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

Cell cycle control of kinesin-mediated transport of Bik1 (CLIP-170) regulates microtubule stability and dynein activation.
Authors: Authors: Carvalho P, Gupta ML, Hoyt MA, Pellman D.
Dev Cell
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The differential roles of budding yeast Tem1p, Cdc15p, and Bub2p protein dynamics in mitotic exit.
Authors: Authors: Molk JN, Schuyler SC, Liu JY, Evans JG, Salmon ED, Pellman D, Bloom K.
Mol Biol Cell
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Crystal structures of a Formin Homology-2 domain reveal a tethered dimer architecture.
Authors: Authors: Xu Y, Moseley JB, Sagot I, Poy F, Pellman D, Goode BL, Eck MJ.
Cell
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A conserved mechanism for Bni1- and mDia1-induced actin assembly and dual regulation of Bni1 by Bud6 and profilin.
Authors: Authors: Moseley JB, Sagot I, Manning AL, Xu Y, Eck MJ, Pellman D, Goode BL.
Mol Biol Cell
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From polyploidy to aneuploidy, genome instability and cancer.
Authors: Authors: Storchova Z, Pellman D.
Nat Rev Mol Cell Biol
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Surfing on microtubule ends.
Authors: Authors: Carvalho P, Tirnauer JS, Pellman D.
Trends Cell Biol
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Processing, localization, and requirement of human separase for normal anaphase progression.
Authors: Authors: Chestukhin A, Pfeffer C, Milligan S, DeCaprio JA, Pellman D.
Proc Natl Acad Sci U S A
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Determinants of S. cerevisiae dynein localization and activation: implications for the mechanism of spindle positioning.
Authors: Authors: Sheeman B, Carvalho P, Sagot I, Geiser J, Kho D, Hoyt MA, Pellman D.
Curr Biol
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The molecular function of Ase1p: evidence for a MAP-dependent midzone-specific spindle matrix. Microtubule-associated proteins.
Authors: Authors: Schuyler SC, Liu JY, Pellman D.
J Cell Biol
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Formin-2, polyploidy, hypofertility and positioning of the meiotic spindle in mouse oocytes.
Authors: Authors: Leader B, Lim H, Carabatsos MJ, Harrington A, Ecsedy J, Pellman D, Maas R, Leder P.
Nat Cell Biol
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