Clonal dynamics towards the development of venetoclax resistance in chronic lymphocytic leukemia
Carmen Herling(University of Cologne), Nima Abedpour(University of Cologne), Jonathan M. Weiss(University of Cologne), Anna Schmitt(University of Cologne), Ron D. Jachimowicz(University of Cologne), Olaf Merkel(University of Cologne), Maria Cartolano(University of Cologne), Sebastian Oberbeck(University of Cologne), Petra Mayer(University of Cologne), Valeska Berg(University of Cologne), Daniel Thomalla(University of Cologne), Nadine Kutsch(University of Cologne), Marius Stiefelhagen(University of Cologne), Paula Cramer(University of Cologne), Clemens‐Martin Wendtner(München Klinik Schwabing), Thorsten Persigehl(University Hospital Cologne), Andreas Saleh(München Klinik), Janine Altmüller(University of Cologne), Peter Nürnberg(University of Cologne), Christian P. Pallasch(University of Cologne), Viktor Achter(University of Cologne), Ulrich Lang(TH Köln - University of Applied Sciences), Barbara Eichhorst(University of Cologne), Roberta Castiglione(University of Cologne), Stephan Schäfer(University of Cologne), Reinhard Büttner(University of Cologne), Karl‐Anton Kreuzer(University of Cologne), Hans Christian Reinhardt(University of Cologne), Michael Hallek(University of Cologne), Lukas P. Frenzel(University of Cologne), Martin Peifer(University of Cologne)
Cited by 193Open Access
Abstract
Abstract Deciphering the evolution of cancer cells under therapeutic pressure is a crucial step to understand the mechanisms that lead to treatment resistance. To this end, we analyzed whole-exome sequencing data of eight chronic lymphocytic leukemia (CLL) patients that developed resistance upon BCL2-inhibition by venetoclax. Here, we report recurrent mutations in BTG1 (2 patients) and homozygous deletions affecting CDKN2A/B (3 patients) that developed during treatment, as well as a mutation in BRAF and a high-level focal amplification of CD274 ( PD-L1 ) that might pinpoint molecular aberrations offering structures for further therapeutic interventions.
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