Demand for Spanish-language cancer Web materials quadruples

Contact: Beth Bukata
bethb@astro.org
703-431-2332
American Society for Therapeutic Radiology and Oncology

Internet resources and access remain scarce

Although Spanish-speaking cancer patients are rapidly increasing their search for patient education resources on the Internet, there are very few Spanish-language Web sites available to provide this information, according to a study presented October 28, 2007, at the American Society for Therapeutic Radiology and Oncology’s 49th Annual Meeting in Los Angeles.

Spanish-speaking cancer patients were also shown to have more limited access to the Internet compared to English-speaking users of cancer information Web sites, based on the user patterns of the two groups.

“There is an urgent need for more Web-based information to be more available to Spanish-speaking patients with cancer, and Internet access needs to be more widely available,” said Charles Simone II, M.D., lead author of the study and a radiation oncologist at the Hospital of the University of Pennsylvania in Philadelphia. “The increased knowledge gained among these patients will help to eliminate healthcare disparities and lead to improved medical outcomes.”

The Spanish-language cancer information Web site, OncoLink en español, quadrupled their number of unique visitors last year, from 7,000 visitors per month in January 2006 to nearly 29,000 monthly visitors by the end of the year. More than 200,000 users visited the Web site in 2006.

In contrast, the English-language version of the site, OncoLink, had nearly 2 million visitors last year, although their number of unique visitors did not increase throughout the year. OncoLink en espanõl was launched in 2005 by OncoLink, one of the oldest and largest Internet-based cancer information resources. Both sites are managed by the University of Pennsylvania.

The study shows that OncoLink en español users were less likely to browse the Internet during weekends and morning hours, compared to the users who browsed OncoLink, suggesting that they are accessing the Internet more through work or specialized services.

In addition to when they accessed the Internet, OncoLink en español users also differed on the types of cancers they searched for, as well as the timing and method of their Internet search patterns.

“Awareness of these differences can assist cancer education Web sites to tailor their content to best meet the needs of their Spanish-speaking users,” said Dr. Simone.

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The study was carried out using AWStats, a Web-data analyzing program, to collect and compare statistical data from the secure servers of both language versions of OncoLink.

For more information on radiation therapy in English and in Spanish, visit http://www.rtanswers.org.

The abstract, “The Utilization of Radiation Oncology Web-based Resources in Spanish-speaking Oncology Patients,” will be presented for poster viewing starting at 10:00 a.m, Sunday, October 28, 2007. To speak to the study author, Charles Simone, II, M.D, please call Beth Bukata or Nicole Napoli October 28-31, 2007, in the ASTRO Press Room at the Los Angeles Convention Center at 213-743-6222 or 213-743-6223. You may also e-mail them at bethb@astro.org or nicolen@astro.org.

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U-M researchers find family of ‘on switches’ that cause prostate cancer

Gene fusions trigger cancer growth, could impact treatment choices

ANN ARBOR, Mich. — Researchers at the University of Michigan Comprehensive Cancer Center have discovered how genes turn on the switch that leads to prostate cancer.

The team discovered that pieces of two chromosomes can trade places with each other and cause two genes to fuse together. The fused genes then override the “off” switch that keeps cells from growing uncontrollably, causing prostate cancer to develop.

By testing these gene fusions in mice and in cell cultures, the researchers showed that the fusions are what cause prostate cancer to develop. But it’s not just one set of genes that fuse. The researchers found that any one of several in a family of genes can become scrambled and fuse. Results of the study appear in the Aug. 2 issue of Nature.

“Each of these switches, or gene fusions, represent different molecular subtypes. This tells us there’s not just one type of prostate cancer. It’s a more complex disease and potentially needs to be treated differently in each patient,” says lead study author Arul Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology, a new U-M center whose goal is to translate research into real world practice.

The gene fusion research is the centerpiece project of the new center. In the current study, researchers found one of several abnormal gene fusions in the prostate cancer tissue samples they tested. In 2005, the researchers identified a prostate-specific gene called TMPRSS2, which fuses with either ERG or ETV1, two genes known to be involved in several types of cancer.

The Nature paper reports on five additional genes that fuse with ERG or ETV1 to cause prostate cancer. Gene fusions were involved in 60 percent to 70 percent of the prostate cancer cell lines the researchers looked at. The genes involved are all controlled by a different mechanism. For example, four of the genes are regulated by androgen, a male sex hormone known to fuel prostate cancer. Androgen deprivation is a common therapy for prostate cancer.

Knowing which gene fusion is involved in an individual patient’s tumor could impact treatment options. If an androgen-regulated gene is involved, androgen therapy would be appropriate. But if the gene fusion involves a gene that represses androgen, the anti-androgen therapy could encourage the cancer’s growth. This may also explain why androgen treatment is not effective for some prostate cancers.

“Typing someone’s prostate cancer by gene fusion can affect the treatment given. We would not want to give androgen to someone whose prostate cancer gene fusion is not regulated by androgen,” says Chinnaiyan, who is the S.P. Hicks Collegiate Professor of Pathology at the U-M Medical School.

