Some Triple Negative Breast Cancer Patients May Benefit from Immunotherapy

Dr. Barbara Pockaj, MD Professor of Surgery Mayo Clinic, ArizonaMedicalResearch.com Interview Invitation
Dr. Barbara Pockaj, MD
Professor of Surgery
Mayo Clinic, Arizona

 

MedicalResearch: What are the main findings of the study?

Dr. Pockaj: The study analyzed 515 triple negative breast cancer samples using a multi-platform approach including whole genome mRNA expression, protein expression, gene copy number changes and gene sequencing for immune markers. The study found that a cohort of the triple negative breast cancer patients had high expression of PD-L1 (program death ligand) and other immune regulators such as CTLA-4 (Cytotoxic T-lymphocyte Antigen) and IDO-1 (indoleamine 2,3-dioxygenase).  High PD-L1 expression was found in patients whose tumors were triple negative and androgen receptor negative.  High PD-L1 expression was related to DNA repair gene abnormalities including BRCA1.


MedicalResearch: Were any of the findings unexpected?

Dr. Pockaj: PD-L1 has been associated with response to immunotherapy.  The finding that BRCA1 mutation carriers may be good candidates for immunotherapy is exciting and unexpected.  In the past patients with BRCA1 and triple negative breast cancer were found to have lymphocytic infiltration into their tumors.  Now we see that there may be a reason for this – the DNA instability found in these tumors.  This could mean that patients with BRCA1 mutations would benefit from immunotherapy.

MedicalResearch: What should clinicians and patients take away from your report?

Dr. Pockaj: The exciting outcomes of immunotherapy seen in the treatment of other cancers such as melanoma, lung, and renal cell may be expanded to patients with breast cancer especially the subset of triple negative breast cancers.

Citation:

Abstract presented at 2014 American Society of Clinical Oncology in Chicago
Abstract No:
1001
Expression of novel immunotherapeutic targets in triple-negative breast cancer.
J Clin Oncol 32:5s, 2014 (suppl; abstr 1001)