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Brian Parkin

Researcher at University of Michigan

Publications -  41
Citations -  1021

Brian Parkin is an academic researcher from University of Michigan. The author has contributed to research in topics: Transplantation & Leukemia. The author has an hindex of 15, co-authored 38 publications receiving 871 citations.

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Activating STAT6 mutations in follicular lymphoma.

TL;DR: The genetic and functional data combined strengthen the recognition of the IL-4/JAK/STAT6 axis as a driver of FL pathogenesis.
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Clonal evolution and devolution after chemotherapy in adult acute myelogenous leukemia

TL;DR: In this article, the authors used SNP 6.0 array-based genomic profiling of acquired copy number aberrations (aCNA) and copy neutral LOH (cnLOH) together with sequence analysis of recurrently mutated genes to characterize paired AML genomes.
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Multiple distinct molecular mechanisms influence sensitivity and resistance to MDM2 inhibitors in adult acute myelogenous leukemia

TL;DR: A detailed characterization of sensitivity and resistance to treatment ex vivo with the MDM2 inhibitor MI219 in AML blasts from 109 patients uncovered a strong and significant association with mutated Flt3 status (Flt3-ITD), which for the first time identified a clinically high-risk group of AML that may particularly benefit from MDM1 inhibitor treatment.
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Acquired genomic copy number aberrations and survival in adult acute myelogenous leukemia.

TL;DR: This study analyzed flow cytometer-sorted, AML blast-derived, and paired, buccal DNA from 114 previously untreated prospectively enrolled AML patients for acquired genomic copy number changes and loss of heterozygosity using Affymetrix SNP 6.0 arrays, and correlations were correlated with patient survival.
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Aggressive chronic lymphocytic leukemia with elevated genomic complexity is associated with multiple gene defects in the response to DNA double-strand breaks

TL;DR: In this article, the authors identify a strong independent effect of radiation resistance on elevated genomic complexity in CLL and describe radiation resistance as a predictor for shortened CLL survival, and identify del17p/p53 aberrations, del11q, del13q14 type II, and CD38 expression as independent predictors of genomic complexity.