Clonal evolution underlying leukemia progression and Richter transformation in patients with ibrutinib-relapsed CLL

Author:

Kadri Sabah1ORCID,Lee Jimmy1ORCID,Fitzpatrick Carrie1ORCID,Galanina Natalie2ORCID,Sukhanova Madina2ORCID,Venkataraman Girish1ORCID,Sharma Shruti1,Long Brad1ORCID,Petras Kristin1,Theissen Megan1,Ming Mei1,Kobzev Yuri1,Kang Wenjun3ORCID,Guo Ailin1,Wang Weige1,Niu Nifang1,Weiner Howard2,Thirman Michael2ORCID,Stock Wendy2,Smith Sonali M.2ORCID,Nabhan Chadi4ORCID,Segal Jeremy P.1,Lu Pin1,Wang Y. Lynn1ORCID

Affiliation:

1. Department of Pathology,

2. Department of Medicine, and

3. Center for Research Informatics, University of Chicago, Chicago, IL; and

4. Cardinal Health Specialty Solutions, Waukegan, IL

Abstract

Key Points Del(18p), together with del(17p)/TP53 mutations, is present at a high frequency before ibrutinib treatment. BTK mutations drive ibrutinib relapse, but del(17p)/TP53 mutations may be dispensable.

Publisher

American Society of Hematology

Subject

Hematology

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