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

2D and 3D multiplexed subcellular profiling of nuclear instability in human cancer.
Authors: Authors: Coy S, Cheng B, Lee JS, Rashid R, Browning L, Xu Y, Chakrabarty SS, Yapp C, Chan S, Tefft JB, Scott E, Spektor A, Ligon KL, Baker GJ, Pellman D, Sorger PK, Santagata S.
bioRxiv
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Heritable transcriptional defects from aberrations of nuclear architecture.
Authors: Authors: Papathanasiou S, Mynhier NA, Liu S, Brunette G, Stokasimov E, Jacob E, Li L, Comenho C, van Steensel B, Buenrostro JD, Zhang CZ, Pellman D.
Nature
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Author 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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ERa-associated translocations underlie oncogene amplifications in breast cancer.
Authors: Authors: Lee JJ, Jung YL, Cheong TC, Espejo Valle-Inclan J, Chu C, Gulhan DC, Ljungström V, Jin H, Viswanadham VV, Watson EV, Cortés-Ciriano I, Elledge SJ, Chiarle R, Pellman D, Park PJ.
Nature
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A tubule-sheet continuum model for the mechanism of nuclear envelope assembly.
Authors: Authors: Zhao G, Liu S, Arun S, Renda F, Khodjakov A, Pellman D.
Dev Cell
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Breakage of cytoplasmic chromosomes by pathological DNA base excision repair.
Authors: Authors: Tang S, Stokasimov E, Cui Y, Pellman D.
Nature
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Decoding complex patterns of oncogene amplification.
Authors: Authors: Pellman D, Zhang CZ.
Nat Genet
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Whole chromosome loss and genomic instability in mouse embryos after CRISPR-Cas9 genome editing.
Authors: Authors: Papathanasiou S, Markoulaki S, Blaine LJ, Leibowitz ML, Zhang CZ, Jaenisch R, Pellman D.
Nat Commun
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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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