HER2 is amplified or overexpressed in 20% to 25% of breast cancers. HER2 is a redundant, robust, and powerful signaling pathway that represents an attractive therapeutic target. Anti-HER2 therapy in the clinic has resulted in significant improvements in patient outcomes and, in recent years, combinations of anti-HER2 therapies have been explored and carry great promise. However, treatment resistance remains a problem. Resistance can be mediated, among others, by pathway redundancy, reactivation, or the utilization of escape pathways. Understanding mechanisms of resistance can lead to better therapeutic strategies to overcome resistance and optimize outcomes.

Resistance to Anti-HER2 Therapies in Breast Cancer / Rimawi, M. F.; De Angelis, C.; Schiff, R.. - (2015), pp. e157-e164. [10.14694/EdBook_AM.2015.35.e157]

Resistance to Anti-HER2 Therapies in Breast Cancer

De Angelis C.
Secondo
;
2015

Abstract

HER2 is amplified or overexpressed in 20% to 25% of breast cancers. HER2 is a redundant, robust, and powerful signaling pathway that represents an attractive therapeutic target. Anti-HER2 therapy in the clinic has resulted in significant improvements in patient outcomes and, in recent years, combinations of anti-HER2 therapies have been explored and carry great promise. However, treatment resistance remains a problem. Resistance can be mediated, among others, by pathway redundancy, reactivation, or the utilization of escape pathways. Understanding mechanisms of resistance can lead to better therapeutic strategies to overcome resistance and optimize outcomes.
2015
Resistance to Anti-HER2 Therapies in Breast Cancer / Rimawi, M. F.; De Angelis, C.; Schiff, R.. - (2015), pp. e157-e164. [10.14694/EdBook_AM.2015.35.e157]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/857304
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