common in men in the United States.”

The study was published online by the Journal of Clinical Oncology, a peer-reviewed journal of the American Society of Clinical Oncology.

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New combination drug controls tumor growth, metastasis in mice


Combination shows greater potency against several diseases.

Bruce Hammond, UC Davis

Researchers at UC Davis, University of Massachusetts and Harvard Medical School have created a combination drug that controls both tumor growth and metastasis. By combining a COX-2 inhibitor, similar to Celebrex, and an epoxide hydrolase (sEH) inhibitor, the drug controls angiogenesis (blood vessel formation), limiting a tumor’s ability to grow and spread. The study appears today (July 14) in the journal Proceedings of the National Academy of Sciences.

“We’ve been studying the effects of COX and sEH inhibitors, both by themselves and in combination, for several years,” said senior author and UC Davis Distinguished Professor Bruce Hammock. “We were surprised to find that the dual inhibitor was more active than higher doses of each compound, either individually or together. By combining the two molecules into one we got much greater potency against several diseases and completely unique effects in terms of blocking tumor growth and metastasis.”

Both COX and sEH enzymes control lipid signaling, which has long been associated with inflammation, cell migration, proliferation, hypertension and other processes. COX inhibitors block production of inflammatory and pain-inducing lipids, while sEH inhibitors preserve anti-hypertensive, anti-inflammatory and analgesic compounds. Separate COX and sEH inhibitors were previously found to work together in reducing inflammation and neuropathic pain.

After testing individual COX-2 and sEH inhibitors, the team synthesized the drug (PTUTB), the first combined COX-2/sEH inhibitor. They then tested the dual inhibitor against human lung and breast tumors, both in vitro and in mice. They found that PTUTB blocked angiogenesis, inhibiting the proliferation of endothelial cells, which are critical to blood vessel formation. This in turn limited tumor growth and metastasis, reducing lung and breast tumor growth by 70 to 83 percent.

In breast and lung cancers, the dual inhibitor blocked angiogenesis, which blocked the growth of solid tumors,” said Hammock. “This represents a new mechanism to control blood vessel and tumor growth.”

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Tweet your way to better health


UCSF study of social media shows potential to convey health messages.

Eleni Linos, UC San Francisco

Twitter and other social media should be better utilized to convey public health messages, especially to young adults, according to a new analysis by researchers at UC San Francisco.

The analysis focused on public conversations on the social media site Twitter around one health issue: indoor tanning beds, which are associated with an increased risk of skin cancer. The researchers assessed the frequency of Twitter mentions related to indoor tanning and tanning health risks during a two week period in 2013. During that timeframe, more than 154,000 tweets (English language) mentioned indoor tanning – amounting to 7.7 tweets per minute. But fewer than 10 percent mentioned any of the health risks, such as skin cancer, that have been linked to indoor tanning.

That offers a potentially valuable forum for conveying important health information directly to the people who might benefit the most from it, but the authors said further research is needed to explore whether that would be effective.

The analysis will be published as an editorial letter in the July 12 issue of The Lancet

“The numbers are staggering,” said senior author Eleni Linos, M.D., Dr.P.H., an assistant professor in the UCSF Department of Dermatology. “With 500 million tweets sent each day and over 1 billion Facebook users, it is clear that social media platforms are the way to go for public health campaigns, especially those focused on young adults.”

Linos has previously published influential research on the harms of indoor tanning beds. The research found that indoor tanning beds can cause non-melanoma skin cancer, with the risk rising the earlier one starts tanning. Indoor tanning has already been established as a risk factor for malignant melanoma, the deadliest form of skin cancer.

In their social media study, the researchers used a Twitter programming application to collect in real time all tweets that mentioned indoor tanning, tanning beds, tanning booths and tanning salons. During the study period in March and April 2013, more than 120,000 people posted at least one tweet about indoor tanning. Altogether, more than 113 million Twitter “followers” were potentially exposed to tweets about indoor tanning, the authors reported.

