Cancers cells co-opt the ancient, multifaceted cellular stress response network in multiple ways to enable malignancy. The role of the cellular stress response network in human cancers is only beginning to be appreciated. We and others have revealed strong associations withactivation of the heat shock response (HSF1)6,7, oxidative stress response (KEAP1/NFE2L2)13 and unfoldedprotein response (ATF4 and XBP1)14 with poor clinical outcomes. Because the cellular stress response network impacts diverse aspects of cell biology, we hypothesize that the activation status of this network will broadly affect how breast cancers respond to a diverse collection of therapeutics.
|Effective start/end date||9/1/16 → 8/31/17|
- Northwestern Memorial Hospital (AGREEMENT 6/9/16)
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