Cancer Institute A national cancer institute
designated cancer center
Profile http://med.stanford.edu/profiles/cancer/researcher/Joseph_Lipsick/
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Joseph (Joe) Lipsick

Academic Appointments

  • Professor of Pathology, Genetics and, by courtesy, of Biology

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Contact Information

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    Personal Information
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Bio

Academic Appointments

Administrative Appointments

  • Director, Genetics Program, SUNY Stony Brook/ Cold Spring Harbor Laboratory/ Brookhaven National Laboratory (1991 - 1993)
  • Associate Chair for Experimental Pathology, Stanford University (1995 - 2002)
  • Member, Committee on Committees, Stanford University (1999 - 2001)
  • Chair, Committee on Committees, Stanford University (2000 - 2001)
  • Director, Cancer Biology Program, Stanford University (2002 - 2005)
  • Member, Steering Committee, Faculty Senate, Stanford University (2011 - 2012)

Honors and Awards

  • Fellow, Leukemia Society of America (1984-1985)
  • Scholar, Leukemia Society of America (1989-1994)
  • Fellow, American Association for the Advancement of Science (2006-present)

Professional Education

B.A.: Oberlin College, English & Biology (1974)
M.D., Ph.D.: UC San Diego, Physiology & Pharmacology (1982)

Research & Scholarship

Current Research and Scholarly Interests

Cancer is caused by mutations in oncogenes and tumor suppressor genes. Mutations are changes in the DNA sequence that may alter gene function. Gain-of-function mutations can activate oncogenes, whereas loss-of-function mutations can inactivate tumor suppressor genes. Our laboratory studies the Myb oncogene family that is mutated in human cancers of blood cells (leukemia), brain, breast, and salivary gland. The proteins encoded by Myb genes bind to DNA and regulate the expression of other genes that control cell division, differentiation, and cell death. The Myb proteins interact with a highly conserved multi-protein complex called the MuvB core. The same complex also interacts with proteins of the Rb tumor suppressor family and the E2F transcription factor family. Work from our laboratory has shown that Myb acts in opposition to Rb-E2F to epigenetically regulate gene expression. We are currently focusing on Drosophila melanogaster (fruit fly) as a model system because of the powerful genetic, genomic, and cell biological tools available in this organism.

Teaching

Courses

2014-15

Prior Year Coursescourses of Joseph Lipsick

Postdoctoral Advisees

Melina Grigorian

Graduate and Fellowship Program Affiliations

Publications

Publications

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