“Indoor tanning has reached alarming rates among young people,” said Linos. “And tanning beds account for hundreds of thousands of skin cancers each year. Through social media, we now have an opportunity to talk about these health risks directly with young people.”

Co-authors include Mackenzie R. Wehner, a Doris Duke Research Fellow at UCSF; Mary-Margaret Chren, M.D., professor of dermatology at UCSF; Melissa L. Shive, a medical student at UCSF; and Jack S. Resneck Jr., M.D., associate professor and vice chair of the UCSF Department of Dermatology.

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Pancreatic surgery complications and impact on hospital costs


UC Davis research challenges current strategies.

Rick Bold, UC Davis

When it comes to a specific type of pancreatic surgery, post-operative complications have a far greater impact on total cost than does how long the patient stays in the hospital, according to a published paper by UC Davis researchers.

The finding, published in JAMA Surgery, challenges current cost-cutting strategies routinely used by administrators and insurers that emphasize shorter lengths of stay in the hospital. Results of the new study point to a different, potentially more effective approach: a focus on reducing surgery complications.

The surgery examined for this study was the pancreaticoduodenectomy, a major operation that involves removal of parts of the stomach, duodenum, pancreas, bile duct and gallbladder. The surgery is performed to remove cancerous tumors or to deal with an inflamed pancreas.

“Hospitals are increasingly motivated to implement clinical care pathways as a method of improving quality of care, with a focus on elimination of excess resource utilization and shortening the hospital length of stay,” said lead author Richard Bold, professor and chief of surgical oncology at the UC Davis Comprehensive Cancer Center. “This study’s results reveal that addressing post-operative complications should be a critical component of these pathways.”

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Robot-assisted technique improves surgeons’ ability to remove kidney tumors


UCLA-led study finds the approach may shorten surgeries, could reduce risk of complications.

Schematic showing the robotic device's proper position during surgery. (Image by Eric Treat, UCLA)

Roughly 50,000 Americans are diagnosed with kidney cancer each year. Most of them have small tumors that doctors discover while screening for other health problems.

The surgeries to remove renal tumors can be difficult, particularly if the cancer is on the posterior side of the kidney and if patients have had previous abdominal surgery, because scar tissue from previous operations usually makes it hard for surgeons to distinguish the normal parts of the body from one another.

Now, a study led by Dr. Jim Hu and researchers at UCLA’s Jonsson Comprehensive Cancer Center has shown that a newer surgical technique called robot-assisted retroperitoneoscopic partial nephrectomy is more effective than other current techniques to remove kidney tumors when the masses are located on the back of the kidney or when a patient has had previous abdominal surgery. RARPN is a minimally invasive laparoscopic procedure in which surgeons use precise robotic arms and magnified, high-definition 3-D cameras.

The study, published online in European Urology, was the largest multicenter study to date on this technique. The five-year project reviewed surgeries for 227 patients whose average age was 60, with most between ages 52 and 66.

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New delivery in living cell signaling


Researchers help find that what was believed to be noise is an important signaling factor.

This gif of membrane-anchored Ras (red) and SOS molecules (green) shows individual SOS molecules corraled in nanofabricated patches where all the Ras molecules they activate can be trapped. (Click for animation)

A breakthrough discovery into how living cells process and respond to chemical information could help advance the development of treatments for a large number of cancers and other cellular disorders that have been resistant to therapy. An international collaboration of researchers, led by scientists with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab) and UC Berkeley, have unlocked the secret behind the activation of the Ras family of proteins, one of the most important components of cellular signaling networks in biology and major drivers of cancers that are among the most difficult to treat.

“Ras is a family of membrane-anchored proteins whose activation is a critical step in cellular signaling, but almost everything we know about how Ras signals are activated has been derived from bulk assays, in solution or in live cells, in which information about the role of the membrane environment and anything about variation among individual molecules is lost,” says Jay Groves, a chemist with Berkeley Lab’s Physical Biosciences Division and UC Berkeley’s Chemistry Department. “Using a supported-membrane array platform, we were able to perform single molecule studies of Ras activation in a membrane environment and discover a surprising new mechanism though which Ras signaling is activated by Son of Sevenless (SOS) proteins.”

