(Posted: 11/27/2012) - Researchers at The University of Texas MD Anderson Cancer Center have tracked down a cancer-promoting protein's pathway into the cell nucleus and discovered how, once there, it fires up a glucose metabolism pathway on which brain tumors thrive. They also found a vital spot along the protein's journey that can be attacked with a type of drug not yet deployed against glioblastoma multiforme, the most common and lethal form of brain cancer. Published online by Nature Cell Biology, the paper further illuminates the importance of pyruvate kinase M2 (PKM2) in cancer development and progression.

(Posted: 11/27/2012) - Discovery of a new drug with high potential to treat Ewing sarcoma, an often deadly cancer of children and young adults, and the previously unknown mechanism behind it, come hand-in-hand in a new study by researchers from Huntsman Cancer Institute (HCI) at the University of Utah. In the lab, researchers found that an enzyme, called lysine specific demethylase (LSD-1), interacts with EWS/FLI to turn off gene expression in Ewing sarcoma. By turning off specific genes, the EWS/FLI-LSD1 complex causes Ewing sarcoma development. The team is now working to further test LSD inhibitors in animal models as they work toward approval of a first-in-man clinical trial.

(Posted: 11/26/2012) - Doctors now use cancer-killing viruses to treat some patients with lethal, fast-growing brain tumors. Clinical trials show that these therapeutic viruses are safe but less effective than expected. A new study led by researchers at the Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) shows that the reason for this is in part due to the patient’s own immune system, which quickly works to eliminate the anticancer virus.

(Posted: 11/23/2012) - Results from a new study conducted by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC-James) show women who wait more than 60 days to begin treatment for advanced breast cancer face significantly higher risks of dying than women who start therapy shortly after diagnosis.

(Posted: 11/23/2012) - Unraveling the mechanism that ovarian cancer cells use to change normal cells around them into cells that promote tumor growth has identified several new targets for treatment of this deadly disease. In the December issue of the American Association for Cancer Research journal Cancer Discovery, a team or researchers from the University of Chicago Medicine (home of the University of Chicago Comprehensive Cancer Center) and Northwestern University Feinberg School of Medicine (home of the Robert H. Lurie Comprehensive Cancer Center) show that ovarian cancer cells induce nearby cells to alter their production of three microRNAs—small strands of genetic material that are important regulators of gene expression.

(Posted: 11/23/2012) - New understanding of molecular changes that convert harmless cells surrounding ovarian cancer cells into cells that promote tumor growth and metastasis provides potential new therapeutic targets for this deadly disease, according to University of Chicago data published in Cancer Discovery, a journal of the American Association for Cancer Research. Researchers set out to learn how normal stromal cells are transformed into cancer-associated fibroblasts, which are found in the tissue immediately surrounding the ovarian cancer cells. Intimate cross talk between cancer-associated fibroblasts and cancer cells boosts tumor growth and metastasis. The University of Chicago is home to the University of Chicago Comprehensive Cancer Center.

(Posted: 11/23/2012) - A pathway called the "Unfolded Protein Response," or UPR, a cell's way of responding to unfolded and misfolded proteins, helps tumor cells escape programmed cell death during the development of lymphoma. Research, led by scientists in the Department of Radiation Oncology from the Perelman School of Medicine, University of Pennsylvania (home of the Abramson Cancer Center), and the Department of Urology, University of California, San Francisco (home of the UCSF Helen Diller Family Comprehensive Cancer Center), shows for the first time that the UPR is active in patients with human lymphomas and mice genetically bred to develop lymphomas. Importantly, when the UPR is inactivated, lymphoma cells readily undergo cell death. Their findings appear online in the Journal of Clinical Investigation and will appear in the December 2012 issue.

(Posted: 11/23/2012) - Epithelial cells are homebodies – they like to attach to things and becoming detached initiates a form of cell suicide known as anoikis (literally "homeless" in Latin). But in order for cancer cells to metastasize they have to leave their homes and to survive while traveling they must resist anoikis – like a third-grader at sleep-away camp. Cancer cells do this by taking a page from the neuron playbook. Neurons are by nature unbound – they grow and link to each other and not to a substrate. Neurons have a protein called TrkB that allows them to survive anoikis; healthy epithelial cells don't have TrkB and so are susceptible to anoikis. Carcinoma cells are epithelial cells gone bad and have learned to act like neurons, inappropriately activating TrkB signaling to escape anoikis. They do it by a mutation that nixes production of a microRNA called miR-200c. When researchers at the University of Colorado Cancer Center reintroduced miR-200c to aggressive, triple-negative breast cancer cells, these cells regained sensitivity to anoikis and self-destructed.

(Posted: 11/23/2012) - A new targeted drug demonstrated its ability to control metastatic gastrointestinal stromal tumor, an uncommon and life-threatening form of sarcoma, after the disease had become resistant to all existing therapies, report investigators at Dana-Farber Cancer Institute who led the worldwide clinical trial. The new study, whose results are being published in The Lancet, demonstrated that the oral drug regorafenib, which inhibits several cancer-promoting kinase enzymes, was able to control GIST for nearly four months longer than placebo in patients for whom imatinib (Gleevec) and sunitinib (Sutent) were no longer effective, a result that was highly significant statistically.

(Posted: 11/21/2012) - The addition of three-dimensional breast imaging—a technology called tomosynthesis—to standard digital mammography significantly increases radiologists' diagnostic accuracy while reducing false positive recall rates, according to the results of a multi-center study led by researchers at the Massachusetts General Hospital in Boston and published in Radiology. Mass General is a component of the Dana-Farber Cancer Institute.