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    Craig J Ceol PhD

    TitleAssistant Professor
    InstitutionUniversity of Massachusetts Medical School
    DepartmentProgram in Molecular Medicine
    AddressUniversity of Massachusetts Medical School
    377 Plantation Street
    Worcester MA 01605
    Phone508-856-5509
      Other Positions
      InstitutionUMMS - School of Medicine
      DepartmentCancer Biology

      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentCancer Biology

      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentInterdisciplinary Graduate Program

      InstitutionUMMS - Programs, Centers and Institutes
      DepartmentBioinformatics and Integrative Biology

        Overview 
        Narrative

        Craig Ceol's Lab Page


        Academic Background

         

        Craig Ceol received his B.S./M.S. degree from Yale University and subsequently worked as an Associate Scientist at Eli Lilly and Company.  He received his Ph.D. from M.I.T. in 2002 and was a postdoctoral fellow at M.I.T. until 2004.  From 2004 to 2008, he was a postdoctoral fellow at Children’s Hospital Boston and Harvard Medical School where he was supported by fellowships from the Damon Runyon Cancer Research Foundation and Charles A. King Trust.  In 2009 he continued his postdoctoral studies as an Instructor in Pediatrics at Harvard Medical School with support from an NIH Pathway to Independence Award.  In 2010, Dr. Ceol joined the Program in Molecular Medicine at the University of Massachusetts Medical School.

        Genetic regulators of melanoma formation using the zebrafish

        Craig Ceol

        Cancer is a genetic disease that results from mutations in genes that control cell growth, division and survival.  Our laboratory seeks to identify the genetic defects that underlie tumor initiation and maintenance and understand the aberrant cellular processes that result from cancer-promoting mutations.  We have focused on malignant melanoma, the most aggressive and deadly skin cancer.  Melanoma arises from melanocytes, which produce the melanin pigments that impart color to skin and are important in the tanning response.  Mutations in the Ras/ERK signaling pathway are involved in converting normal melanocytes into melanomas.  In particular, mutations that overactive the BRAF serine/threonine kinase, a downstream effector of Ras signaling, are found in 60-70% of all melanomas.  These mutations are also present in benign melanocytic nevi - more commonly referred to as moles - indicating that other genetic alterations cooperate with oncogenic BRAF to generate melanomas.  We aim to identify these alterations and study how they cooperate with oncogenic BRAF to promote melanoma.

        Zebrafish Model

         

        We primarily utilize a zebrafish model of melanoma. Zebrafish melanocytes are externally visible, and single cells can be visualized in a living animal.  Together with a p53 mutation, human oncogenic BRAF can induce melanoma formation in zebrafish.  We developed a high-throughput method to express candidate oncogenes in zebrafish melanocytes (see figure below) and have tested whether genes that are recurrently amplified and overexpressed in human melanomas can accelerate tumor formation.  In these studies, we identified the SETDB1 histone methyltransferase as a new melanoma oncogene, highlighting the role of chromatin methylation and dysregulated transcription in tumorigenesis.  We are currently assessing additional candidates, including copy number altered genes and melanocyte lineage factors, for roles in melanoma.  In addition, we are probing how different cell subpopulations within a tumor are involved in its maintenance.  Ultimately our goal is to identify genes and cells that may serve as diagnostic and prognostic markers of disease as well as therapeutic targets. 

         



        Post Docs

        A postdoc position is available to study in Dr. Ceol's lab.Click here to apply.