Rearrangements in chromosomes and fused genes are known to play a role in blood cell cancers like leukemia and lymphoma, and in Ewing’s sarcoma. A fused gene combination that plays a role in chronic myelogenous leukemia led researchers to develop the drug Gleevec, which has dramatically improved survival rates for that disease.

Chinnaiyan believes the prostate gene fusions will eventually lead to similar treatments for prostate cancer.

“More immediately, we hope to develop tests for diagnosis or prognosis. But long-term, we hope this will lead to better therapies to treat prostate cancer. The key challenge is to find a drug that would go after this gene fusion,” Chinnaiyan says.

The gene fusion technology has been licensed to San Diego-based Gen-Probe Inc., which is working on a screening tool to detect gene fusions in urine. The tool could one day supplement or replace the prostate specific antigen, or PSA, test currently used to screen for prostate cancer.

The idea of translating laboratory research findings into a test or treatment that will impact patients is central to the new Michigan Center for Translational Pathology. The center brings together experts in genomics, proteomics and bioinformatics to look at common patterns and potential targets in cancer and other diseases. This is the first center of its kind in the nation in that it is associated with one of 39 National Cancer Institute-designated “comprehensive” cancer centers, a premier medical school and a large health system with both clinicians and patients.

The center’s goal is to study the genes, proteins and other markers on cells to develop new diagnostic tests or screening tools as well as targeted treatments for cancer and other diseases, with the key being to translate these laboratory discoveries into clinical applications.

Chinnaiyan and his team have received numerous awards and honors, including the American Association for Cancer Research Team Science Award for their previously published work on gene fusions, and the Specialized Program of Research Excellence Outstanding Investigator award. The new Center for Translational Pathology supported in part by the Prostate Cancer Foundation, which has offered to match up to $1 million dollars in donations to support work related to developing therapies against prostate cancer gene fusions at the university.

“Mapping of the human genome was only the beginning. Equipped with the comprehensive analysis of the human genome, we can now systematically examine the blueprint of disease at the molecular level. This essential knowledge may lead to better diagnostic tests and promising new treatments for cancer, cardiovascular disease, diabetes and other illnesses,” Chinnaiyan says.

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For information about the Michigan Center for Translational Pathology, go to http://www.med.umich.edu/mctp.

About 218,890 men will be diagnosed with prostate cancer this year, and 27,050 will die from the disease, according to the American Cancer Society. The gene fusion work is not currently available for treatment or diagnosis, and no clinical trials are currently recruiting. For information about prostate cancer and currently available treatments, go to http://www.mcancer.org or call the U-M Cancer AnswerLine at 800-865-1125.

In addition to Chinnaiyan, U-M study authors were Scott Tomlins; Saravana Dhanasekaran, Ph.D.; Bharathi Laxman; Qi Cao; Beth Helgeson; Xuhong Cao; David Morris, M.D.; Anjana Menon; Xiaojun Jing; Bo Han; James Montie, M.D.; Kenneth Pienta, M.D.; Diane Roulston; Rajal Shah, M.D.; Sooryanarayana Varambally, Ph.D.; and Rohit Mehra, M.D. Mark Rubin, M.D., from Brigham and Women’s Hospital, Dana-Farber Cancer Institute and Harvard Medical School is also a study author.

Funding for the study came from the U.S. Department of Defense, the National Institutes of Health, the Early Detection Research Network, the Prostate Cancer Foundation and Gen-Probe Inc.

The University of Michigan has filed for a patent on the detection of gene fusions in prostate cancer, on which Tomlins, Mehra, Rubin and Chinnaiyan are co-inventors. The diagnostic field of use has been licensed to Gen-Probe Inc. Chinnaiyan also has a sponsored research agreement with Gen-Probe; however, GenProbe has had no role in the design or experimentation of this study, nor has it participated in the writing of the manuscript.

Reference: Nature, Vol. 448, No. 7153, Aug. 2, 2007

Contact: Nicole Fawcett
nfawcett@umich.edu
734-764-2220
University of Michigan Health System

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New research provides hope for childhood cancer sufferers

Dr Richard Lock, Head of the Leukaemia Biology Program at the Children’s Cancer Institute Australia for Medical Research, Sydney, along with collaborators from the Childrens Hospital Los Angeles and University of Southern California, USA, recently published their findings in the prestigious scientific journal Blood.

ALL is the most common form of childhood cancer. Over the years, improvements in primary therapy have increased the cure rate to approximately 80 percent. However, for the 20 percent of patients who relapse, the majority will die.

“When used in combination with common drugs administered in ALL therapy, ABT-737 has the ability to enhance the combined toxicity of these drugs against the leukaemia cells with minimal effects on the normal cells of the body,” said Dr Lock.

Resistance to common therapeutic drugs is associated with poor long-term outcomes in leukaemia patients. In the study, the effects of ABT-737 in combination with three common chemotherapeutic agents: L-Asparaginase, vincristine and dexamethasone, were tested on a number of ALL cell lines under conditions which were considered clinically relevant for the disease.

