Clonal dynamics towards the development of venetoclax resistance in chronic 
lymphocytic leukemia

Herling, C. D.; Abedpour, N.; Weiss, J.; Schmitt, A.; Jachimowicz, R. D.; Merkel, O.; Cartolano, M.; Oberbeck, S.; Mayer, P.; Berg, V.; Thomalla, D.; Kutsch, N.; Stiefelhagen, M.; Cramer, P.; Wendtner, C. M.; Persigehl, T.; Saleh, A.; Altmuller, J.; Nurnberg, P.; Pallasch, C.; Achter, V.; Lang, U.; Eichhorst, B.; Castiglione, R.; Schafer, S. C.; Buttner, R.; Kreuzer, K. A.; Reinhardt, H. C.; Hallek, M.; Frenzel, L. P.; Peifer, M.

doi:10.1038/s41467-018-03170-7

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Clonal dynamics towards the development of venetoclax resistance in chronic lymphocytic leukemia

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Jachimowicz, R. D.
Jachimowicz – Mechanisms of DNA Repair, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/29463802
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Citation

Herling, C. D., Abedpour, N., Weiss, J., Schmitt, A., Jachimowicz, R. D., Merkel, O., et al. (2018). Clonal dynamics towards the development of venetoclax resistance in chronic lymphocytic leukemia. Nat Commun, 9(1), 727. doi:10.1038/s41467-018-03170-7.

Cite as: https://hdl.handle.net/21.11116/0000-000B-488E-5

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.