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Philip C. Hanawalt

Academic Appointments

  • Dr. Morris Herzstein Professor in Biology and Professor of Dermatology

Contact Information

  • Academic Offices
    Personal Information
    Email Tel (650) 723-2424
    Alternate Contact
    Yolanda Madrid Administrative Assistant Tel Work 650-723-2424

Bio

Academic Appointments

Administrative Appointments

  • Chair, Department of Biological Sciences, Stanford University (1982 - 1989)
  • Chair, Second Senate ad hoc Committee on the Professoriate, Stanford University (1988 - 1990)
  • Director, Biophysics Graduate Program, Stanford University (1968 - 1985)
  • Member, School Planning Group, Humanities and Sciences, Stanford Universtiy (1991 - 1993)
  • Board of Trustees, Oberlin College (1998 - 2007)
  • Editorial Board, Proceedings of the National Academy of Sciences USA (2000 - present)
View All 27administrative appointments of Philip Hanawalt

Honors and Awards

  • AACR-Princess Takamatsu Lectureship, American Association for Cancer Research (April 2011)
  • The Dr. Morris Herzstein Professorship in Biology, Stanford University (2008 -)
  • Howard H. and Jessie T. Watkins University Professor, Stanford University (1997 - 2002)
  • Member, National Academy of Sciences, USA (1989)
  • Peter and Helen Bing Award for Distinguished Teaching, Stanford University (1992)
  • Excellence in Teaching Award, Northern California Chapter, Phi Beta Kappa (1991)
View All 27honors and awards of Philip Hanawalt

Professional Education

Ph.D.: Yale University, Biophysics (1959)
M.S.: Yale University, Physics (1955)
B.A.: Oberlin College, Physics (1954)

Research & Scholarship

Current Research and Scholarly Interests

Hanawalt has been a productive researcher in the field of DNA repair since his pioneering discovery of repair replication in E. coli in 1963. In 1982 Hanawalt and his colleagues reported the first example of intragenomic DNA repair heterogeneity: chemical adducts in alpha DNA in African green monkey kidney cells were not as efficiently repaired as in the genome overall. Hanawalt and his colleagues then discovered that repair of some types of damage is selective; active genes are preferentially repaired, and in fact a special repair pathway, termed transcription-coupled repair (TCR), operates on the transcribed strands of expressed genes. TCR was documented in mammalian cells, in E. coli, and in yeast chromosomal and plasmid borne genes. The discovery of TCR in Hanawalt’s laboratory has had profound implications for the fields of mutagenesis, environmental carcinogenesis, aging, and risk assessment.
The prototype recQ gene was discovered in E. coli in Hanawalt’s laboratory, and we now know of five homologues in humans including the genes mutated in the cancer prone hereditary diseases: Bloom’s syndrome, Werner’s syndrome, and Rothman Thompson syndrome.
More recent studies have focused upon the regulation of TCR and the global genomic nucleotide excision repair (GGR) pathway. Features of the TCR pathway (defective in Cockayne syndrome) include the possibility of "gratuitous TCR" at transcription pause sites in undamaged DNA. The GGR pathway was shown to be controlled through the SOS stress response in E. coli and through the activated product of the p53 tumor suppressor gene in human cells. These regulatory systems particularly affect the efficiency of repair of the predominant UV-induced photoproduct, the cyclobutane pyrimidine dimer, as well as that of chemical carcinogen DNA adducts, such as benzo(a)pyrene diol-epoxide and benzo(g)chrysene. Rodent cells (typically lacking the p53-controlled GGR pathway) are unable to carry out efficient GGR of some lesions. Therefore, caution should be exercised in the interpretation of results from such systems for risk assessment in genetic toxicology.

Teaching

Courses

2014-15

Prior Year Coursescourses of Philip Hanawalt

Graduate and Fellowship Program Affiliations

Publications

Publications

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Publication Topics

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