CDK9 inhibition by dinaciclib potently suppresses Mcl-1 to induce durable apoptotic responses in aggressive MYC-driven B-cell lymphoma in vivo

Gareth P. Gregory(Peter MacCallum Cancer Centre), Simon J. Hogg(Peter MacCallum Cancer Centre), Lev M. Kats(Peter MacCallum Cancer Centre), Eva Vidacs(Peter MacCallum Cancer Centre), Adele J. Baker(Peter MacCallum Cancer Centre), Omer Gilan(The University of Melbourne), Marcus Lefebure(Peter MacCallum Cancer Centre), Benjamin Martin(Peter MacCallum Cancer Centre), Mark A. Dawson(The University of Melbourne), Ricky W. Johnstone(Peter MacCallum Cancer Centre), Jake Shortt(The University of Melbourne)
Leukemia
January 12, 2014
Cited by 142Open Access
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Abstract

either as false negatives of the PCR or as false positives of MFC. We can thus conclude that the junction region of the IgH rearrangement in MM is stable and can be used as a target for MRD assessment by ASO RQ-PCR and more, also by deep-sequencing methods, as it constantly identifies the myeloma cells responsible for relapse. n conclusion, our results show that, in the dominant myeloma clone, the CDR3 region of IGH remains constant across all the stages of disease evolution. This major clone signature is not modified by clinical or biological changes in the disease nor under different treatment pressures; accordingly, it would thus be responsible for disease relapses and progression, and could be used as a MRD target. Assuming that the CDR3 region remains stable, the recently raised concept of clonal tiding


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