4 New Genetic Risk Factors Identified For Testicular Cancer

Main Category: Cancer / Oncology
Also Included In: Men's Health;??Genetics
Article Date: 14 May 2013 - 1:00 PDT Current ratings for:
4 New Genetic Risk Factors Identified For Testicular Cancer

A new study looking at the genomes of more than 13,000 men identified four new genetic variants associated with an increased risk of testicular cancer, the most commonly diagnosed type in young men today. The findings from this first-of-its-kind meta-analysis were reported online in Nature Genetics by researchers at the Perelman School of Medicine at the University of Pennsylvania.

The discovery of these genetic variations - chromosomal "typos," so to speak - could ultimately help researchers better understand which men are at high risk and allow for early detection or prevention of the disease.

"As we continue to cast a wider net, we identify additional genetic risk factors, which point to new mechanisms for disease," said Katherine L. Nathanson, MD, associate professor in the division of Translational Medicine and Human Genetics within the department of Medicine. "Certain chromosomal regions, what we call loci, are tied into testicular cancer susceptibility, and represent a promising path to stratifying patients into risk groups - for a disease we know is highly heritable."

Tapping into three genome-wide association studies (GWAS), the researchers, including Peter A. Kanetsky, PhD, MPH, an associate professor in the department of Biostatistics and Epidemiology, analyzed 931 affected individuals and 1,975 controls and confirmed the results in an additional 3,211 men with cancer and 7,591 controls. The meta-analysis revealed that testicular germ cell tumor (TGCT) risk was significantly associated with markers at four loci - 4q22, 7q22, 16q22.3, and 17q22, none of which have been identified in other cancers. Additionally, these loci pose a higher risk than the vast majority of other loci identified for some common cancers, such as breast and prostate.

This brings the number of genomic regions associated with testicular cancer up to 17 - including eight new ones reported in another study in this issue of Nature Genetics.

Testicular cancer is relatively rare; however, incidence rates have doubled in the past 40 years. It is also highly heritable. If a man has a father or son with testicular cancer, he has a four-to six-fold higher risk of developing it compared to a man with no family history. That increases to an eight-to 10-fold higher risk if the man has a brother with testicular cancer.

Given this, researchers continue to investigate genetic variants and their association with cancer.

In 2009, Dr. Nathanson and colleagues uncovered variation around two genes - KITLG and SPRY4 - found to be associated with an increased risk of testicular cancer. The two variants were the first striking genetic risk factors found for this disease at the time. Since then, several more variants have been discovered, but only through single GWAS studies.

"This analysis is the first to bring several groups of data together to identify loci associated with disease," said Dr. Nathanson, "and represent the power of combining multiple GWAS to better identify genetic risk factors that failed to reach genome-wide significance in single studies."

The team also explains how the variants associated with increased cancer risk are the same genes associated with chromosomal segregation. The variants are also found near genes important for germ cell development. These data strongly supports the notion that testicular cancer is a disorder of germ cell development and maturation.

"TGCT is unique in that many of the loci are very good biological candidates due to their role in male germ cell development," said Dr. Nathanson. "Disruptions in male germ cell development lead to tumorigenesis, and presumably also to infertility. These conditions have been linked before, epidemiologically, and genes implicated in both of our prior studies, but this study reinforces that connection."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. This study was supported in part by Intramural Research Program of the National Cancer Institute and the National Institutes of Health grant (R01CA114478).
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No Benefit Offered By Bevacizumab For Newly Diagnosed Glioblastoma

Main Category: Cancer / Oncology
Also Included In: Neurology / Neuroscience
Article Date: 04 Jun 2013 - 0:00 PDT Current ratings for:
No Benefit Offered By Bevacizumab For Newly Diagnosed Glioblastoma

The angiogenesis inhibitor bevacizumab (Avastin) failed to increase overall survival (OS) or statistically significant progression-free survival (PFS) for glioblastoma patients in the frontline setting, according to research led by researchers at The University of Texas MD Anderson Cancer Center.

