New Therapy—New Hope for Aggressive Breast Cancer -- Research Summary
BACKGROUND: About 10 to 20 percent of breast cancers—more than one out of every 10—are found to be triple negative. Triple negative breast cancer (TNBC) is a cancer that tests negative for estrogen receptors, HER2, and progesterone receptors. If a woman is to test negative for all three factors, than she has triple-negative breast cancer, meaning that the patient will not respond to hormonal therapy or treatments that target HER2 receptors. Triple negative breast cancer is more often seen in African American women, Hispanic/Latina women, and younger women. Triple negative breast cancer is also more aggressive than most cancers and it is less likely to be seen on a mammogram. This cancer is known to be reoccurring and it is more likely to spread to other parts of the body. (Source: http://www.breastcancer.org/symptoms/diagnosis/trip_neg and http://ww5.komen.org/uploadedFiles/Content_Binaries/KOMEED079100.pdf)
TREATMENT: TNBC is treated with a combination of surgery, radiation, and chemotherapy. Since it tests negative for the three receptors, it isn’t treated with hormone or targeted therapy. If the cancer is caught early enough, it can be treated. Chemotherapy works well in TNBC. It may work even better for TNBC than for other types of breast cancer. (Source: http://ww5.komen.org/uploadedFiles/Content_Binaries/KOMEED079100.pdf
NEW THERAPY: PARP inhibitors, also known as poly ADP-ribose polymerase, are now being studied to treat patients with triple negative breast cancer. One study in 2011 found that the PARP inhibitor boosted overall survival to a median 12.3 months compared with 7.7 months with chemotherapy alone, according to Joyce O’Shaughnessy, MD, of Baylor Sammons Cancer Center in Dallas. Patients on the drug showed similar gains in objective response, clinical benefit, and progression-free survival, with no significant difference in adverse events in the open-label phase II trial. Normal cells favor a BRCA ½-dependant process to repair double-strand breaks in DNA, which are caused by radiation and some chemotherapy. Although patients with BRAC1 or BRCA2 mutations have one functional allele that keeps this mechanism in play for normal cells, cancer cells usually inactivate that allele (allele is one or two more versions of a gene). PARP inhibitors exploit that vulnerability by keeping double-strand breaks from being repaired in cells without the BRCA repair function. Triple negative tumors share characteristics with BRCA1 breast tumors and may have other genetic lesions that impair double-strand repair. However, researchers say to use caution. This trial included only 123 patients with metastatic breast cancer negative for estrogen receptor (ER), progesterone receptor (PR), and HER2 overexpression, which is a small cohort. (Source: http://www.medpagetoday.com/HematologyOncology/BreastCancer/24195) MORE.