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01.10.2010 | Viewpoint | Ausgabe 5/2010

Breast Cancer Research 5/2010

Can phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibition ERase them all?

Zeitschrift:
Breast Cancer Research > Ausgabe 5/2010
Autoren:
Dominique S Meyer, Mohamed Bentires-Alj
Wichtige Hinweise

Competing interests

The authors declare that they have no competing interests.

Abstract

Seventy percent of breast tumors are estrogen receptor (ER) positive. Although endocrine therapy is successful for the majority of patients with ER-positive tumors, approximately 30% show de novo or acquired resistance and the underlying molecular mechanisms and biomarkers that predict such resistance remain elusive. Two recent papers report that hyperactivation of the phosphatidylinositol 3-kinase (PI3K) pathway produces resistance to tamoxifen. This raises the possibility that combining endocrine therapy and PI3K inhibition may be more effective than monotherapy for treating ER-positive breast tumors, either as first-line therapy for tumors with high PI3K activity or after the development of resistance to endocrine therapy.

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