Autophagy, inflammation, and breast cancer risk

Katherine L. Cook, Robert Clarke

Research output: Chapter in Book/Report/Conference proceedingChapter


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 languageEnglish (US)
Title of host publicationAutophagy
Subtitle of host publicationCancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging Volume 12
Number of pages14
ISBN (Electronic)9780128121467
ISBN (Print)9780128121474
StatePublished - Jan 1 2017
Externally publishedYes


  • Autophagy
  • Breast cancer risk
  • Estrogen receptor
  • HER2
  • Immune cells
  • Inflammation
  • Microbiome
  • Obesity
  • Progesterone receptor


Dive into the research topics of 'Autophagy, inflammation, and breast cancer risk'. Together they form a unique fingerprint.

Cite this