Back to Journals » Breast Cancer: Targets and Therapy » Volume 9

Current perspectives on CHEK2 mutations in breast cancer

Authors Apostolou P, Papasotiriou I

Received 21 January 2017

Accepted for publication 20 April 2017

Published 12 May 2017 Volume 2017:9 Pages 331—335

DOI https://doi.org/10.2147/BCTT.S111394

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Professor Pranela Rameshwar


Panagiotis Apostolou, Ioannis Papasotiriou

Department of Molecular Medicine, Research Genetic Cancer Centre S.A. (R.G.C.C. S.A.), Florina, Greece

Abstract: Checkpoint kinase 2 (CHEK2) is a serine/threonine kinase which is activated upon DNA damage and is implicated in pathways that govern DNA repair, cell cycle arrest or apoptosis in response to the initial damage. Loss of kinase function has been correlated with different types of cancer, mainly breast cancer. CHEK2 functionality is affected by different missense or deleterious mutations. CHEK2*1100delC and I157T are most studied in populations all over the world. Although these variants have been identified in patients with breast cancer, their frequency raises doubts about their importance as risk factors. The present article reviews the recent advances in research on CHEK2 mutations, focusing on breast cancer, based on the latest experimental data.

Keywords: CHEK2, breast cancer

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]