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Alfonso Bellacosa, MD, PhD

Professor
Adjunct Professor, Department of Microbiology and Immunology, Lewis Katz School of Medicine, Temple University
Adjunct Professor, College of Science and Technology, Temple University
Adjunct Associate Professor, Department of Biochemistry, Drexel University College of Medicine
Research Program
Educational Background
- PhD, Genetics, University of Paris, 2001-2004
- Postgraduate School of Hematology, Catholic University Medical School, Rome, 1988-1992
- MD, Catholic University Medical School, Rome, 1982-1988
- University of Naples Second Medical School, 1981-1982
Honors & Awards
- PhD, avec la mention Très Honorable, 2004
- "Sir Paul Girolami" Award for Innovative Research in Biology and Medicine, presented by Nobel Laureates Edmund Fischer and Rita Levi-Montalcini, 1993
- Fellowship from the Italian Association for Cancer Research, 1992-1994
- Postdoctoral Fellowship from the "Lawrence Greenwald Foundation for Research on Leukemia and Lymphoma," 1989-1991
- MD, 110/110 Summa Cum Laude, 1988
Research Program
Research Interests
- Role of DNA Repair in the stability of the genome and epigenome
- Regulation of DNA methylation and DNA demethylation in development and cancer
- Targeted epigenetic therapy
- Hereditary Cancer
Lab Overview
The goal of our research is to clarify how alterations in genomic and epigenomic stability of CpG sequences lead to altered development and cancer formation. Mutations are often the consequence of defective DNA repair; we are particularly interested in the mammalian DNA repair enzymes that protect the integrity of CpG sequences in DNA: MBD4 and TDG. This is important because mutations at CpG sites represent about one third of all point mutations in cancer. In addition, CpG sites are also important for regulation of gene activity by an epigenetic process called DNA methylation. We discovered a role of TDG in active DNA demethylation (Cortellino et al. Cell, 2011), which is highly relevant in the context of the recently identified oxidized cytosine variants that have expanded the information content of the genome: TDG is the only enzyme that efficiently removes 5-formylcytosine and 5-carboxylcytosine produced by the TET dioxygenases.
We are also interested in innovative approaches of cancer prevention and therapy that are rationally based on the analysis of genetic and epigenetic alterations of cancer cells.
Finally, we are interested in the molecular basis of hereditary cancer syndromes.

Contact Information
Alfonso.Bellacosa@fccc.edu
Office Phone: 215-728-2813
Fax: 215-214-1590
Office: P3041
Lab: P3023

Contact Information
Alfonso.Bellacosa@fccc.edu
Office Phone: 215-728-2813
Fax: 215-214-1590
Office: P3041
Lab: P3023
Professor
Adjunct Professor, Department of Microbiology and Immunology, Lewis Katz School of Medicine, Temple University
Adjunct Professor, College of Science and Technology, Temple University
Adjunct Associate Professor, Department of Biochemistry, Drexel University College of Medicine
Research Program
Education
Educational Background
- PhD, Genetics, University of Paris, 2001-2004
- Postgraduate School of Hematology, Catholic University Medical School, Rome, 1988-1992
- MD, Catholic University Medical School, Rome, 1982-1988
- University of Naples Second Medical School, 1981-1982
Honors & Awards
- PhD, avec la mention Très Honorable, 2004
- "Sir Paul Girolami" Award for Innovative Research in Biology and Medicine, presented by Nobel Laureates Edmund Fischer and Rita Levi-Montalcini, 1993
- Fellowship from the Italian Association for Cancer Research, 1992-1994
- Postdoctoral Fellowship from the "Lawrence Greenwald Foundation for Research on Leukemia and Lymphoma," 1989-1991
- MD, 110/110 Summa Cum Laude, 1988
Research Profile
Research Interests
- Role of DNA Repair in the stability of the genome and epigenome
- Regulation of DNA methylation and DNA demethylation in development and cancer
- Targeted epigenetic therapy
- Hereditary Cancer
Lab Overview
The goal of our research is to clarify how alterations in genomic and epigenomic stability of CpG sequences lead to altered development and cancer formation. Mutations are often the consequence of defective DNA repair; we are particularly interested in the mammalian DNA repair enzymes that protect the integrity of CpG sequences in DNA: MBD4 and TDG. This is important because mutations at CpG sites represent about one third of all point mutations in cancer. In addition, CpG sites are also important for regulation of gene activity by an epigenetic process called DNA methylation. We discovered a role of TDG in active DNA demethylation (Cortellino et al. Cell, 2011), which is highly relevant in the context of the recently identified oxidized cytosine variants that have expanded the information content of the genome: TDG is the only enzyme that efficiently removes 5-formylcytosine and 5-carboxylcytosine produced by the TET dioxygenases.
We are also interested in innovative approaches of cancer prevention and therapy that are rationally based on the analysis of genetic and epigenetic alterations of cancer cells.
Finally, we are interested in the molecular basis of hereditary cancer syndromes.
Lab Staff
