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On Saturday 9 December 92017 during an oral abstract session at the 59th Annual meeting American Society of Hematology (ASH), Lukas P. Frenzel of the Center of Integrated Oncology Cologne-Bonn at the University of Cologne in Cologne, Germany, on behalf of his colleagues, presented results from their clinical study, which was designed to better understand the genetic causes of treatment resistance towards venetoclax in chronic lymphocytic leukemia (CLL).
This abstract (#263), “Mechanisms of Venetoclax Resistance in Chronic Lymphocytic Leukemia,” was presented during Oral Session: 641. “Biology and Pathophysiology, excluding Therapy: Therapeutic Resistance in CLL”. The summary here provides data from the presentation at the session and may supersede date in the pre-published ASH abstract.
While this was a small exploratory study, it’s notable that the mutations in BTG1 and homozygous deletions in CDKN2A/B occurred in a relatively large percentage of patients. Whole exome sequencing from 8 of these patients before the initiation of venetoclax therapy and at the time of venetoclax resistance revealed diverse patterns of clonal evolution.
The authors of this study agreed that in order to further pinpoint genetic mechanisms of venetoclax resistance, larger studies with repeated longitudinal sampling of CLL cell material under therapy and at disease progression/relapse are necessary.
Michael Hallek | ASCO 2018 | The potential of venetoclax for CLL patients with 17p deletion
Michael Hallek | ASCO 18 | The potential of venetoclax for CLL patients with 17p deletion
ASH 2017 | Combination of venetoclax and ibrutinib: promising phase II results in high-risk and R/R CLL
The investigators noted that ibrutinib plus venetoclax was both safe and active in CLL patients.
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