The study was presented at the American Society of Clinical Oncology 2013 Annual Meeting by Mark Gilbert, M.D., professor in MD Anderson's Department of Neuro-Oncology.

Glioblastoma is both the most common and lethal form of brain cancer. More than 12,000 people will be diagnosed with the disease in 2013, with an average survival rate of less than 18 months, said Gilbert.

Bevacizumab works as a monoclonal antibody against VEGF-A, which is produced by glioblastoma to stimulate blood vessel growth. The angiogenesis inhibitor first showed promise in glioblastoma as clinicians reported positive results treating the disease under approved compassionate use. Numerous institutional studies then found similar results: a 35-40 percent objective response rate, or tumor shrinkage, of more than 50 percent, and a six-month PFS rate in the mid-30 percent, said Gilbert. With those findings, in May, 2009, the FDA granted an accelerated registration of bevacizumab in the second line setting.

However, before this trial, no randomized, double-blind studies with the drug in glioblastoma had been conducted.

"Obviously, glioblastoma is a cancer with too few effective therapies," said Gilbert, who also holds the Blanche Bender Professorship in Cancer Research. "When we launched this study, those in the field of brain cancer - both the scientific and patient communities - were excited. Bevacizumab recently received approval in the second-line (recurrent disease) setting, and we knew some physicians were already giving the drug as a frontline therapy - even with virtually no data to support that decision. It was important from a patient care and regulatory standpoint that we conduct this trial."

The Phase III, international study (RTOG 0825) was a collaboration of three cooperative groups: RTOG, NCCTG and ECOG.

The randomized, double-blind, placebo-controlled study registered 978 and enrolled 637 patients, respectively, all of whom were newly diagnosed with glioblastoma. Participants underwent surgery to resect some or most of the tumor, received the standard of care of chemoradiation with temozolomide, and were randomized to receive either bevacizumab or placebo. The study was designed with two primary endpoints: PFS and OS.

Two distinguishing factors of the study design include: crossover to bevacizumab in the placebo arm at the time of progression, and longitudinal assessment of symptom burden, neurocognitive function and quality of life.

"With the crossover, we could determine the possible overall, or progression free survival benefits that could distinguish the potential benefits of early versus later use of bevacizumab," Gilbert said. "Also, there may be some alternative advantages for delaying progression in the disease. In order to interpret that possible delay in progression, it was important to understand what the quality of the survival of that possible progression free survival interval."

A third distinction: the study was designed to look at the impact of pre-specified molecular markers -- a nine-gene signature expression and MGMT methylation -- to determine if a subgroup that specifically benefited from bevacizumab could be identified.

The researchers found no difference in OS between the bevacizumab and placebo arms, 15.7 and 16.1 months, respectively. PFS did not reach the pre-set level statistical significance -- although longer ??in those taking bevacizumab upfront (10.7 months), compared to in those receiving placebo (7.3 months).

Bevacizumab was associated with a higher rate of toxicities, including hypertension, bleeding, deep vein thrombosis and pulmonary embolism, and gastrointestinal perforation. Those on the therapy also experienced increase rates of symptom burden and neurocognitive decline, as well decreased quality of life, compared to those on placebo.

When looking at the molecular markers, no subgroup of patients that benefitted from bevacizumab could be identified, said Gilbert.

Despite the disappointing findings, Gilbert stressed that the study did not find that bevacizumab had no place in the management of glioblastoma.

"Ultimately, our study showed that bevacizumab has the same benefit whether given early or late and because of the risk of extra toxicity upfront, its used can be reserved as a later treatment for most patients," said Gilbert.

