University of California San Francisco
Helen Diller Family Comprehensive Cancer Center
Robert Judson, PhD

Robert Judson, PhD

Assistant Researcher, Sandler Faculty Fellow, UCSF

Cancer Center Program Memberships

Cancer Genetics

Research Summary

Melanoma is the most deadly skin cancer, and the incidence of the disease has been increasing steadily for about three decades. In 2016, we expect over 75,000 new diagnoses and about 10,000 deaths in the United States. Metastasized melanomas are notorious for their ability to acquire resistance to even the most promising treatments, usually resulting in a fatal recurrence. Perhaps most tragic, melanoma is among the most common cancers in young adults, ages 20 to 39. Better methods of predicting and preventing this disease would have significant impact on the lives of these patients and the economic burden of treatment.

At the root of melanoma is a cell state transition – the reprogramming of a melanocyte functioning under one specific set of operations into a different cell type that has lost some of its cellular programs and acquired others. What causes this transition to occur? Melanoma, like many cancers, has traditionally been viewed as a strictly genetic disease - progression is driven though the accumulation of genetic mutations that confer survival advantages and oncogenic phenotypes. One consequence of this progressive hit model is that treatment is reactionary – no individual cell is at greater or less risk of progression, but rather a cancer cell is only identified after it has obtained the causal mutation.

This progressive hit model is almost certainly over-simplified. Much of previous research has focused on “surviving cells” – for example, the few cells that progressed to form a tumor in a patient or mouse model, or cells that successfully transform into lines in culture. The interests of my research group can be generalized by the inverse question: “If one in ten (or more accurately, ten thousand) mutated melanocytes successfully form a melanoma – what prevented the rest from doing so and why?” Answering this question will flesh out the progressive hit model by providing both an understanding of the diversity of phenotypic consequences established oncogenic mutations can have on individual cells and by identifying the non-genetic factors that result in cells being permissive to transformation. With the goal of developing novel strategies for early diagnostics and prevention, my research group uses a combination of primary tumor sequencing, microRNA-based network dissection, CRISPR/Cas9-based engineering of melanomas from primary melanocytes, and digital holographic quantitative cytometry to study the networks of genes that prevent normal melanocytes and primary melanomas from acquiring oncogenic programs.

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Wesleyan University, B.A., 05/05, Mol. Biology & Biochemistry
National Institutes of Health, 09/07, Biochemistry
University of California, San Francisco, Ph.D., 12/12, Biomedical Sciences

Professional Experience

  • 2004 – 2005
    Research Assistant, Georgetown University
  • 2005 – 2007
    Postbaccalaureate Fellow, National Institutes of Health, NICHD
  • 2007 – 2012
    Graduate Student Researcher, University of California, San Francisco
  • 2013 – 2014
    Postdoctoral Fellow, University of California, San Francisco
  • 2014 – present
    Sandler Faculty Fellow, University of California, San Francisco

Honors & Awards

  • 2004
    Goldwater Scholarship, Barry Goldwater Excellence in Education Foundation
  • 2005
    Graduated University Honors: Wesleyan’s highest honor awarded to 0-2 graduating seniors a year.
  • 2005
    Graham Prize for Excellence in Natural Sciences, Wesleyan University
  • 2005
    Hawk Prize for Excellence in Biochemistry, Wesleyan University
  • 2007 – 2010
    National Sciences Foundation Graduate Research Fellowship
  • 2010
    UC Cancer Research Coordinating Committee Fellowship, UCSF
  • 2011
    Julius R. and Patricia A. Krevans Fellowship, UCSF
  • 2012
    Northern California Association of Phi Beta Kappa Graduate Fellowship
  • 2013
    UCSF Faculty Fellow, University of California, San Francisco
  • 2014
    NIH Common Fund DP5 Early Independence Award
  • 2016-2017
    Seeding Bold Ideas Award, Marcus Program in Precision Medicine
  • 2017
    Cancer Center Impact Award, Helen Diller Family Comprehensive Cancer Center, UCSF

