Adam Bailis, PhD
Associate Dean of Research, Jefferson College of Health Professions
Professor
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Adam Bailis, PhD
Associate Dean of Research, Jefferson College of Health Professions
Professor
Research & Clinical Interests
My laboratory has studied genome instability in the form of mutations, loss of heterozygosity, and chromosomal rearrangements, and their role in tumorigenesis. These genetic changes result from endogenous processes, such as DNA replication failure, oxidative metabolism and age-related telomere erosion, as well as exposure to exogenous agents, such as chemotherapeutic chemicals, and radiation. A broad array of DNA repair mechanisms addresses this damage in human cells and maintains genome stability. We have focused most directly on homology directed repair (HDR), which is essential for life in humans, indicative of its critical role in the repair of endogenous DNA damage. HDR factors, such as BRCA1 and BRCA2 are also important tumor suppressors reflecting their prominent role in genome stabilization. Many cancers are found to be defective for BRCA1 or BRCA2. Intriguingly, reducing the level of another DNA repair protein, RAD52, in BRCA-defective tumor cells is lethal but has little effect on normal cells. This “synthetic lethality” indicates that RAD52 would be an excellent target for chemotherapeutic assault as it would kill tumors without affecting normal tissue. Such a strategy could revolutionize cancer treatment by replacing drugs that cause dangerous side effects with drugs that are more targeted to the tumor and much better tolerated. However, the same attributes that make RAD52 an excellent chemotherapeutic target also make it difficult to develop drugs against, as killing BRCA-defective cells and having little effect on normal cells provide little opportunity for study. This is addressed by our recent discovery that RAD52 repairs broken chromosomes in budding yeast where this repair is not required for viability. This provides the opportunity to distinguish between compounds that affect RAD52 function and general cellular poisons. This system is being used for the high-throughput screening of compound libraries for inhibitors of RAD52 function, and to study their effects at the molecular level in order to develop them into safe and effective chemotherapeutic drugs.
Education
PhD - Albert Einstein College of Medicine, Bronx, NY - 1987
PhD Candidate - University of South Carolina, Columbia, SC, - 1983
BA - University of Delaware, Newark, DE- 1982
Publications
- Variants of the human RAD52 gene confer defects in ionizing radiation resistance and homologous recombination repair in budding yeast
- The RAD52 S346X variant reduces risk of developing breast cancer in carriers of pathogenic germline BRCA2 mutations
- Discovery of mutations in homologous recombination genes in African-American women with breast cancer
- Homologous recombination in budding yeast expressing the human RAD52gene reveals a Rad51-independent mechanism of conservative double-strand break repair
- Alleles of the homologous recombination gene, RAD59, identify multiple responses to disrupted DNA replication in Saccharomyces cerevisiae
Fellowship
Postdoctoral Fellowship - Department of Genetics and Development, Columbia College of Physicians and Surgeons, Columbia University, NY, NY - 1993
Awards
- Irell & Manella Graduate School of Biological Sciences Excellence in Teaching Award, 2003
- Irell & Manella Graduate School of Biological Sciences Excellence in Teaching Award, 2002
- Taber Outstanding Graduate Student Award, 1982, University of South Carolina
- Degree with Honors and Distinction, 1982, University of Delaware, Newark, DE