Complementary studies detailing quality of life, symptom burden and molecular findings will all be presented by MD Anderson faculty at the meeting.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Abstract 1

In addition to Gilbert, others on the international study include: Kenneth D. Adalpe, M.D., Paul D. Brown, M.D., Ritsuko Komaki, M.D., Eric Sulman, M.D. Ph.D., and Jeffrey Wefel, all of MD Anderson; James Dignam, Ph.D., and Minhee Won, both of RTOG; Minesh Mehta, M.D., professor, University of Maryland Medical Center; Deborah T. Blumenthal, M.D., Tel Aviv Sourasky Medical Center; Michael A. Vogelbaum, M.D., Ph.D., Cleveland Clinic Foundation; Howard Colman, M.D., Ph.D., Huntsman Cancer Institute; Arnab Chakravarti, M.D., Arthur James Cancer Center; Robert Jeraj, Ph.D., University of Wisconsin; Terri S. Armstrong, Ph.D., University of Texas Health Science Center School of Nursing; Kurt Jaeckle, M.D., Mayo Clinic Florida; David Schiff, M.D., University of Virginia Medical Center; James Atkins, M.D., National Surgical Adjuvant Breast and Bowel Project and SCCC-CCOP; David Brachman, M.D., Arizona Oncology Services Foundation; and Maria Werner-Wasik, M.D., Thomas Jefferson University Hospital.

Gilbert is on Roche's advisory board; Genentech financially supported the 0825 study; it was also supported by NCI U10CA 21661, U10 CA37422.

University of Texas M. D. Anderson Cancer Center

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posted by Greg P. on 4 Jun 2013 at 1:16 pm

Wow! This is blockbuster news! In one study, patients who were expected to benefit the most from Avastin based on "genetic" testing had the worst survival rates.

Bevacizumab-induced tumor calcifications can be elicited in glioblastoma microspheroid culture and represent massive calcium accumulation death (MCAD) of tumor endothelial cells

http://precedings.nature.com/documents/7069/version/1

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A Wide Variety Of Advanced Cancers Harbor Abnormalities In HER2 Gene

Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 04 Jun 2013 - 1:00 PDT Current ratings for:
A Wide Variety Of Advanced Cancers Harbor Abnormalities In HER2 Gene

The HER2 growth-factor gene is known to be over-active in breast and gastro-esophageal cancers. But now, irregularities in the genes 's expression - among them mutations, amplifications, substitutions, and translocations - have been found in 14 different advanced solid tumors.

The results of the study of more than 2,000 tumors, presented at the annual meeting of the American Society of Clinical Oncology (ASCO), both surprised researchers and provided hope that some of these tumors might benefit from the three anti-HER2 therapies now in clinical use.

"No one ever thought that there would be such a variety of genomic alterations in HER2 in this many solid tumors," says Massimo Cristofanilli, MD, FACP, Professor of Medical Oncology and Director of the Jefferson Breast Center at the Kimmel Cancer Center and Thomas Jefferson University Hospital.

"But this may be good news, both clinically and scientifically," he says. "It tells us that these tumors might benefit from treatment that we already have on hand, and, from a research perspective, it builds on the idea that it is the genomic profile of a tumor that is relevant in providing biological information for planning of personalized treatments - not where the cancer is located or where it develops.'

Dr. Cristofanilli presented the results of the study in an oral presentation at the ASCO meeting. He is one of a group of co-authors from many institutions who donated tumor samples to Foundation Medicine, a cancer diagnostics company in Cambridge, Massachusetts. Foundation Medicine led and paid for the study.

Dr. Cristofanilli contributed about 50 metastatic breast tumor samples for the analysis, and found out that one of his patients with advanced triple negative breast cancer had a HER2 mutation. "My patient was treated with Herceptin as well as chemotherapy, and derived clinical benefit," he says. "No one looks for HER2 mutations in this form of breast cancer. To me, this makes the case for the value of genome-driven therapy."

In the study, Foundation Medicine conducted a genetic screen of more than 182 genes and 14 genetic rearrangements known to be linked to cancer in 2,223 tumor specimens. Twenty different advanced solid cancers were represented.

Researchers found HER2 alterations in 14 types of solid tumors, including 29 percent of esophageal, 20 percent of uterine, 14 percent of breast, 12 percent of stomach carcinomas, and 6 percent of all lung cancer samples.

They also found HER2 irregularities varied widely - 4.9 percent of specimens had 116 different HER2 alterations. That included 58 percent with amplifications, 25 percent with substitutions, 14 percent with indels (insertions/deletions of DNA), 2 percent with splice site variants, 2 percent with translocations, 5 percent with multiple alterations, and 2 tumors had both HER2 substitution and amplification.

