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THERE’S

POWER

IN

KNOWING

Does your metastatic breast cancer (MBC) patient have a
gBRCA* mutation?
*germline BRCA.

THERE’S POWER IN TESTING

gBRCA IN
BREAST CANCER (BC)

THERE’S POWER IN TESTING

Patients with DNA repair deficiencies such as a gBRCA mutation are significantly more likely to develop early onset of breast cancer.1,2

IT’S IMPORTANT TO TEST

IT’S IMPORTANT TO TEST

RECOMMENDED DURING THE WORKUP FOR RECURRENT OR STAGE IV DISEASE

According to the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Breast Cancer, for patients with HER2-negative disease eligible for single-agent therapy, strongly consider germline BRCA1/2 testing3

More about testing

WHO TO TEST

WHO TO TEST

~15% of adult HER2- MBC patients were tested for a gBRCA mutation

According to a real-world retrospective analysis of testing rate data in 11,542 TNBC and HR+/HER2- MBC patients from 2011 to 20174

WHEN TO TEST
FOR A gBRCA MUTATION

Testing for a gBRCA mutation at MBC diagnosis may help inform treatment planning5

MORE ABOUT WHEN TO TEST

ABOUT PARP

PARP enzymes and BRCA proteins play a role in maintaining DNA replication and cell survival.
Tumor cells with a gBRCA mutation are dependent on PARP and other repair proteins for DNA repair.6,7

NORMAL CELL7-11

NORMAL CELL
PARP and BRCA bind to DNA to repair damage

BRCA-MUTATED TUMOR CELL7,9-11

BRCA-MUTATED TUMOR CELL
Bound PARP recruits proteins to repair single-strand DNA breaks and disassociates upon completion

BRCA=breast cancer susceptibility gene; HER2=human epidermal growth factor receptor 2; HR=hormone receptor; PARP=poly-ADP ribose polymerase; TNBC=triple-negative breast cancer.

 

References: 1. National Institutes of Health. National Cancer Institute. BRCA mutations: cancer risk and genetic testing. What are BRCA1 and BRCA2? National Institutes of Health Web site. https://www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet#q5. Accessed May 10, 2018. 2. Breastcancer.org. Study estimates breast cancer risk by age for women with BRCA mutations. Breastcancer.org Web site. http://www.breastcancer.org/research-news/risk-estimates-by-age-for-brca-mutations. Accessed May 29, 2018. 3. Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Breast Cancer V.1.2018. © National Comprehensive Cancer Network, Inc. 2018. All rights reserved. Accessed April 23, 2018. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way. 4. Quek R, Mardekian J. Real-world clinical outcomes and treatment patterns among metastatic breast cancer (MBC) patients with germline BRCA mutation (gBRCAmut). J Clin Oncol. In press. 5. American Society of Clinical Oncology. Genetic testing. American Society of Clinical Oncology Web site. https://www.asco.org/practice-guidelines/cancer-care-initiatives/genetics-toolkit/genetic-testing. Accessed April 6, 2018. 6. Gavande NS, VanderVere-Carozza PS, Hinshaw HD, et al. DNA repair targeted therapy: the past or future of cancer treatment? Pharmacol Ther. 2016;160:65-83. 7. Livraghi L, Garber JE. PARP inhibitors in the management of breast cancer: current data and future prospects. BMC Med. 2015;13:188. doi:10.1186/s12916-015-0425-1. 8. Shao G, Lilli DR, Patterson-Fortin J, Coleman KA, Morrissey DE, Greenberg RA. The Rap80-BRCC36 de-ubiquitinating enzyme complex antagonizes RNF8-Ubc13-dependent ubiquitination events and DNA double strand breaks. Proc Natl Acad Sci U S A. 2009;106(9):3166-3171. 9. Lee JM, Ledermann JA, Kohn EC. PARP inhibitors for BRCA1/2 mutation-associated and BRCA-like malignancies. Ann Oncol. 2014;25(1):32-40. 10. Lupo B, Trusolino L. Inhibition of poly(ADP-ribosyl)ation in cancer: old and new paradigms revisited. Biochim Biophys Acta. 2014;1846(1):201-215. 11. Rouleau M, Patel A, Hendzel MJ, Kaufmann SH, Poirier GG. PARP inhibition: PARP1 and beyond. Nat Rev Cancer. 2010;10(4):293-301. doi:10.1038/nrc2812.

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