Philip C. Hanawalt
Academic Appointments
- Professor, Biology (School of Humanities and Sciences)
- Member, Bio-X
- Member, Stanford Cancer Institute
- Professor, Dermatology
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 723-2424Alternate Contact Yolanda Madrid Administrative Assistant Email Tel Work 650-723-2424
Professional Overview
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)
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)
Professional Education
| Ph.D.: | Yale University, Biophysics (1959) |
| M.S.: | Yale University, Physics (1955) |
| B.A.: | Oberlin College, Physics (1954) |
Graduate & Fellowship Program Affiliations
Internet Links
Scientific Focus
Current Research 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 Hanawalts 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 Hanawalts laboratory, and we now know of five homologues in humans including the genes mutated in the cancer prone hereditary diseases: Blooms syndrome, Werners 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.
Publications
- Anchoring nascent RNA to the DNA template could interfere with transcription. Biophys J. 2011; (3): 675-84
- DNA slip-outs cause RNA polymerase II arrest in vitro: potential implications for genetic instability. Nucleic Acids Res. 2011; (17): 7444-54
- Mechanisms and implications of transcription blockage by guanine-rich DNA sequences. Proc Natl Acad Sci U S A. 2010; (29): 12816-21
- Transcription-coupled nucleotide excision repair of a gene transcribed by bacteriophage T7 RNA polymerase in Escherichia coli. DNA Repair (Amst). 2010; (9): 958-63
- New applications of the Comet assay: Comet-FISH and transcription-coupled DNA repair. Mutat Res. 2009 Jan-Feb; (1): 44-50
- Peptide nucleic acid (PNA) binding and its effect on in vitro transcription in friedreich's ataxia triplet repeats. Mol Carcinog. 2009; (4): 299-308
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