Anti-HER2 therapies such as Herceptin can also treat HER2 mutations, and may also help block HER2 that is altered in the ways seen in the study, Dr. Cristofanilli says.

"This study highlights the need to study a broad range of genes at a high level of sensitivity and specificity when searching for novel targets of therapy," he says. "Widespread use of this approach could provide more treatment options and enable more rapid accrual to ongoing and planned trials of agents targeting pathways under study."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Dr. Cristofanilli declares no conflicts of interest related to this study.
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posted by John M. on 4 Jun 2013 at 11:37 am

I often think of cancer as a disease where the body doesn't attack its own tissue and autoimmune diseases as a disease where it attacks it too much. So it occurs to me that like cancer maybe some autoimmune diseases of different organs may be caused by the same underlying genetic mutation and therefore you could determine if drugs that treat one type of autoimmune disease might treat others . . .

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Sorafenib Stops Tumor Growth And Provides The First Effective Treatment For Thyroid Cancer Patients Who Progress Following Standard Therapies

Main Category: Cancer / Oncology
Also Included In: Endocrinology;??Ear, Nose and Throat
Article Date: 04 Jun 2013 - 0:00 PDT Current ratings for:
Sorafenib Stops Tumor Growth And Provides The First Effective Treatment For Thyroid Cancer Patients Who Progress Following Standard Therapies

The kidney and liver cancer drug sorafenib holds metastatic thyroid cancer at bay for nearly twice as long as a placebo, according to results of a randomized phase III trial, which was presented by a researcher from the Abramson Cancer Center and the Perelman School of Medicine at the University of Pennsylvania in a plenary session during the American Society of Clinical Oncology's annual meeting (Abstract #4).

If approved for use in thyroid cancer patients by the Food and Drug Administration, sorafenib (Nexavar), a kinase inhibitor that mediates tumor cell division and growth of tumor blood vessels, would be the first effective agent for this patient population. Thyroid cancer is highly curable through surgery and radioactive iodine treatment, but about 10 percent of the 60,000 patients who are diagnosed with the disease each year fail to respond to standard therapies, with tumors eventually appearing in the lymph nodes, bones, lungs, and other sites. The only other drug for advanced thyroid cancer, doxorubicin, which was approved in 1974, is not used because it is highly toxic and is not effective.

"Until we began using sorafenib, we had no medical options for these patients who suffered due to progression of their disease," said Marcia S. Brose, MD, PhD, an assistant professor of Otolaryngology and Head and Neck Surgery and Hematology/Oncology, who led the study, which is known as DECISION. "Now, we can give patients hope - a breakthrough medication that can stop the progression of the disease for 5 months. This trial is the first step in a promising series of clinical trials to identify new drugs that are shifting the horizon for patients with advanced thyroid cancer."

Of the 417 metastatic thyroid cancer patients studied in the multicenter, international trial, 207 were randomized to take sorafenib, an oral drug, and 210 to a placebo arm. Twelve percent of patients experienced tumor shrinkage in the sorafenib arm, compared to 0.5 percent of patients taking a placebo. Importantly, the therapy also appeared to thwart disease progression even among many of those whose tumors did not regress: 42 patients who took sorafenib had stable disease after six months, compared to 33 percent of those in the placebo group.

Among patients taking sorafenib, median progression-free survival was 10.8 months, compared to 5.8 months among the placebo group. Patients taking the placebo were allowed to cross over into the sorafenib arm once their disease progressed; 70 percent of them did so. Overall survival data is not yet available.

