| REVIEW ARTICLE |
|
| Year : 2022 | Volume
: 59
| Issue : 5 | Page : 130-141 |
Management of human epidermal growth factor receptor 2–negative metastatic breast cancer: Role of poly adenosine diphosphate (ADP-ribose) polymerase inhibitors
Ashok Kumar Vaid1, Chetan Deshmukh2, Nitesh Rohatgi3, Joydeep Ghosh4
1 Department of Medical Oncology, Medanta - The Medicity, Gurugram, Haryana, India
2 Department of Medical Oncology, Dinanath Mangeshkar Hospital, Pune, Maharashtra, India
3 Department of Medical Oncology, Max Superspeciality Hospital, Saket, New Delhi, India
4 Department of Medical Oncology, TMC, Kolkata, West Bengal, India
Correspondence Address:
Ashok Kumar Vaid
Department of Medical Oncology, Medanta - The Medicity, Gurugram, Haryana
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijc.IJC_30_21
Human epidermal growth factor receptor 2 (HER2)-negative subset is the most heterogeneous group of metastatic breast cancers (MBCs) as it includes both hormone receptor (HR)-positive and HR-negative breast cancer (or TNBC), which have different therapies and treatment challenges. Though endocrine therapy (ET) remains the treatment backbone in HR-positive HER2-negative cases, about 40% of the patients show intrinsic or acquired resistance to ET due to multiple mechanisms. Combining different therapies such as ET and other targeted therapies with or without chemotherapy fails to give continued benefit, unlike cyclin-dependent kinase (CDK) 4/6 inhibitors that have shown a great benefit. TNBC has conventionally been treated ineffectively with systemic chemotherapy. Recently, poly (ADP-ribose) polymerase inhibitors (PARPi) have emerged for HER2-negative breast cancer (BC) patients, including TNBC. Olaparib and talazoparib have recently been approved in germline BRCA-mutated (gBRCAm) HER2-negative MBC. Additionally, ongoing trials of PARPi in combination with various therapies are expected to provide more and better treatment options for gBRCAm HER2-negative breast cancer.
[FULL TEXT] [PDF]*
|