Selected Publications

  1. Zhang Y, Judson RL. Evaluation of holographic imaging cytometer holomonitor M4® motility applications. Cytometry A. 2018 Nov; 93(11):1125-1131.
    View on PubMed
  2. Zeng H, Jorapur A, Shain AH, Lang UE, Torres R, Zhang Y, McNeal AS, Botton T, Lin J, Donne M, Bastian IN, Yu R, North JP, Pincus L, Ruben BS, Joseph NM, Yeh I, Bastian BC, Judson RL. Bi-allelic Loss of CDKN2A Initiates Melanoma Invasion via BRN2 Activation. Cancer Cell. 2018 07 09; 34(1):56-68.e9.
    View on PubMed
  3. Shain AH, Joseph NM, Yu R, Benhamida J, Liu S, Prow T, Ruben B, North J, Pincus L, Yeh I, Judson R, Bastian BC. Genomic and Transcriptomic Analysis Reveals Incremental Disruption of Key Signaling Pathways during Melanoma Evolution. Cancer Cell. 2018 07 09; 34(1):45-55.e4.
    View on PubMed
  4. Yeh I, Lang UE, Durieux E, Tee MK, Jorapur A, Shain AH, Haddad V, Pissaloux D, Chen X, Cerroni L, Judson RL, LeBoit PE, McCalmont TH, Bastian BC, de la Fouchardière A. Combined activation of MAP kinase pathway and ß-catenin signaling cause deep penetrating nevi. Nat Commun. 2017 09 21; 8(1):644.
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  5. Hejna M, Jorapur A, Song JS, Judson RL. High accuracy label-free classification of single-cell kinetic states from holographic cytometry of human melanoma cells. Sci Rep. 2017 09 20; 7(1):11943.
    View on PubMed
  6. Huskey NE, Guo T, Evason KJ, Momcilovic O, Pardo D, Creasman KJ, Judson RL, Blelloch R, Oakes SA, Hebrok M, Goga A. CDK1 inhibition targets the p53-NOXA-MCL1 axis, selectively kills embryonic stem cells, and prevents teratoma formation. Stem Cell Reports. 2015 Mar 10; 4(3):374-89.
    View on PubMed
  7. Parchem RJ, Ye J, Judson RL, LaRussa MF, Krishnakumar R, Blelloch A, Oldham MC, Blelloch R. Two miRNA clusters reveal alternative paths in late-stage reprogramming. Cell Stem Cell. 2014 May 01; 14(5):617-31.
    View on PubMed
  8. Judson RL, Greve TS, Parchem RJ, Blelloch R. MicroRNA-based discovery of barriers to dedifferentiation of fibroblasts to pluripotent stem cells. Nat Struct Mol Biol. 2013 Oct; 20(10):1227-35.
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  9. Greve TS, Judson RL, Blelloch R. microRNA control of mouse and human pluripotent stem cell behavior. Annu Rev Cell Dev Biol. 2013; 29:213-239.
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  10. Subramanyam D, Lamouille S, Judson RL, Liu JY, Bucay N, Derynck R, Blelloch R. Multiple targets of miR-302 and miR-372 promote reprogramming of human fibroblasts to induced pluripotent stem cells. Nat Biotechnol. 2011 May; 29(5):443-8.
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  11. Swarbrick A, Woods SL, Shaw A, Balakrishnan A, Phua Y, Nguyen A, Chanthery Y, Lim L, Ashton LJ, Judson RL, Huskey N, Blelloch R, Haber M, Norris MD, Lengyel P, Hackett CS, Preiss T, Chetcuti A, Sullivan CS, Marcusson EG, Weiss W, L'Etoile N, Goga A. miR-380-5p represses p53 to control cellular survival and is associated with poor outcome in MYCN-amplified neuroblastoma. Nat Med. 2010 Oct; 16(10):1134-40.
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  12. Melton C, Judson RL, Blelloch R. Opposing microRNA families regulate self-renewal in mouse embryonic stem cells. Nature. 2010 Feb 04; 463(7281):621-6.
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  13. Judson RL, Babiarz JE, Venere M, Blelloch R. Embryonic stem cell-specific microRNAs promote induced pluripotency. Nat Biotechnol. 2009 May; 27(5):459-61.
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  14. Ebina H, Chatterjee AG, Judson RL, Levin HL. The GP(Y/F) domain of TF1 integrase multimerizes when present in a fragment, and substitutions in this domain reduce enzymatic activity of the full-length protein. J Biol Chem. 2008 Jun 06; 283(23):15965-74.
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  15. Atwood-Moore A, Yan K, Judson RL, Levin HL. The self primer of the long terminal repeat retrotransposon Tf1 is not removed during reverse transcription. J Virol. 2006 Aug; 80(16):8267-70.
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