Groves, who is also a Howard Hughes Medical Institute (HHMI) investigator, is the corresponding author of a paper in Science that reports this discovery. The paper is titled “Ras activation by SOS: Allosteric regulation by altered fluctuation dynamics.” The lead authors were Lars Iversen and Hsiung-Lin Tu, both members of Groves’ research group at the time of the study.


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Upending a cancer dogma


Cyclin D, long believed to promote cancer, actually activates tumor suppressor.

Steven Dowdy, UC San Diego

Researchers at the UC San Diego School of Medicine say a protein essential to regulating cell cycle progression – the process of cell division and replication – activates a key tumor suppressor, rather than inactivating it as previously thought.

“The finding is the result of literally 20 years of work in my lab,” said Steven F. Dowdy, Ph.D., professor in the Department of Cellular and Molecular Medicine at UC San Diego. “It completely turns upside-down what was thought to be a fundamental aspect of cell cycle progression in all cancer cells driven by one of the most common genetic pathways mutated in cancer, namely the p16-cyclin D pathway.”

he findings are published in the journal eLife.

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Biomarker predicts effectiveness of brain cancer treatment


UC San Diego researchers study microRNAs.

Clark Chen, UC San Diego

Researchers at the UC San Diego School of Medicine have identified a new biomarker that predicts whether glioblastoma – the most common form of primary brain cancer – will respond to chemotherapy. The findings are published in the July print issue of Oncotarget.

“Every patient diagnosed with glioblastoma is treated with a chemotherapy called temozolomide. About 15 percent of these patients derive long-lasting benefit,” said Clark C. Chen, M.D., Ph.D., vice chairman of academic affairs, Division of Neurosurgery, UC San Diego School of Medicine, and the study’s principal investigator. “We need to identify which patients benefit from temozolomide and which another type of treatment. All therapies involve risk and the possibility of side effects. Patients should not undergo therapies if there’s no likelihood of benefit.”

To pinpoint which patients were most likely respond to temozolomide, the researchers studied microRNAs that control the expression of a protein called methyl-guanine-methyl-transferase or MGMT. This protein dampens the cancer-killing effect of temozolomide. Tumors with high levels of MGMT are associated with a poor response to temozolomide therapy.

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Surgical biopsy proves safe for selected late-stage lung cancer patients


UC Davis findings should promote use of targeted treatments.

David Cooke, UC Davis

Researchers at UC Davis have determined that surgical biopsies can be safely performed on select patients with late-stage non-small cell lung cancer, which should enhance their access to drugs that target specific genetic mutations such as epidermal growth factor receptor (EGFR).

The findings, which will be published in the July issue of General Thoracic Surgery, address a common problem in treatment for advanced lung cancer: insufficient tumor tissue available for molecular analysis, which is required before prescribing targeted therapy.

“We will be allowing more people to be eligible for clinical trials, and ultimately that will provide value to the patient and access to treatments they may not have had otherwise,” said study lead author David T. Cooke, assistant professor and head of general thoracic surgery at UC Davis Medical Center.

In many cases of late-stage lung cancer, surgical biopsy is deemed too dangerous, so less invasive approaches are used, including fine needle aspiration and core needle biopsies.

“With clinical trials of new targeted therapies, an exhausting level of testing is performed,” Cooke said.  “With non-invasive biopsies, often there is not enough volume of cells collected to do the molecular testing.”

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Forbes, Buffett honor UCSF donor


Chuck Feeney recognized after decades of stealth philanthropy.

Chuck Feeney, after decades of anonymous and stealth philanthropy, has been caught in the spotlight by earning a Forbes 400 Lifetime Achievement Award.

