Richard J. Baer, PhD

  • Professor of Pathology and Cell Biology (in the Institute for Cancer Genetics)
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Overview

Dr. Richard J. Baer is the Deputy Director of the Institute for Cancer Genetics at Columbia University Irving Medical Center and serves as Professor of Pathology & Cell Biology. He earned his B.A. in Biological Sciences from Rutgers College and completed his Ph.D. in Microbiology at Rutgers University in 1981. Dr. Baer's research focuses on understanding the tumor-suppressing mechanisms of the BRCA1 gene, which is pivotal in preventing the formation of basal-like triple-negative breast cancer, a particularly aggressive cancer subtype. His work has emphasized the BRCA1/BARD1 complex and its role in genome stability, exploring how this complex functions and its impact on cancer development when disrupted. Through biochemical and cellular approaches, Dr. Baer's laboratory also investigates related factors such as the DNA repair protein CtIP

Academic Appointments

  • Professor of Pathology and Cell Biology (in the Institute for Cancer Genetics)

Administrative Titles

  • Deputy Director, Institute for Cancer Genetics

Research

Women who carry germline mutations in the BRCA1 tumor suppressor gene are prone to develop basal-like triple-negative breast tumors, an especially lethal subtype of human breast cancer. Richard Baer studies the mechanisms by which BRCA1 suppresses tumor formation and how these mechanisms are disrupted in BRCA1 mutation carriers. In vivo, BRCA1 exists in the form of a heterodimer with another structurally-related tumor suppressor, the BARD1 protein. Most of the cellular functions attributed to BRCA1, including its critical activities in genome stability and tumor suppression, are mediated by the BRCA1/BARD1 heterodimer. The Baer laboratory uses biochemical, cellular, and organismal approaches to characterize the BRCA1/BARD1 complex and its associated factors, such as the DNA repair protein CtIP. These studies seek to define the biological functions of the BRCA1/BARD1 pathway, particularly with respect to maintenance of genome stability, and how the loss of these functions promotes breast and ovarian cancer.

Research Interests:

  • Cancer etiology
  • Hereditary breast and ovarian cancer
  • BRCA1/BARD1 pathway
  • Genome instability

Selected Publications

  • Liu X, Wang XS, Lee BJ, Wu-Baer FK, Lin X, Shao Z, Estes VM, Gautier J, Baer R, Zha S. CtIP is essential for early B cell proliferation and development in mice. J Exp Med. 2019. PMID: 31097467, DOI: 10.1084/jem.20181139
  • Billing D, Horiguchi M, Wu-Baer F, Taglialatela A, Leuzzi G, Nanez SA, Jiang W, Zha S, Szabolcs M, Lin CS, Ciccia A, Baer R. The BRCT Domains of the BRCA1 and BARD1 Tumor Suppressors Differentially Regulate Homology-Directed Repair and Stalled Fork Protection. Mol Cell. 2018. PMID: 30244837, DOI: 10.1016/j.molcel.2018.08.016
  • Chia G, Agudo J, Treff N, Sauer MV, Billing D, Brown BD, Baer R, Egli D. Genomic instability during reprogramming by nuclear transfer is DNA replication dependent. Nat Cell Biol. 2017. PMID: 28263958, DOI: 10.1038/ncb3485
  • Reczek CR, Szabolcs M, Stark JM, Ludwig T, Baer R. The interaction between CtIP and BRCA1 is not essential for resection-mediated DNA repair or tumor suppression. J Cell Biol. 2013. PMID: 23712259, DOI: 10.1083/jcb.201302145
  • Shakya R, Reid LJ, Reczek CR, Cole F, Egli D, Lin CS, deRooij DG, Hirsch S, Ravi K, Hicks JB, Szabolcs M, Jasin M, Baer R, Ludwig T. BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not its E3 ligase activity. Science. 2011. PMID: 22034435, DOI: 10.1126/science.1209909
  • Shakya R, Szabolcs M, McCarthy E, Ospina E, Basso K, Nandula S, Murty V, Baer R, Ludwig T. The basal-like mammary carcinomas induced by Brca1 or Bard1 inactivation implicate the BRCA1/BARD1 heterodimer in tumor suppression. Proc Natl Acad Sci USA. 2008. PMID: 18443292, DOI: 10.1073/pnas.0711032105
  • Laufer M, Nandula SV, Modi AP, Wang S, Jasin M, Murty VV, Ludwig T, Baer R. Structural requirements for the BARD1 tumor suppressor in chromosomal stability and homology-directed DNA repair. J Biol Chem. 2007.
    PMID: 17848578, DOI: 10.1074/jbc.M705198200
  • Wu-Baer F, Lagrazon K, Yuan W, Baer R. The BRCA1/BARD1 heterodimer assembles polyubiquitin chains through an unconventional linkage involving lysine residue K6 of ubiquitin. J Biol Chem. 2003. PMID: 12890688, DOI: 10.1074/jbc.C300249200
  • Baer R, Ludwig T. The BRCA1/BARD1 heterodimer, a tumor suppressor complex with ubiquitin E3 ligase activity. Curr Opin Genet Dev. 2002. PMID: 11790560, DOI: 10.1016/s0959-437x(01)00269-6
  • Yu X, Wu LC, Bowcock AM, Aronheim A, Baer R. The C-terminal (BRCT) domains of BRCA1 interact in vivo with CtIP, a protein implicated in the CtBP pathway of transcriptional repression. J Biol Chem. 1998. PMID: 9738006, DOI: 10.1074/jbc.273.39.25388
  • Wu LC, Wang ZW, Tsan JT, Spillman MA, Phung A, Xu XL, Yang MC, Hwang LY, Bowcock AM, Baer R. Identification of a RING protein that can interact in vivo with the BRCA1 gene product. Nat Genet. 1996. PMID: 8944023, DOI: 10.1038/ng1296-430
  • Baer R. TAL1, TAL2 and LYL1: a family of basic helix-loop-helix proteins implicated in T cell acute leukaemia. Semin Cancer Biol. 1993. PMID: 8142619, DOI:
  • Xia Y, Brown L, Yang CY, Tsan JT, Siciliano MJ, Espinosa R, Le Beau MM, Baer RJ. TAL2, a helix-loop-helix gene activated by the (7;9)(q34;q32) translocation in human T-cell leukemia. Proc Natl Acad Sci USA. 1991. PMID: 1763056, DOI: 10.1073/pnas.88.24.11416
  • Brown L, Cheng JT, Chen Q, Siciliano MJ, Crist W, Buchanan G, Baer R. Site-specific recombination of the tal-1 gene is a common occurrence in human T cell leukemia. EMBO J. 1990. PMID: 2209547
  • Chen Q, Cheng JT, Tasi LH, Schneider N, Buchanan G, Carroll A, Crist W, Ozanne B, Siciliano MJ, Baer R. The tal gene undergoes chromosome translocation in T cell leukemia and potentially encodes a helix-loop-helix protein. EMBO J. 1990. PMID: 2303035

For a complete list of publications, please visit PubMed.gov