Discovery Of Inflammatory Circuit That Triggers Breast Cancer Offers New Therapeutic Target For Treatment And Prevention
Although it's widely accepted that inflammation is a critical underlying factor in a range of diseases, including the progression of cancer, little is known about its role when normal cells become tumor cells. Now, scientists from the Florida campus of The Scripps Research Institute have shed new light on exactly how the activation of a pair of inflammatory signaling pathways leads to the transformation of normal breast cells to cancer cells. The study, led by Jun-Li Luo, an assistant professor at Scripps Florida, was published online before print by the journal Molecular Cell. The scientists' discovery points to the activation of a self-sustaining signaling circuit that inhibits a specific RNA, a well-known tumor suppressor that helps limit the spread of cancer (metastasis). Therapies that disable this circuit and halt this miRNA repression could have the potential to treat cancer.
The infamous BRCA genes do not act alone in causing cancer; there is a molecular syndicate at work preventing the way cells normally repair breaks in DNA that is at the root of breast cancer. But finding all of the BRCA molecular collaborators has been elusive. Researchers at the Perelman School of Medicine at the University of Pennsylvania and the University of Oulu, Finland, published their discovery of a mutation in the Abraxas gene, which interacts with the well-known breast-cancer gene BRCA1, in Science Translational Medicine this week. The mutation affects the ability of the Abraxas protein to enter the nucleus and bind to sites adjacent to damaged DNA. Abraxas organizes a large BRCA1 protein-containing complex that is required to fix DNA-damage. A mutated Abraxas protein impairs the BRCA1 complex's ability to migrate to sites of DNA damage and repair breaks.
The use of an injectable, clot-preventing drug known as Low Molecular Weight Heparin to treat patients with advanced cancer complicated by blood clots increased steadily between 2000 and 2007, according to a new study published in The Oncologis t, funded by the National Cancer Institute and led by Kaiser Permanente Colorado. However, despite previous research indicating LMWH is the preferred first-line treatment for cancer patients experiencing blood clots, use of LMWH is low compared to another commonly used anticoagulant, warfarin. The study was conducted by a team of Kaiser Permanente researchers from Colorado, Oregon, Washington and Northern California, Dana-Farber Cancer Institute and Group Health Research Institute. Venous thromboembolism, or blood clots, are common and serious complications in cancer patients.
Based on a study of nearly 2, 000 breast cancer patients, researchers at the Swedish Cancer Institute in Seattle say that, in women between the ages of 40 and 49, breast cancers detected by mammography have a better prognosis. The study appears in the March issue of Radiology. "In our study, women aged 40 to 49 whose breast cancer was detected by mammography were easier to treat and had less recurring disease and mortality, because their cancer was found at an earlier stage, " said Judith A. Malmgren, Ph.D., president of HealthStat Consulting, Inc. Dr. Malmgren and a team of researchers reviewed breast cancer patient data from a dedicated registry at the Swedish Cancer Institute's community cancer center. The researchers analyzed data on 1, 977 breast cancer patients between the ages of 40 and 49 who were treated between 1990 and 2008.
The trefoil factor 3 (TFF3) protein protects and maintains the integrity of the epithelial surface in the normal breast. New research has found that while TFF3 protein expression is higher in well-differentiated low grade tumors and therefore associated with features of a good prognosis, it has a more sinister role in breast cancer invasion and metastasis. The report is published in the March issue of the American Journal of Pathology. "Our findings suggest that TFF3 is regulated by estrogen and has beneficial properties in breast epithelia, " says lead investigator Felicity E.B. May, PhD, of the Northern Institute for Cancer Research and the Department of Pathology at Newcastle University, UK. "We propose that early during breast tumorigenesis, TFF3 retains its association with normal functionality of breast epithelial cells.