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Mitchell L. Leibowitz
Researcher at Harvard University
Publications - 8
Citations - 1236
Mitchell L. Leibowitz is an academic researcher from Harvard University. The author has contributed to research in topics: Chromothripsis & Genome. The author has an hindex of 6, co-authored 8 publications receiving 910 citations. Previous affiliations of Mitchell L. Leibowitz include Howard Hughes Medical Institute & University of Virginia.
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Journal ArticleDOI
Genome-wide mapping and assembly of structural variant breakpoints in the mouse genome
Aaron R. Quinlan,Royden A. Clark,Svetlana Sokolova,Mitchell L. Leibowitz,Yujun Zhang,Matthew E. Hurles,Joshua Chang Mell,Ira M. Hall +7 more
TL;DR: An algorithm to localize SV breakpoints by paired-end mapping, and a general approach for the genome-wide assembly and interpretation of breakpoint sequences are developed, which demonstrate that HYDRA accurately maps diverse classes of SV, including those involving repetitive elements such as transposons and segmental duplications.
Journal ArticleDOI
Chromothripsis and beyond: rapid genome evolution from complex chromosomal rearrangements
TL;DR: The impact of massive chromosomal change for the development of diseases such as cancer and for evolution more generally is considered and current models for underlying mechanisms are summarized.
Posted ContentDOI
Chromothripsis as an on-target consequence of CRISPR-Cas9 genome editing
Mitchell L. Leibowitz,Mitchell L. Leibowitz,Stamatis Papathanasiou,Phillip A. Doerfler,Logan J. Blaine,Yu Yao,Cheng-Zhong Zhang,Mitchell J. Weiss,David Pellman,David Pellman +9 more
TL;DR: It is shown that CRISPR-Cas9-mediated DNA breaks generate abnormal nuclear structures—micronuclei and chromosome bridges—that trigger chromothripsis, an on-target toxicity that may be minimized by cell manipulation protocols or screening but cannot be completely avoided in many genome editing applications.
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Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms
Ankit Malhotra,Michael R. Lindberg,Gregory G. Faust,Mitchell L. Leibowitz,Royden A. Clark,Ryan M. Layer,Aaron R. Quinlan,Ira M. Hall +7 more
TL;DR: These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.
Journal ArticleDOI
Chromothripsis: A New Mechanism for Rapid Karyotype Evolution
TL;DR: The genomic features of chromothripsis are reviewed and recent progress on understanding its mechanism is summarized, including new work indicating that one mechanism to generate chromothRIpsis is through the physical isolation of chromosomes in abnormal nuclear structures (micronuclei).