Circulating tumor cells — established in metastatic breast cancer for predicting a woman’s chance of recurrence and survival — have now shown similar value in early-stage breast cancer. As one of the first studies and the largest to show this new predictive value, its findings may help determine which earlier stage breast cancer patients need additional treatment and intervention in the adjuvant setting.
Lead author and principal investigator: Anthony Lucci, M.D., professor in MD Anderson’s Department of Surgical Oncology
Reported in the July 2012 edition of Lancet Oncology.
See MD Anderson’s online Newsroom and CancerFrontline for more information on these and other basic, translational and clinical research findings at MD Anderson.
Clinical tool indicates radiation benefit
A new nomogram, or clinical model, demonstrates accuracy in predicting the benefit of radiation therapy in older women — ages 66-79 — with breast cancer. The study may offer clinical guidance to physicians so they can help determine which patients in this age group will likely benefit from radiation therapy. As the U.S. population ages, it is critical to establish indications for radiation therapy. A 57% increase in breast cancer diagnoses in older women is projected during the next two decades.
Lead author: Benjamin Smith, M.D., assistant professor in MD Anderson’s Department of Radiation Oncology
Reported in the Aug. 10, 2012, edition of The Journal of Clinical Oncology.
Genetic change caused by sun damage
It’s been a burning question in melanoma research: Tumor cells are full of ultraviolet (UV)-induced genetic damage caused by sunlight exposure, but which mutations drive this cancer? The sheer abundance of these passenger mutations has obscured the search for genetic driver mutations that actually matter in melanoma development and progression. Researchers, however, have now identified six genes with driving mutations in melanoma, three of which have recurrent “hotspot” mutations as a result of damage inflicted by UV light.
Co-senior author: Lynda Chin, M.D., professor and chair of MD Anderson’s Department of Genomic Medicine; in collaboration with scientists at the Broad Institute of MIT and Harvard, and Dana-Farber Cancer Institute
Reported in the July 20, 2012, issue of the journal Cell.
Marker identifies, attacks stem cells
Breast cancer stem cells wear a new nametag on the cell surface called GD2 ganglioside (a group of glycosphingolipids found principally on the surface of some nerve cells). Presence of GD2 serves part as nametag and part bull’s-eye, identifying them as potent tumor-generating cells and flagging their vulnerability to the drug triptolide. This drug stymied cancer growth in cell line experiments and also resulted in smaller tumors and prolonged survival in mouse models. Drug development for clinical trials is close.
Co-senior authors: Michael Andreeff, M.D., Ph.D., professor in MD Anderson’s Departments of Leukemia and Stem Cell Transplantation and Cellular Therapy, and Sendurai Mani, Ph.D., assistant professor in MD Anderson’s Department of Molecular Pathology and co-director of the Metastasis Research Center
Reported in the June 1, 2012, edition of the Journal of Clinical Investigation.
Specialized protein activates major player in cancer
Researchers have found a chain of events that promotes Herceptin resistance in breast cancer and activation of glucose metabolism (glycolysis), which cancer cells primarily use to fuel their growth and survive. This discovery is potentially important for understanding and addressing Herceptin resistance in breast cancer. The effect on glucose metabolism also could have implications for other types of solid tumor cancers, including prostate, because they rely so heavily on glycolysis.
Senior author: Hui-Kuan Lin, Ph.D., associate professor in MD Anderson’s Department of Molecular and Cellular Oncology
Reported in the May 25, 2012, issue of Cell.
Therapies for rheumatoid arthritis do not increase cancer risk
Biologic therapies developed for patients with rheumatoid arthritis during the last decade have caused concern about possible links to cancer. However, results from the largest systematic review of these drugs — including 29,423 adult patients from 63 randomized controlled trials — showed no statistically significant increased risk of any type of cancer in patients treated with these biologic response modifiers (BRMs), compared to other medications.
Rheumatoid arthritis affects approximately 1% of the population and can lead to significant morbidity, joint deformity and impaired quality of life. Researchers compared the safety of all nine BRMs currently approved by the U.S. Food and Drug Administration against a placebo or traditional disease-modifying, anti-rheumatic drug. They worked with the Cochrane Collaboration, an independent, non-profit organization that houses the largest collection of records of randomized, controlled trials in the world.
Senior author: Maria Suarez-Almazor, M.D., professor in the Department of General Internal Medicine
Reported in the Sept. 5, 2012, issue of the Journal of the American Medical Association.
Cancer stem cells found among low-PSA cells
Prostate cancer cells that defy treatment and display heightened tumor-generating capacity can be identified by levels of prostate specific antigen (PSA) expressed in the tumor cells. Using a new technique, researchers were able, for the first time, to separate low-PSA and high-PSA prostate cancer cells, leading to the discovery that a low-PSA population of cancer stem cells appears to be an important source of castration-resistant prostate cancer.
Low-PSA cells were found to be both self-renewing and capable of differentiating into other prostate cancer cell types upon division. The findings demonstrate the need to develop new therapeutics that will target low-PSA prostate cancer cells that can be combined with hormone therapy to wipe out cancer cells and prevent recurrence.
Senior author: Dean Tang, Ph.D., professor in MD Anderson’s Department of Molecular Carcinogenesis
Reported in the May 3, 2012, edition of Cell Stem Cell.