Gilbert Chu

Clinical Focus

• Cancer > GI Oncology
• Oncology

Honors and Awards

• Giulio Racah Prize, International School of Subnuclear Physics, Erice, Italy (1973)
• Rita Allen Award, Rita Allen Foundation (1988-1993)
• Clinical Scientist Award for Translational Research, Burroughs-Wellcome Fund (1997-2002)
• Kaiser Award for Preclinical Teaching, Stanford University (2003, 2007)

Professional Education

Graduate & Fellowship Program Affiliations

• Biochemistry
• Biophysics
• Cancer Biology
• Immunology
• Medicine
• Molecular and Genetic Medicine

Web Site Links

• Chu Lab Home Page:

Research Interests

Our laboratory focuses on understanding how cells respond to DNA damage. Our research currently involves three areas that interact with each other: repair of ionizing radiation damage, repair of ultraviolet radiation damage, and transcriptional responses to DNA damage in cancer patients.

To understand how cells target DNA damaged by ultraviolet radiation for nucleotide excision repair, we identified UV-damaged DNA binding activity (UV-DDB). We showed that the p48 gene, encoding one of the subunits of UV-DDB, is mutated in xeroderma pigmentosum group E patients, and transcriptionally activated after DNA damage by p53. UV-DDB enhances global genomic repair and suppresses UV-induced mutagenesis.

To understand how cells repair DNA damaged by ionizing radiation, we study the non-homologous end joining pathway, which repairs double-strand breaks produced by ionizing radiation and V(D)J recombination. We wish to understand how joining optimizes the preservation of DNA sequence. We are currently studying the joining reaction with purified proteins to determine how the DNA ends are brought together, processed, and rejoined.

We have used microarrays to study the transcriptional response to ionizing radiation in lymphoblastoid cells from cancer patients with adverse reactions to radiation therapy. To interpret the microarray data, we invented new methods to analyze microarray data, including SAM (Significance Analysis of Microarrays). We successfully identified genes whose transcriptional responses predict risk for radiation toxicity. These results provide hope that treatment toxicity will soon be predicted by clinical tests.

Publications

• Local false discovery rate facilitates comparison of different microarray experiments. Hong WJ, Tibshirani R, Chu G. Nucleic Acids Res. 2009
• Cernunnos/XLF promotes the ligation of mismatched and noncohesive DNA ends. Tsai CJ, Kim SA, Chu G. Proc Natl Acad Sci U S A. 2007; 104 (19): 7851-6
• Processing of DNA for nonhomologous end-joining by cell-free extract. Budman J, Chu G. EMBO J. 2005; 24 (4): 849-60
• Significance analysis of microarrays applied to the ionizing radiation response. Tusher VG, Tibshirani R, Chu G. Proc Natl Acad Sci U S A. 2001; 98 (9): 5116-21
• Xeroderma pigmentosum p48 gene enhances global genomic repair and suppresses UV-induced mutagenesis. Tang JY, Hwang BJ, Ford JM, Hanawalt PC, Chu G. Mol Cell. 2000; 5 (4): 737-44