In presenting the award, billionaire Warren Buffett referred to Feeney as his hero, and Bill Gates’ hero as well. “He should be everybody’s hero,” Buffett remarked.

Feeney, through his philanthropic arm The Atlantic Philanthropies, is UC San Francisco’s single greatest benefactor, giving more than a quarter of a billion dollars over the years. Proof of his epic generosity is visible most prominently at Mission Bay, where he has provided indispensable support to state-of-the-art buildings and created the environment for the remarkable science that goes on within them.

“Chuck’s approach to giving is based on backing great people in achieving demonstrable outcomes. As he has noted, ‘you should think of your philanthropic efforts as a business – out to achieve a demonstrable result,’” said Feeney’s business partner, Steve Denning, who accepted the honor on his behalf.

Feeney’s deep and wide investment in UCSF is evidence of his confidence in UCSF’s ability to deliver on its promise as a world-class bioscience center.

His most recent gift to UCSF has been to Global Health Sciences, enabling UCSF to build Mission Hall, which will house its global health researchers, scientists, and students under the same roof for the first time. The building opens this fall.

Feeney also has given generously to the building of the Smith Cardiovascular Research Building, Helen Diller Family Cancer Research Building, and the UCSF Medical Center at Mission Bay, which opens its doors in 2015.

“Chuck Feeney is an extraordinary human being – a visionary, a humanitarian, and a pragmatist,” said Interim Chancellor Sam Hawgood, M.B.B.S. “These traits have made him an indispensable partner in our evolution as a global health science hub. We are thrilled that he is being recognized for the magnitude of his remarkable generosity around the world.”

Committed to “giving while living,” Feeney transferred nearly all his and his family’s assets to The Atlantic Philanthropies with the intent to give it all away during his lifetime. For the first 15 years, Feeney swore The Atlantic Philanthropies staff to secrecy and gave anonymously, until he was outed by Forbes Magazine. By 2016, Atlantic Philanthropies will close its books, having emptied its $7.5 billion coffers into the promising causes Feeney has carefully chosen over the years.

“Chuck Feeney has changed the face of philanthropy,” said Hawgood. “Giving while living substantially increases the value of a gift both emotionally and financially. The working relationship we have with Chuck has been a source of inspiration for us all, personally and professionally.”

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Specialty pharmacy program helps patients adhere to oral chemotherapy


UC Davis cancer center plans to expand the program this fall.

Patients enrolled in the program can make an appointment with a pharmacist or a nurse practitioner any time they have a question about their drug regimen.

A UC Davis program designed to better manage cancer patients taking oral chemotherapy drugs has demonstrated that one-on-one counseling, education and monitoring can improve adherence to potentially life-saving cancer treatments.

The rise in oral chemotherapy development and use has heightened the need for coordinated cancer care. Oncology pharmacists and physicians worked together at UC Davis Comprehensive Cancer Center to create the Medication Adherence Pilot Program to ensure that patients stick to their regimens to safely maximize the drugs’ effectiveness and minimize or manage side effects.

Oral chemotherapy prescriptions are on the rise because many newer drugs, which target individual genes involved in tumor growth, are being developed in oral formulations, said Ted Wun, a medical oncologist and chief of the Division of Hematology and Oncology.

In addition, oral chemotherapy agents are created to allow for more continuous exposure of the drug in the patient over time, which can be more effective and may be less toxic. When oral treatment is prescribed exclusively, patients require fewer office visits and may get a greater sense of control over their treatment, Wun said.

Unlike traditional chemotherapy, which takes place in special infusion centers with nursing care, patients taking oral chemotherapy drugs may experience potentially life-threatening side effects without the information or immediate support they need. Or, patients may stop taking the medication or not follow the directions correctly, which can affect treatment efficacy, produce misleading treatment results and cause higher mortality.