The most common adverse events observed among patients taking sorafenib included hand-foot skin reaction, diarrhea, alopecia, rash, fatigue, weight loss and hypertension, all of which are consistent with findings from previous trials of the drug for its approved indications.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Bayer HealthCare Pharmaceuticals and Onyx Pharmaceuticals provided funding for the trial. Editor's note: Dr. Brose has received consulting fees and honoraria from these companies.
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University of Pennsylvania School of Medicine. (2013, June 4). "Sorafenib Stops Tumor Growth And Provides The First Effective Treatment For Thyroid Cancer Patients Who Progress Following Standard Therapies." Medical News Today. Retrieved from
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Researchers reveal new potential means to suppress tumor growth

Main category: Cancer / Oncology
Also included in: genetics
Article Date: June 5, 2013-0:00 PDT current ratings for:
Researchers reveal new potential means to suppress tumor growth

Researchers at the University of California, San Diego School of Medicine, with colleagues at the University of Rochester Medical Center have identified a new mechanism that seems to remove the tumor growth, opening up the possibility of developing a new class of anti-cancer drugs.

Written in first editions online this week by the proceedings of the Academy national of Sciences (PNAS), Willis X. Li, Ph.d., Professor in the Department of medicine at UC San Diego, reports that a particular form of signaling called STAT5A protein stabilizes the formation of heterochromatin (a form of chromosomal DNA), which in turn removes the ability of cancer cells to give instructions to multiply and grow.

Specifically, Li and his colleagues concluded that the place of STAT form promotes and stabilizes the heterochromatin, which keeps DNA closely packed and inaccessible to transcription factors. "As a result, genes 'buried' in heterochromatin are not expressed," said Li.

Phosphorylation is a fundamental cellular function in which a phosphate group is added to a protein or molecule, the cause to activate or disable or modify its function. A STAT place lack of this phosphate group.

Li said that in previous studies with the fruit flies, the place of STAT caused chromatin form to condense in heterochromatin, while the phosphorylated version prompted the dispersal and loss of the heterochromatin, promoting the expression of genes.

"STAT site promotes and stabilizes the formation of heterochromatin, which in turn removes the gene transcription," Li said. "when we have expressed either HP1 (the central element of the heterochromatin) or place STAT5A in human cancer cells, several genes important for the growth of the cancer are removed." These cancer cells do not grow as fast or as large as their cancer cells parental control in xenograft models mouse."

Most suppressors tumor known, such as p53 or Rb function by inhibiting the progression of the cell cycle or by stimulating cell death or apoptosis. Li said their findings indicate a potential new way to inhibit the expression of the genes of cancer and could constitute a new class of tumour suppressors.

"We are trying to identify drugs to small molecules that can promote the formation of heterochromatin without stopping cell division or causing the death of the cell," he said. "These drugs, if found, may be effective in treating cancer with fewer side effects."

Article adapted by Medical News Today press release original. Click on "references" tab above for the source.
Visit our cancer / Oncology section for the latest news on this subject. Co-authors are Xiaoyu Hu, Amy Tsurumi and Hartmut Land, Department of biomedical genetics, University of Rochester Medical Center; Pranabananda Dutta, Jinghong Li and Jingtong Wang, Department of medicine, UCSD.
Funding of this research came, in part, grants from the National Institutes of Health R01CA131326 and RO1CA138249 and a leukemia & Lymphoma Society Research Scholar grant.
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10 Years On Tamoxifen Halves Breast Cancer Recurrence Risk

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Main Category: Breast Cancer
Also Included In: Cancer / Oncology
Article Date: 03 Jun 2013 - 4:00 PDT
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10 Years On Tamoxifen Halves Breast Cancer Recurrence Risk

Survivors who take tamoxifen for ten years have half the risk of dying from estrogen receptor positive breast cancer, researchers from Cancer Research UK reported at the ASCO Annual Meeting in Chicago, Illinois, USA.

Lead researcher, Dr Daniel Rea reported that the "aTTom" study demonstrated that estrogen receptor positive breast cancer patients who took tamoxifen for longer than five years were much less likely to suffer cancer recurrence or die from the disease. Currently, the recommended period for tamoxifen therapy is five years.

The study involved 6,953 adult females with breast cancer. 580 patients from 3,468 women took tamoxifen for ten years, while 672 of 3,485 patients stopped tamoxifen after five years.

