Stanford School of Medicine
Community Academic Profiles

Joseph (Joe) Lipsick

Email:
Profile: http://med.stanford.edu/profiles/Joseph_Lipsick/
Academic Appointments
Appointment
Organization
Professor
Professor
Member
Member
Graduate & Fellowship Program Affiliations
 
Honors & Awards
Title
Organization
Date(s)
Fellow
Leukemia Society of America
1984-1985
Scholar
Leukemia Society of America
1989-1994
Fellow
American Association for the Advancement of Science
2006-present
Administrative Appointments
Title
Organization
Start Year
End Year
Director, Genetics Program
SUNY Stony Brook/ Cold Spring Harbor Laboratory/ Brookhaven National Laboraotry
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
Professional Education
Degree
Awarding Institution
Field of Study
Year of Graduation
B.A.
Oberlin College
English & Biology
1974
M.D., Ph.D.
UC San Diego
Physiology & Pharmacology
1982
Postdoctoral Advisees
Hong Wen
Web Site Links
Research/Lab website:   Myb World (Lipsick Lab Homepage)
Research Interests

Since participating in the initial identification of the protein product of the v-Myb oncogene as a postdoctoral fellow, I have dedicated my research career to understanding the function of the highly conserved Myb oncogene family. We initially focused on the retroviral v-Myb oncogene and its cellular homologue, c-Myb. More recently we have focused on the fruit fly Drosophila melanogaster as a model organism for understanding the human Myb oncogene family. We created the first null mutants of the sole Drosophila Myb gene, and showed that the absence of Myb resulted in mitotic abnormalities including chromosome condensation defects, aneuploidy, polyploidy, and aberrant spindle formation. In collaboration with the laboratory of Michael Botchan (UC Berkeley), we also showed that Myb was required for the site-specific initiation of DNA replication that occurs during chorion gene amplification in adult ovarian follicle cells. We ourselves then showed that the absence of Myb causes a failure in the normal progression of chromosome condensation from heterchromatin to euchromatin. Most recently, we have found that Myb acts in opposition to repressive E2F and RB proteins to epigenetically regulate the expression of key components of the spindle assembly checkpoint and spindle pole regulatory pathways.

To investigate the functional evolution of the three Myb genes present in all vertebrate species, we tested which if any of these vertebrate Myb genes could complement a Drosophila Myb null mutant. We found that B-Myb, but neither A-Myb nor C-Myb, could complement the defects in proliferation and differentiation seen in Myb null Drosophila hemocytes. These results argue strongly that Drosophila Myb is in fact the orthologue of vertebrate B-Myb. Therefore, studies of Drosophila Myb are likely to be highly informative about the function of vertebrate B-Myb. Importantly, elevated levels of B-Myb expression are a clinically significant predictor of poor prognosis in human breast cancer and other malignancies.

Publications
  • Wen H, Andrejka L, Ashton J, Karess R, Lipsick JS "Epigenetic regulation of gene expression by Drosophila Myb and E2F2-RBF via the Myb-MuvB/dREAM complex." Genes Dev 2008; 22: 5: 601-14 More »
  • Manak JR, Wen H, Tran V, Andrejka L, Lipsick JS "Loss of Drosophila Myb interrupts the progression of chromosome condensation." Nat Cell Biol 2007; 9: 5: 581-7 More »
  • Wang DM, Sevcikova S, Wen H, Roberts S, Lipsick JS "v-Myb represses the transcription of Ets-2." Oncogene 2006; More »
  • Fu SL, Ganter B, Lipsick JS "Myb proteins inhibit fibroblast transformation by v-Rel." Mol Cancer 2006; 5: 1: 54 More »
  • Lipsick JS, "synMuv verite--Myb comes into focus." Genes Dev 2004; 18: 23: 2837-44 More »
59 publications:   view full list

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