Amity L. Manning
Biology & Biotechnology
BS Brandeis University 2002
PhD Geisel School of Medicine at Dartmouth 2008

Work in my lab is focused on defining the cellular mechanisms that maintain genome stability in normal cells and understanding how these pathways are corrupted in cancer cells. Genomic instability is a feature common in cancer that leads to aneuploidy and intra-tumor heterogeneity.  Whole chromosome instability (CIN) results from underlying defects in mitotic chromosome segregation and leads to gains and losses of entire whole chromosomes.  The ability of CIN cancer cells to ‘shuffle’ their genomic content can lead to gains of oncogenes, loss of tumor suppressors, and promotes tumor cell evolution. The resulting genomic heterogeneity between cells within a single tumor can hamper the identification of effective therapies and promote acquired drug resistance. The existence of genomic instability represents a major difference between cancer cells and the normal cells from which they are derived. As such, manipulation of CIN may represent a point of weakness that can be exploited. Experimental evidence has suggested that both increasing and suppressing CIN may be therapeutically valuable, though the most appropriate mechanisms by which to alter CIN, as well as the cancer contexts where this would be most advantageous remain unclear. Using a combination of molecular and cell biological approaches, together with bioinformatics and imaging techniques, my group aims to identify changes associated with genomic instability in cancer and exploit these changes to identify novel therapeutic targets and enhance cancer cell death. I look forward to working with students both in class and in lab to gain a better understanding of cancer cell biology and to make meaningful contributions to cancer research.

Life Sciences & Bioengineering Center 4025
Lab website
Manning Lab

Research Interests

Cancer cell biology
Cell cycle progression and cell division
Genomic instability
Chromatin structure and regulation
Tumor Suppressors

Scholarly Work

Manning AL, Yazinski S, Bryll,A, Zou L, Dyson NJ. 2014. Suppression of genome instability in pRB deficient cells by enhancement of chromosome cohesion. Mol. Cell. 53(6):993-1004. PMID: 24613344.
Manning AL, Benes C, Dyson NJ. 2014. Whole Chromosome instability resulting from the synergistic effects of pRB and p53 inactivation. Oncogene. 33(19): 2487-94. PMID. 23792446.
Black JC, Manning AL, Van Rechem C, Kim J, Ladd B, Cho J, Pineda CM, Murphy N, Daniels DL, Montagna C, Lewis PW, Glass K, Allis CD, Dyson NJ, Getz G, Whetstine JR. 2013. KDM4A lysine demethylase induces site-specific copy gain and rereplication of regions amplified in tumors. Cell. 154(3):541-55. PM
Manning AL, Bakhoum SF, Maffini S, Correia-Melo C, Maiato H, Compton DA. 2010. CLASP1, astrin and Kif2b form a molecular switch that regulates kinetochore-microtubule dynamics to promote mitotic progression and fidelity. EMBO J. 29(20): 3531-43. PMID 20852589
Manning AL, Longworth MS, Dyson NJ. 2010. Loss of pRB causes centromere dysfunction and chromosomal instability. Genes Dev. 24(13): 1364-76. PMID 20551165
Proteomic analysis of pRb loss highlights a signature of decreased mitochondrial oxidative phosphorylation. Nicolay BN, Danielian PS, Kottakis F, Lapek JD Jr, Sanidas I, Miles WO, Dehnad M, Tschöp K, Gierut JJ, Manning AL, Morris R, Haigis K, Bardeesy N, Lees JA, Haas W, Dyson NJ.

Amity Manning Receives Smith Family Foundation Award for Research on the Molecular Biology of Cancer Cells
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