Dr Rea reported that: 25% of the 10-year tamoxifen patients had fewer recurrences of breast cancer than those on just five years of therapyThere were 23% fewer deaths in the 10-year tamoxifen groupDr Daniel Rea, who is based at the University of Birmingham, England, said:

"These results are important as they establish that giving tamoxifen for longer than the current standard of five years significantly cuts the risk of breast cancer returning.

Doctors are now likely to recommend continuing tamoxifen for an extra five years and this will result in many fewer breast cancer recurrences and breast cancer deaths worldwide. Tamoxifen is cheap and widely available so this could have an immediate impact."

Approximately three-quarters of all breast cancers are of the estrogen receptor positive kind. This type of breast cancer benefits from hormone therapy. Estrogen, a female hormone, encourages breast cancers to grow by activating estrogen receptors. Tamoxifen works by blocking these receptors, thus making it much harder for the cancer to recur after surgery or invade the other breast.

Tamoxifen side effects - patients on tamoxifen may experience menopausal-type symptoms, including hot flashes (UK: hot flushes) and night sweats. A Norwegian study found that acupuncture reduces menopausal symptoms in tamoxifen patients by 50%. More rarely, tamoxifen has also been linked to an increased risk of developing blood clots, endometrial cancer and stroke.

Stroke risk did not rise with 10 years of tamoxifen therapy compared to five years, the researchers found. However, the risk of endometrial cancer did increase. Fortunately, endometrial cancer is usually diagnosed in the early stages of the disease, when it can be treated successfully.

According to the researchers, thirty breast cancer deaths would be prevented for every endometrial cancer death due to long-term tamoxifen therapy.

Professor Richard Gray, who is based at the University of Oxford and was also presenting the aTTom trial results at ASCO, said:

"Five years of tamoxifen is already an excellent treatment but there have been concerns that giving it for longer might not produce extra benefits and could even be harmful. The aTTom study establishes that the benefits of taking tamoxifen for longer greatly outweigh the risks.

Kate Law, director of clinical research at Cancer Research UK, said: "Large clinical trials like aTTom are vitally important to understand how drugs such as tamoxifen work and how best to use them. We need these sorts of studies so we can be sure the benefits from cancer drugs outweigh the side-effects that they may have."

The aTTom trial was funded by the Medical Research Council, UK.

A trial led by Oxford University's Clinical Trial Service Unit reported in The Lancet (December 2012 issue) that taking tamoxifen for ten years after breast cancer surgery is more effective than five years. The study was called ATLAS.

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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Inostics' Blood-Based Mutation Testing Receives CLIA Certification

Main Category: Cancer / Oncology
Also Included In: Regulatory Affairs / Drug Approvals;??Blood / Hematology
Article Date: 04 Jun 2013 - 2:00 PDT Current ratings for:
Inostics' Blood-Based Mutation Testing Receives CLIA Certification

Inostics, a molecular diagnostics company that provides blood-based mutation testing, received CLIA (Clinical Laboratory Improvement Amendments) licensure for its clinical laboratory located in Baltimore, MD. This marks a critical milestone for the clinical adoption of this non-invasive molecular approach for the analysis of tumor biomarkers.

"Due to the non-invasiveness and real-time reflection of tumor genetics, the OncoBEAM blood test represents a valuable tool to complement clinical decision making. We are extremely excited to be able to bring this solution to cancer patients as OncoBEAM tests offer a significant enhancement to clinical care over traditional tissue-based molecular testing," Dr. Frank Diehl, CSO of Inostics, said.

The OncoBEAM blood test is based on BEAMing technology which combines emulsion based digital PCR with flow cytometry. This technology enables the molecular analysis of tumor DNA shed from primary and metastatic tumors, found circulating in the blood of patients.

Due to its non-invasiveness, OncoBEAM blood tests introduce new possibilities for the management of various cancers like skin, colorectal, breast, and lung cancer. Now a simple blood draw can support clinical decision making in the context of therapy selection, assessment of drug response, resistance and recurrence monitoring, and detection of minimal residual disease (MRD).

Article adapted by Medical News Today from original press release. Source: Source: Inostics
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