Heat shock 70 kDa protein 5/glucose-regulated protein 78 "AMP"ing up autophagy

Katherine L. Cook, Robert Clarke

Research output: Contribution to journalShort surveypeer-review

24 Scopus citations


Breast cancer is one of the most prevalent cancers in women, with more than 240,000 new cases reported in the United States in 2011. Classification of breast cancer based upon hormone and growth factor receptor profiling shows that approximately 70% of all breast cancers express estrogen receptor-α. Thus, drugs that either block estrogen biosynthesis (aromatase inhibitors like Letrozole), or compete with estrogen for estrogen receptor (ER) binding (selective ER modulators including tamoxifen; TAM) and/or cause ER degradation (selective estrogen receptor downregulators such as fulvestrant), are among the most prescribed targeted therapeutics for breast cancer. However, overall clinical benefit from the use of these drugs is often limited by resistance; ER+ breast cancers either fail to respond to endocrine therapies initially (de novo resistance), or they respond and then lose sensitivity over time (acquired resistance). While several preclinical studies postulate how antiestrogen resistance occurs, for the most part, the molecular mechanism(s) of resistance is unknown.

Original languageEnglish (US)
Pages (from-to)1827-1829
Number of pages3
Issue number12
StatePublished - Dec 2012
Externally publishedYes

Bibliographical note

Funding Information:
K.C. is supported by a DOD Breast Cancer Research Program Postdoctoral Fellowship (BC112023). This research was also supported in part by awards from the U.S. Department of Health and Human Services (R01-CA131465 and U54-CA149147) to R.C.


  • AMP-activated protein kinase
  • Antiestrogen resistance
  • Autophagy
  • Breast cancer
  • Glucose-regulated protein 78
  • MTOR
  • Unfolded protein response


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