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CDK4/6 Inhibition in Breast Cancer: Mechanisms of Response and Treatment Failure

CDK4/6 Inhibition in Breast Cancer: Mechanisms of Response and Treatment Failure Curr Breast Cancer Rep (2017) 9:26–33 DOI 10.1007/s12609-017-0232-0 TRANSLATIONAL RESEARCH (TA KING AND EA MITTENDORF, SECTION EDITORS) CDK4/6 Inhibition in Breast Cancer: Mechanisms of Response and Treatment Failure 1 1 Ana C. Garrido-Castro & Shom Goel Published online: 1 February 2017 Springer Science+Business Media New York 2017 Abstract Introduction Purpose of review The purpose of this review is to de- scribe the role of D-type cyclins and cyclin-dependent In order for a healthy cell to divide, it must pass through each kinases (CDKs) 4 and 6 in breast cancer and to discuss stage of the cell cycle in a sequential and tightly orchestrated potential biomarkers for sensitivity or resistance to fashion. The control of cellular proliferation is governed by a CDK4/6 inhibitors. vast array of molecular players, most important of which are the Recent findings A small number of preclinical and clini- cyclins and their partner kinases, the cyclin-dependent kinases cal studies have explored potential mechanisms of (CDKs). Given the fundamental role of dysregulated cellular CDK4/6 inhibitor response and resistance in breast can- proliferation in cancers, it is not surprising, therefore, that the cer. Putative markers of response include estrogen re- development of drugs that inhibit the cyclin/CDK axes http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Breast Cancer Reports Springer Journals

CDK4/6 Inhibition in Breast Cancer: Mechanisms of Response and Treatment Failure

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References (68)

Publisher
Springer Journals
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Medicine & Public Health; Oncology; Internal Medicine; Surgical Oncology
ISSN
1943-4588
eISSN
1943-4596
DOI
10.1007/s12609-017-0232-0
Publisher site
See Article on Publisher Site

Abstract

Curr Breast Cancer Rep (2017) 9:26–33 DOI 10.1007/s12609-017-0232-0 TRANSLATIONAL RESEARCH (TA KING AND EA MITTENDORF, SECTION EDITORS) CDK4/6 Inhibition in Breast Cancer: Mechanisms of Response and Treatment Failure 1 1 Ana C. Garrido-Castro & Shom Goel Published online: 1 February 2017 Springer Science+Business Media New York 2017 Abstract Introduction Purpose of review The purpose of this review is to de- scribe the role of D-type cyclins and cyclin-dependent In order for a healthy cell to divide, it must pass through each kinases (CDKs) 4 and 6 in breast cancer and to discuss stage of the cell cycle in a sequential and tightly orchestrated potential biomarkers for sensitivity or resistance to fashion. The control of cellular proliferation is governed by a CDK4/6 inhibitors. vast array of molecular players, most important of which are the Recent findings A small number of preclinical and clini- cyclins and their partner kinases, the cyclin-dependent kinases cal studies have explored potential mechanisms of (CDKs). Given the fundamental role of dysregulated cellular CDK4/6 inhibitor response and resistance in breast can- proliferation in cancers, it is not surprising, therefore, that the cer. Putative markers of response include estrogen re- development of drugs that inhibit the cyclin/CDK axes

Journal

Current Breast Cancer ReportsSpringer Journals

Published: Feb 1, 2017

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