Abstract
Breast cancer is the most prevalent cancer in women, with more than 246,000 new cases diagnosed annually. Based upon receptor profiling, breast cancer can be classified into estrogen receptor (ER) positive, human epidermal growth factor-2 receptor (HER2) overexpressing, or triple negative (TN) that are ER negative, progesterone receptor negative, and HER2 normal. Targeted therapy options, such as selective ER modulators or aromatase inhibitors for ER+ breast cancer, or HER2-targeted antibodies and EGFR inhibitors for HER2-overexpressing breast cancers, improve overall survival rates. TN breast cancers are limited to cytotoxic chemotherapeutic options. Unfortunately, many of these tumors develop resistance to treatments, which limit the curative potential of these therapies. Autophagy, a cellular process of “self-eating,” is implicated as a possible contributor to therapy resistance in breast cancer. Autophagy plays an important role in inflammation and immune responses, which may impact breast cancer risk and therapeutic responsiveness.
Original language | English (US) |
---|---|
Title of host publication | Autophagy |
Subtitle of host publication | Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging Volume 12 |
Publisher | Elsevier |
Pages | 359-372 |
Number of pages | 14 |
ISBN (Electronic) | 9780128121467 |
ISBN (Print) | 9780128121474 |
DOIs | |
State | Published - Jan 1 2017 |
Externally published | Yes |
Keywords
- Autophagy
- Breast cancer risk
- Estrogen receptor
- HER2
- Immune cells
- Inflammation
- Microbiome
- Obesity
- Progesterone receptor