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Published on: December 26, 2016
Intratumoural inflammation and endocrine resistance in breast cancer
Jill I Murray1, Nathan R West1, Leigh C Murphy1
1Deeley Research CentreBritish Columbia Cancer Agency, 2410 Lee Avenue, Victoria, British Columbia, Canada V8R 6V5Translational Gastroenterology UnitNuffield Department of Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UKDepartment of Biochemistry and Medical Genetics and the Manitoba Institute of Cell BiologyUniversity of Manitoba and CancerCare Manitoba, 675 McDermot Avenue, Winnipeg, Manitoba, CanadaDepartment of Biochemistry and MicrobiologyUniversity of Victoria, Victoria, British Columbia, CanadaDepartment of Pathology and Laboratory MedicineUniversity of British Columbia, Vancouver, British Columbia, Canada.
Abstract:
It is becoming clear that inflammation-associated mechanisms can affect progression of breast cancer and modulate responses to treatment. Estrogen receptor alpha (ERα (ESR1)) is the principal biomarker and therapeutic target for endocrine therapies in breast cancer. Over 70% of patients are ESR1-positive at diagnosis and are candidates for endocrine therapy. However, ESR1-positive tumours can become resistant to endocrine therapy. Multiple mechanisms of endocrine resistance have been proposed, including suppression of ESR1. This review discusses the relationship between intratumoural inflammation and endocrine resistance with a particular focus on inflammation-mediated suppression of ESR1.
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