Angelika Amon

Angelika Amon

Kathleen and Curtis Marble Professor of Cancer Research; Investigator, Howard Hughes Medical Institute

Angelika Amon examines cell growth and division, and how errors in this process contribute to cancer and aging.

617-258-8964

Phone

76-561

Office

Erica Burds

Assistant

617-258-6559

Assistant Phone

Education

  • PhD, 1993, University of Vienna
  • BS, 1989, Biology, University of Vienna

Research Summary

We study cell growth and division. Specifically, we investigate how macromolecule biosynthesis is coordinated with cell division, and how chromosome segregation is is regulated by intracellular and extracellular cues. We also analyze the consequences of chromosome mis-segregation on cell and organismal physiology, and how these repercussions can lead to cancer and aging.

Awards

  • Nakasone Award, Human Frontier Science Program, 2020
  • Breakthrough Prize in Life Sciences, 2019
  • Vilcek Foundation Prize in Biomedical Science, 2019
  • American Academy of Arts and Sciences, Member, 2017
  • Elected Foreign Associate to EMBO, 2015
  • Elected Foreign Associate to the Austrian Academy of Sciences, 2015
  • Genetics Society of America Medal, 2014
  • Ernst Jung Prize for Medicine, 2013
  • National Academy of Sciences, Member, 2010
  • National Academy of Sciences Award in Molecular Biology, 2008
  • Paul Marks Prize, 2007
  • ASBMB Amgen Award, 2007
  • Alan T. Waterman Award, 2003
  • Eli Lilly and Company Research Award, 2003
  • Howard Hughes Medical Institute, HHMI Investigator, 2000

Key Publications

  1. Chromosome Mis-segregation Generates Cell-Cycle-Arrested Cells with Complex Karyotypes that Are Eliminated by the Immune System. Santaguida, S, Richardson, A, Iyer, DR, M'Saad, O, Zasadil, L, Knouse, KA, Wong, YL, Rhind, N, Desai, A, Amon, A et al.. 2017. Dev Cell 41, 638-651.e5.
    doi: 10.1016/j.devcel.2017.05.022PMID:28633018
  2. Aneuploidy Causes Non-genetic Individuality. Beach, RR, Ricci-Tam, C, Brennan, CM, Moomau, CA, Hsu, PH, Hua, B, Silberman, RE, Springer, M, Amon, A. 2017. Cell 169, 229-242.e21.
    doi: 10.1016/j.cell.2017.03.021PMID:28388408
  3. Single-chromosome Gains Commonly Function as Tumor Suppressors. Sheltzer, JM, Ko, JH, Replogle, JM, Habibe Burgos, NC, Chung, ES, Meehl, CM, Sayles, NM, Passerini, V, Storchova, Z, Amon, A et al.. 2017. Cancer Cell 31, 240-255.
    doi: 10.1016/j.ccell.2016.12.004PMID:28089890
  4. Spatial signals link exit from mitosis to spindle position. Falk, JE, Tsuchiya, D, Verdaasdonk, J, Lacefield, S, Bloom, K, Amon, A. 2016. Elife 5, .
    doi: 10.7554/eLife.14036PMID:27166637
  5. Regulated Formation of an Amyloid-like Translational Repressor Governs Gametogenesis. Berchowitz, LE, Kabachinski, G, Walker, MR, Carlile, TM, Gilbert, WV, Schwartz, TU, Amon, A. 2015. Cell 163, 406-18.
    doi: 10.1016/j.cell.2015.08.060PMID:26411291

Recent Publications

  1. The environmental stress response causes ribosome loss in aneuploid yeast cells. Terhorst, A, Sandikci, A, Keller, A, Whittaker, CA, Dunham, MJ, Amon, A. 2020. Proc Natl Acad Sci U S A 117, 17031-17040.
    doi: 10.1073/pnas.2005648117PMID:32632008
  2. Spindle pole bodies function as signal amplifiers in the Mitotic Exit Network. Campbell, IW, Zhou, X, Amon, A. 2020. Mol Biol Cell 31, 906-916.
    doi: 10.1091/mbc.E19-10-0584PMID:32074005
  3. Relevance and Regulation of Cell Density. Neurohr, GE, Amon, A. 2020. Trends Cell Biol 30, 213-225.
    doi: 10.1016/j.tcb.2019.12.006PMID:31980346
  4. Context is everything: aneuploidy in cancer. Ben-David, U, Amon, A. 2020. Nat Rev Genet 21, 44-62.
    doi: 10.1038/s41576-019-0171-xPMID:31548659
  5. Evaluation of Chen et al.: Overexpression of Protein Complexes and Aneuploidy. Amon, A. 2019. Cell Syst 9, 107-108.
    doi: 10.1016/j.cels.2019.08.004PMID:31465727
  6. Protein aggregation mediates stoichiometry of protein complexes in aneuploid cells. Brennan, CM, Vaites, LP, Wells, JN, Santaguida, S, Paulo, JA, Storchova, Z, Harper, JW, Marsh, JA, Amon, A. 2019. Genes Dev 33, 1031-1047.
    doi: 10.1101/gad.327494.119PMID:31196865
  7. Why haploinsufficiency persists. Morrill, SA, Amon, A. 2019. Proc Natl Acad Sci U S A 116, 11866-11871.
    doi: 10.1073/pnas.1900437116PMID:31142641
  8. Aneuploidy drives lethal progression in prostate cancer. Stopsack, KH, Whittaker, CA, Gerke, TA, Loda, M, Kantoff, PW, Mucci, LA, Amon, A. 2019. Proc Natl Acad Sci U S A 116, 11390-11395.
    doi: 10.1073/pnas.1902645116PMID:31085648
  9. Excessive Cell Growth Causes Cytoplasm Dilution And Contributes to Senescence. Neurohr, GE, Terry, RL, Lengefeld, J, Bonney, M, Brittingham, GP, Moretto, F, Miettinen, TP, Vaites, LP, Soares, LM, Paulo, JA et al.. 2019. Cell 176, 1083-1097.e18.
    doi: 10.1016/j.cell.2019.01.018PMID:30739799
  10. The Mitotic Exit Network integrates temporal and spatial signals by distributing regulation across multiple components. Campbell, IW, Zhou, X, Amon, A. 2019. Elife 8, .
    doi: 10.7554/eLife.41139PMID:30672733
More Publications

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Photo credit: Samara Vise