Laboratory of Cancer Cell Biology

Research

Dr. Neil Ganem’s laboratory uses a combination of high-resolution microscopy, genome-wide RNAi screening, cell biology, and bioinformatics to study the causes and consequences of genome instability in human cancer. Dr. Ganem’s lab seeks to define the tumor suppression mechanisms that limit the proliferation of highly abnormal aneuploid cells, as well as to identify the common genetic adaptations made by cancer cells to overcome these growth barriers.

Current projects in the lab are aimed at:

1) Identifying the cellular defects that trigger activation of the Hippo tumor suppressor pathway in aneuploid cells.

2) Examining the consequences of oncogenic signaling on mitotic fidelity and chromosome segregation.

3) Characterizing novel regulators of growth factor signaling and the Hippo pathway, as uncovered by a functional RNAi screen.

Dr. Ganem is currently accepting Rotation Students.

People

Principal Investigator

Neil J. Ganem, Ph.D.

Associate Professor of Pharmacology, Physiology & Biophysics and Medicine

Graduate Students

Amanda Bolgioni

Sanghee Lim

Lab Members

Allison Matthews

Hatim Mustaly

Tenny Mudianto

Lab Alumni

Elizabeth Shenk, Ph.D.
Position: Staff Scientist at Alliance Pharmaceuticals, Boston, MA

Lab Photos

Publications

Selected Publications:

Ganem NJ*, and Pellman D. 2012. Linking abnormal mitosis with the acquisition of DNA damage. J Cell Biol. 199(6):871-878. PMID: 2329895. PMCID: PMC 3518222 . *Corresponding author.

Highlighted in Biobytes Podcast: https://rupress.org/jcb/article/199/6/871/36973/Linking-abnormal-mitosis-to-the-acquisition-of-DNA

Crasta K, Ganem NJ, Dagher R, Lantermann AB, Ivanova EV, Pan Y, Nezi L, Protopopov A, Chowdhury D, and Pellman D. 2012. Errors in mitosis cause DNA breaks and chromosome pulverization. Nature. 482(7383):53-58. PMID:22258507. PMCID:PMC 3271137. .

Highlighted in Nature Reviews Cancer, “Shattered details” Research Highlights, 12:153.

Ganem NJ, Godinho SA, and Pellman D. 2009. A mechanism linking extra centrosomes to chromosome instability. Nature. 460:278-282.

Highlighted in Nature, “Making the paper: Neil Ganem”, 460:149; Current Biology, “Cancer: CINful Centrosomes” Dispatch, 19(15):642-645; Nature Reviews Cancer, “Chromosomal Instability: It’s about the geometry” Research Highlights, 9:529.

Kwon M, Godinho SA, Chandhok NS, Ganem NJ, Azioune A, Thery M, and Pellman D. 2008. Mechanisms to suppress multipolar divisions in cancer cells with extra centrosomes. Genes Dev.22(16):2189-2203.

Highlighted in Cell, “A Tale of too many centrosomes” Minireview, 134(4):572-575; Nature Reviews in Molecular Cell Biology, “Cancer Biology: The counting game” Research Highlight, 9:669; Genes and Development, “Multiple Centrosomes: together they stand, divided they fall” Perspective, 22 (17):22911-6; and Cancer Cell, “Actin and Microtubules: Working together to control spindle polarity” Preview, 14(3):197-199.

Ganem NJ, Storchova Z, and Pellman D. 2007. Tetraploidy, aneuploidy, and cancer. Curr Opin Genet Dev. 17:157-162.

Ganem NJ, and Pellman D. 2007. Limiting the proliferation of polyploid cells. Cell. 131:437-440.

Manning AL*, Ganem NJ*, Bakhoum SF, Wagenbach M, Wordeman L, and Compton DA. 2007. The kinesin-13 proteins Kif2a, Kif2b, and Kif2c/MCAK have distinct roles during mitosis in human cells. Mol. Biol. Cell. 18(8):2970-2979. *Co-first authors.

Couch RD, Ganem NJ, Zhou M, Popov V, Honda T, Veenstra T, Sporn MB, and Anderson AC. 2005. 2-cyano-3,12-dioxooleana-1,9(11)-diene-28-oic acid (CDDO) disrupts microtubule polymerization: A possible mechanism contributing to apoptosis. J Mol Pharm. 69:1158-1165.

Ganem NJ, and Compton DA. 2006. Functional roles of poleward microtubule flux during mitosis.Cell Cycle. 5:481-485.

Ganem NJ, Upton K, and Compton DA. 2005. Efficient mitosis in human cells lacking poleward microtubule flux. Curr. Biol. 15(20): 1827-1832.

Highlighted in Current Biology, “Microtubule flux: what is it good for?” Dispatch, 15(25):966-968.

Ganem NJ, and Compton DA. 2004. The KinI kinesin Kif2a is required for bipolar spindle assembly through a functional relationship with MCAK. J Cell Biol. 166(4): 473-478.