ABT-737, developed by Abbott Laboratories, acts by inhibiting the Bcl-2 family of proteins. These proteins are expressed in ALL and inhibit the mechanisms responsible for destroying leukaemia cells. High levels of expression of Bcl-2 is linked with chemoresistance in a variety of cancers.

“There is a critical need for new drugs with novel mechanisms of action that might improve the outcome for relapsed ALL patients,” said Dr Lock.

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The manuscript is available online at http://bloodjournal.hematologylibrary.org/papbyrecent.dtl Children’s Cancer Institute Australia for Medical Research is associated with the University of NSW and Sydney Children’s Hospital.

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Dealing deadly cancers a knockout punch

Contact: Cathy Ward
cathy.ward@oncolyticsbiotech.ca
403-670-7370
Oncolytics Biotech Inc.

New scientific evidence is helping to build a compelling case for oncolytic viruses as a first-line and adjunctive treatment for many cancers.

Reovirus, a non-pathogenic virus under development at Calgary, Alberta-based Oncolytics Biotech, has shown powerful anti-cancer activity against cultured tumor cells, in animal models, and in human clinical trials. Oncolytics’ proprietary reovirus formulation, Reolysin®, is active against numerous cancers, including intractable sarcomas and melanomas.

Recent studies also indicate that Reolysin works synergistically with standard anti-cancer drugs, providing significantly stronger responses than either agent alone.

In addition, other studies completed in the past year have shown Reolysin has the ability to prime patients’ immune systems against their particular cancer, leading to additional cancer cell killing. It is through this second “inflammatory” mechanism that researchers hope Reolysin will bring about long-term remissions of once-untreatable cancers.

At the Fourth International Conference on Oncolytic Viruses as Cancer Therapeutics in March 2007 in Scottsdale, Arizona, several presentations focused on reovirus efficacy alone or in combination with standard chemotherapies.

In one study, investigators examined the tumor-killing ability of reovirus plus cisplatin, a standard chemotherapy agent, in a mouse melanoma model that included both cultured cells and live animals. The results of the preclinical study showed that the combination of reovirus and cisplatin was significantly more effective than cisplatin or reovirus alone at killing melanoma cancer cells in a mouse model. The investigators intend to explore the mechanism of this promising synergistic action in further detail in future preclinical work.

Another presentation at the Arizona conference reported on the use of Reolysin plus the cancer drug cyclophosphamide in an animal model of melanoma. When treated with both agents, test animals experienced enhanced tumor regression compared with either agent alone, and without additional toxicity. Oncolytics has permission from the U.K. regulatory authorities to test Reolysin in three separate human trials in combination with the cancer drugs gemcitabine, paclitaxel/carboplatin and docetaxel.

Perhaps the most exciting findings of Reolysin combination therapy were reported at the American Association for Cancer Research Annual Meeting in April, 2007. In mice transplanted with a human colon cancer, Reolysin plus gemcitabine completely eradicated the tumors in four of five test animals. It is rare to see the virtual elimination of tumours as well as the long-lasting therapeutic effect that was observed in this study.

“Combination therapy results for reovirus in animals are particularly encouraging because they suggest that Reolysin can improve the anti-tumor activity of standard chemotherapy agents in advanced cancer patients without causing additional toxicity,” said Dr. Karl Mettinger, Chief Medical Officer of Oncolytics.

Physicians often prefer to treat cancer with multiple agents, but toxicity limits these approaches. Since reovirus typically is not pathogenic in humans nor associated with severe toxicity in clinical studies, its co-administration is not expected to increase a treatment’s overall toxicity.

Dual Mechanism

Reovirus works by entering and replicating within cancer cells containing an activated ras pathway, a mutation present in about two-thirds of all human cancers. Reovirus enters a cancer cell, makes thousands of copies of itself, and then causes the cell to burst, which releases viruses that infect and kill adjacent cancer cells. Normal cells are not harmed.

In addition to killing cancer cells directly, reovirus is believed to activate an anti-tumor immune response through the body’s natural killer cells and T cells. Through this mechanism, which persists for weeks or months, the body continues to fight off cancer long after the virus clears from the body.

Future directions

On April 11, 2007, Oncolytics announced it had initiated a Phase II trial to evaluate intravenous administration of Reolysin in patients with sarcomas that have metastasized to the lung. For patients with deadly soft tissue sarcoma, the lungs are the most common site of metastatic disease. To date, surgery has been the only effective therapy for metastatic sarcoma.

The multi-center, Phase II study follows successful completion of systemic administration trials with Reolysin in the U.K. and the U.S. This will be the second of several Phase II trials Oncolytics plans for 2007. The Company also has a collaborative agreement with the U.S. National Cancer Institute to conduct multiple clinical trials with Reolysin which are expected to begin in 2007, including a Phase II melanoma trial and a Phase I/II ovarian cancer trial.

“It is hoped that the trials will clearly show that Reolysin alone or in combination with either radiation or chemotherapy can stop or reverse the growth of advanced cancers without adding harmful side effects,” said Dr. Mettinger.

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