David Pellman

David Pellman, M.D.

Margaret M. Dyson Professor of Pediatric Oncology (Dana-Farber Cancer Institute)
Professor of Cell Biology (HMS)
HHMI Investigator

David Pellman, M.D. is the Margaret M. Dyson Professor of Pediatric Oncology at the Dana-Farber Cancer Institute, a Professor of Cell Biology at Harvard Medical School, an Investigator of the Howard Hughes Medical Institute, and the Associate Director for Basic Science at the Dana-Farber/Harvard Cancer Center.  He received his undergraduate and medical degrees from the University of Chicago.  During medical school, he did research at the Rockefeller University.  His postdoctoral fellowship was at the Whitehead Institute/Massachusetts Institute of Technology.

The Pellman Lab works on the mechanism of cell division and how certain cell division errors drive rapid genome evolution.  The normal processes studied in the laboratory have included spindle positioning and asymmetric cell division, the mechanism of spindle assembly and cytokinesis, and the mechanism of nuclear envelope assembly and how it is coordinated with chromosome segregation.  The mutational processes studied in David’s group are particularly important for cancer, but have relevance for genome evolution in other contexts.  Current projects include: the mechanism of a newly discovered mutational process called “chromothripsis”, how the architecture and integrity of the nuclear envelope impacts genome maintenance, and the role of cytoplasmic chromatin in triggering innate immune proinflammatory signaling. The lab uses a variety of approaches which include, molecular genetics, biochemistry, and imaging.  Currently there is a heavy emphasis on using a combination of live-cell imaging and single-cell genome sequencing developed in the lab (“Look-Seq”) to relate the consequences of cell division errors to genome alterations. 

Dana Farber Cancer Institute

Dept. of Pediatrics, Mayer-612

450 Brookline Ave

Boston, MA 02115

Lab phone: 617-632-4918

Lab fax: 617-632-5363

Chromothripsis as an on-target consequence of CRISPR-Cas9 genome editing.
Authors: Authors: Leibowitz ML, Papathanasiou S, Doerfler PA, Blaine LJ, Sun L, Yao Y, Zhang CZ, Weiss MJ, Pellman D.
Nat Genet
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The Ubiquitin Ligase TRAIP: Double-Edged Sword at the Replisome.
Authors: Authors: Wu RA, Pellman DS, Walter JC.
Trends Cell Biol
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Angelika Amon (1967-2020).
Authors: Authors: Pellman D.
Nat Cell Biol
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The coordination of nuclear envelope assembly and chromosome segregation in metazoans.
Authors: Authors: Liu S, Pellman D.
Nucleus
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Factors promoting nuclear envelope assembly independent of the canonical ESCRT pathway.
Authors: Authors: Lee IJ, Stokasimov E, Dempsey N, Varberg JM, Jacob E, Jaspersen SL, Pellman D.
J Cell Biol
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Publisher Correction: Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing.
Authors: Authors: Cortés-Ciriano I, Lee JJ, Xi R, Jain D, Jung YL, Yang L, Gordenin D, Klimczak LJ, Zhang CZ, Pellman DS, Park PJ.
Nat Genet
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Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer.
Authors: Authors: Ge JY, Shu S, Kwon M, Jovanovic B, Murphy K, Gulvady A, Fassl A, Trinh A, Kuang Y, Heavey GA, Luoma A, Paweletz C, Thorner AR, Wucherpfennig KW, Qi J, Brown M, Sicinski P, McDonald TO, Pellman D, Michor F, Polyak K.
Nat Commun
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Mechanisms generating cancer genome complexity from a single cell division error.
Authors: Authors: Umbreit NT, Zhang CZ, Lynch LD, Blaine LJ, Cheng AM, Tourdot R, Sun L, Almubarak HF, Judge K, Mitchell TJ, Spektor A, Pellman D.
Science
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Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing.
Authors: Authors: Cortés-Ciriano I, Lee JJ, Xi R, Jain D, Jung YL, Yang L, Gordenin D, Klimczak LJ, Zhang CZ, Pellman DS, Park PJ.
Nat Genet
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Mitotic CDK Promotes Replisome Disassembly, Fork Breakage, and Complex DNA Rearrangements.
Authors: Authors: Deng L, Wu RA, Sonneville R, Kochenova OV, Labib K, Pellman D, Walter JC.
Mol Cell
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