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James A. Lautenberger, Ph.D.

Portait Photo of James Lautenberger
Basic Research Laboratory
Staff Scientist
Center for Cancer Research
National Cancer Institute
Building 560, Room 21-18
P.O. Box B
Frederick, MD 21702-1201
Phone:  
301-846-5296
Fax:  
301-846-1686
E-Mail:  
lautenbj@mail.nih.gov

Biography

Dr. Lautenberger received his B.S. degree from the University of Rochester and a Ph.D. from the University of California, Berkeley. His Ph.D. thesis work, performed in the laboratory of Dr. Stuart Linn, consisted of the characterization of the Escherichia coli B modification methylase. After postdoctoral training at the University of North Carolina, Chapel Hill, under Drs. Clyde Hutchison III and Marshall Edgell, Dr. Lautenberger joined the National Cancer Institute. In Dr. Takis Papas's laboratory at the NCI, his accomplishments included the molecular cloning of the v-myc oncogene, bacterial expression of the HTLV-I envelope protein allowing the development of an assay for the virus in blood, and demonstration that antisense oligonucleotides derived from the ETS1 proto-oncogene sequence inhibit endothelial cell migration. Dr. Lautenberger later joined Dr. Stephen O'Brien's Laboratory of Genomic Diversity (LGD) where he characterized admixture linkage disequilibrium in African Americans and investigated host-genetic influences on HIV/AIDS infection and progression.

Research

My research involves discovering associations between human genes and disease outcomes. I recently have participated in the analysis of genome-wide association studies (GWAS) for AIDS and nasopharyngeal carcinoma (NPC) in the NCI Laboratory of Human Diversity (LGD). The LGD AIDS GWAS has detected a novel association between several SNPs in the PARD3B gene on chromosome 2 and the rate of progression to AIDS-defining clinical conditions. A plausible role for PARD3B in HIV/AIDS biology exists since the PARD3B product has been shown to bind several SMAD proteins including SMAD3 and SMAD4 that are associated with tat-mediated transcription of the HIV-1 LTR. A paper describing this association has recently been accepted for publication (Troyer et al., J. Inf. Dis., in press). In addition to the PARD3B association, several SNPs near the CCR5 gene on chromosome 3 were found to be significantly associated with infection susceptibility reconfirming this previously described association. In performing these analyses I have developed expertise in the management of large clinical data sets, the management of large sets of genotypic data, and the detection of genotype-phenotype associations with categorical and survival analysis techniques.

This page was last updated on 2/27/2013.