Clonal selection and double-hit events involving tumor suppressor genes underlie relapse in myeloma

Author:

Weinhold Niels1,Ashby Cody1,Rasche Leo1,Chavan Shweta S.1,Stein Caleb1,Stephens Owen W.1,Tytarenko Ruslana1,Bauer Michael A.1,Meissner Tobias2,Deshpande Shayu1,Patel Purvi H.1,Buzder Timea1,Molnar Gabor1,Peterson Erich A.1,van Rhee Frits1,Zangari Maurizio1,Thanendrarajan Sharmilan1,Schinke Carolina1,Tian Erming1,Epstein Joshua1,Barlogie Bart1,Davies Faith E.1,Heuck Christoph J.1,Walker Brian A1,Morgan Gareth J.1

Affiliation:

1. Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR; and

2. Department of Molecular and Experimental Medicine, Avera Cancer Institute, La Jolla, CA

Abstract

Key PointsHits in driver genes and bi-allelic events affecting tumor suppressors increase apoptosis resistance and proliferation rate–driving relapse. Excessive biallelic inactivation of tumor suppressors in high-risk cases highlights the need for TP53-independent therapeutic approaches.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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