“Patients are monitored when they’re here, but when they go home, it’s harder to monitor,” said Josephine Lai, the cancer center’s pharmacy supervisor, who has been assessing oral chemotherapy adherence rates since 2012. “Unlike other chronic care medications, oral chemo drugs can be more complicated. For example, one agent, Xeloda (capecitabine), is taken every 12 hours within 30 minutes of a meal for two weeks followed by a one-week break, before a new cycle begins. Sometimes we see people who didn’t realize they had a break in between their cycles.”

To improve patient care, Lai and colleagues in the UC Davis Departments of Pharmacy and Internal Medicine, and the Division of Hematology and Oncology launched the Cancer Center Medication Adherence Pilot Program in September 2013.

Patients enrolled in the program can make an appointment with a pharmacist or a nurse practitioner anytime they have a question about their drug regimen. Pharmacists also check in regularly each month to monitor patients’ progress, notify oncologists of any issues and offer practical tips, such as how to maintain a medication calendar or handle a missed dose.

Early indications suggest the program is working. In one assessment of 44 patients enrolled in the pilot program, 92 percent adhered to their drug regimens. Today, 80 patients at UC Davis Comprehensive Cancer Center are enrolled in the program. Beginning this fall, the cancer center will employ a full-time pharmacist dedicated to the program, offering the services to all UC Davis cancer patients.

“This is a great example of interdisciplinary collaboration among pharmacists, physicians, nurse practitioners and nurses,” said Lai. “And for our patients, who already face enough challenges, we hope it makes their cancer care a little easier.”

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Biologists find ‘missing link’ in production of protein factories in cells


UC San Diego discovery could lead to better understanding, potential treatment of cancer.

Biologists at UC San Diego have found the “missing link” in the chemical system that enables animal cells to produce ribosomes—the thousands of protein “factories” contained within each cell that manufacture all of the proteins needed to build tissue and sustain life.

Their discovery, detailed in the June 23 issue of the journal Genes & Development, will not only force a revision of basic textbooks on molecular biology, but also provide scientists with a better understanding of how to limit uncontrolled cell growth, such as cancer, that might be regulated by controlling the output of ribosomes.

Ribosomes are responsible for the production of the wide variety of proteins that include enzymes; structural molecules, such as hair, skin and bones; hormones like insulin; and components of our immune system such as antibodies. Regarded as life’s most important molecular machine, ribosomes have been intensively studied by scientists (the 2009 Nobel Prize in Chemistry, for example, was awarded for studies of its structure and function). But until now researchers had not uncovered all of the details of how the proteins that are used to construct ribosomes are themselves produced.

In multicellular animals such as humans, ribosomes are made up of about 80 different proteins (humans have 79 while some other animals have a slightly different number) as well as four different kinds of RNA molecules. In 1969, scientists discovered that the synthesis of the ribosomal RNAs is carried out by specialized systems using two key enzymes: RNA polymerase I and RNA polymerase III. But until now, scientists were unsure if a complementary system was also responsible for the production of the 80 proteins that make up the ribosome.

That’s essentially what the UC San Diego researchers headed by Jim Kadonaga, a professor of biology, set out to examine. What they found was the missing link — the specialized system that allows ribosomal proteins themselves to be synthesized by the cell.

“We found that ribosomal proteins are synthesized via a novel regulatory system with the enzyme RNA polymerase II and a factor termed TRF2,” Kadonaga says.  “For the production of most proteins, RNA polymerase II functions with a factor termed TBP, but for the synthesis of ribosomal proteins, it uses TRF2.”

“The discovery of this specialized TRF2-based system for ribosome biogenesis,” he adds, “provides a new avenue for the study of ribosomes and its control of cell growth, and should lead to a better understanding and potential treatment of diseases such as cancer.”

Other authors of the paper were UC San Diego biologists Yuan-Liang Wang, Sascha Duttke and George Kassavetis, and Kai Chen, Jeff Johnston, and Julia Zeitlinger of the Stowers Institute for Medical Research in Kansas City, Missouri. Their research was supported by two grants from the National Institutes of Health (1DP2OD004561-01 and R01 GM041249).

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