        Bibliographic 
        selected publications
        List All   |   Timeline
        1. Iyengar S, Houvras Y, Ceol CJ. Screening for Melanoma Modifiers using a Zebrafish Autochthonous Tumor Model. J Vis Exp. 2012; (69).
          View in: PubMed
        2. Lian CG, Xu Y, Ceol C, Wu F, Larson A, Dresser K, Xu W, Tan L, Hu Y, Zhan Q, Lee CW, Hu D, Lian BQ, Kleffel S, Yang Y, Neiswender J, Khorasani AJ, Fang R, Lezcano C, Duncan LM, Scolyer RA, Thompson JF, Kakavand H, Houvras Y, Zon LI, Mihm MC, Kaiser UB, Schatton T, Woda BA, Murphy GF, Shi YG. Loss of 5-hydroxymethylcytosine is an epigenetic hallmark of melanoma. Cell. 2012 Sep 14; 150(6):1135-46.
          View in: PubMed
        3. Richardson J, Zeng Z, Ceol C, Mione M, Jackson IJ, Patton EE. A zebrafish model for nevus regeneration. Pigment Cell Melanoma Res. 2011 Apr; 24(2):378-81.
          View in: PubMed
        4. Ceol CJ, Houvras Y, Jane-Valbuena J, Bilodeau S, Orlando DA, Battisti V, Fritsch L, Lin WM, Hollmann TJ, Ferré F, Bourque C, Burke CJ, Turner L, Uong A, Johnson LA, Beroukhim R, Mermel CH, Loda M, Ait-Si-Ali S, Garraway LA, Young RA, Zon LI. The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset. Nature. 2011 Mar 24; 471(7339):513-7.
          View in: PubMed
        5. North TE, Goessling W, Peeters M, Li P, Ceol C, Lord AM, Weber GJ, Harris J, Cutting CC, Huang P, Dzierzak E, Zon LI. Hematopoietic stem cell development is dependent on blood flow. Cell. 2009 May 15; 137(4):736-48.
          View in: PubMed
        6. Freeman JL, Ceol C, Feng H, Langenau DM, Belair C, Stern HM, Song A, Paw BH, Look AT, Zhou Y, Zon LI, Lee C. Construction and application of a zebrafish array comparative genomic hybridization platform. Genes Chromosomes Cancer. 2009 Feb; 48(2):155-70.
          View in: PubMed
        7. Ceol CJ, Houvras Y, White RM, Zon LI. Melanoma biology and the promise of zebrafish. Zebrafish. 2008 Dec; 5(4):247-55.
          View in: PubMed
        8. Goessling W, North TE, Lord AM, Ceol C, Lee S, Weidinger G, Bourque C, Strijbosch R, Haramis AP, Puder M, Clevers H, Moon RT, Zon LI. APC mutant zebrafish uncover a changing temporal requirement for wnt signaling in liver development. Dev Biol. 2008 Aug 1; 320(1):161-74.
          View in: PubMed
        9. Langenau DM, Keefe MD, Storer NY, Jette CA, Smith AC, Ceol CJ, Bourque C, Look AT, Zon LI. Co-injection strategies to modify radiation sensitivity and tumor initiation in transgenic Zebrafish. Oncogene. 2008 Jul 10; 27(30):4242-8.
          View in: PubMed
        10. White RM, Sessa A, Burke C, Bowman T, LeBlanc J, Ceol C, Bourque C, Dovey M, Goessling W, Burns CE, Zon LI. Transparent adult zebrafish as a tool for in vivo transplantation analysis. Cell Stem Cell. 2008 Feb 7; 2(2):183-9.
          View in: PubMed
        11. Ceol CJ, Pellman D, Zon LI. APC and colon cancer: two hits for one. Nat Med. 2007 Nov; 13(11):1286-7.
          View in: PubMed
        12. Harrison MM, Ceol CJ, Lu X, Horvitz HR. Some C. elegans class B synthetic multivulva proteins encode a conserved LIN-35 Rb-containing complex distinct from a NuRD-like complex. Proc Natl Acad Sci U S A. 2006 Nov 7; 103(45):16782-7.
          View in: PubMed
        13. Ceol CJ, Stegmeier F, Harrison MM, Horvitz HR. Identification and classification of genes that act antagonistically to let-60 Ras signaling in Caenorhabditis elegans vulval development. Genetics. 2006 Jun; 173(2):709-26.
          View in: PubMed
        14. Ceol CJ, Horvitz HR. A new class of C. elegans synMuv genes implicates a Tip60/NuA4-like HAT complex as a negative regulator of Ras signaling. Dev Cell. 2004 Apr; 6(4):563-76.
          View in: PubMed
        15. Thomas JH, Ceol CJ, Schwartz HT, Horvitz HR. New genes that interact with lin-35 Rb to negatively regulate the let-60 ras pathway in Caenorhabditis elegans. Genetics. 2003 May; 164(1):135-51.
          View in: PubMed
        16. Ceol CJ, Horvitz HR. dpl-1 DP and efl-1 E2F act with lin-35 Rb to antagonize Ras signaling in C. elegans vulval development. Mol Cell. 2001 Mar; 7(3):461-73.
          View in: PubMed
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