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James J. Goedert, M.D.

Senior Investigator

James J. Goedert, M.D.

James J. Goedert, M.D.

Organization:National Cancer Institute
Division of Cancer Epidemiology & Genetics, Infections and Immunoepidemiology Branch
Address:NCI Shady Grove
Room 6E106
Phone:240-276-7103
E-mail:goedertj@mail.nih.gov

Biography

Dr. Goedert earned a B.A. degree in psychology from Yale University and an M.D. from Loyola University Stritch School of Medicine. He received postgraduate training at Georgetown University Hospital, and he is board certified in internal medicine and medical oncology. Dr. Goedert joined the NCI Epidemiology and Biostatistics Program as a medical staff fellow in 1980. He was appointed chief of the AIDS and Cancer Section of the Viral Epidemiology Branch in 1992, and served as chief of the Branch from 1995 to 2008. Dr. Goedert received the PHS Outstanding Service Medal and the International AIDS Society's 1992 International LIFE Prize for his study of twins born to HIV-1-infected mothers. He was elected chair of the NCI Faculty of HIV and Cancer Associated Viruses in 2001, and he serves on the NCI Special Studies Institutional Review Board and on the editorial boards of several journals.

Research Interests

The epidemiology of infection-associated malignancies provides the scientific underpinnings for large-scale, effective public health and clinical interventions. It also affords opportunities for insight on basic mechanisms of carcinogenesis.

The human microbiome and cancer

The microbiome refers to the sum of all of the gene sequences in a community of microbes. Rapidly improving, high-throughput DNA amplification and sequencing technologies are being used to characterize the microbial communities that reside on and in the human body, as well as their associations with disease. In collaboration with the Center for Genome Sciences at Washington University in St. Louis and with the Department of Preventive Medicine at the University of Southern California, we have launched a study to compare the fecal microbiome of twin pairs who are discordant for Hodgkin lymphoma. Specifically, the variable region of the 16S rRNA gene, which is present in all bacteria, will be amplified and sequenced. To test the hygiene hypothesis, that links Hodgkin lymphoma to fewer exposures in childhood, the study postulates that Hodgkin cases and people with fewer oral exposures in early childhood will have less diversity in their fecal microbiome.

We also have launched a pair of studies, one within DCEG and the second in collaboration with Kaiser Permanente Colorado and the Institute of Genome Sciences at the University of Maryland Medical School, to determine whether systemic estrogen levels are associated with particular members of the fecal microbiota or with higher levels of fecal microbial beta-glucuronidase activity. If so, modulation of the intestinal microbiota or its functions might be employed to reduce the risk of postmenopausal breast cancer, which is directly related to higher systemic estrogen levels.

HIV/AIDS and cancer

Infection with human immunodeficiency virus (HIV) causes the acquired immunodeficiency syndrome (AIDS). People with HIV/AIDS have a markedly increased risk of Kaposi sarcoma (KS), non-Hodgkin lymphomas (NHL), and Hodgkin lymphoma (HL). Their risk for KS and NHL is substantially reduced by controlling HIV infection with combination antiretroviral therapy (cART). HIV-associated HL risk also is reduced, but only with at least six months of effective cART. In contrast to KS and NHL, for which the risk is inversely related to CD4 count, HL risk is highest with 100-200 CD4 cells/uL, which is moderately but not extremely severe immune deficiency. We recently found evidence for an abrupt increase in HL risk during the first six weeks after initiation of cART, suggesting that HL may be a manifestation of the immune reconstitution inflammatory syndrome (IRIS).

Using data from the HIV AIDS Cancer Match (HACM), we showed that HIV-infected women in the U.S. had a highly significant deficit in breast cancer risk during the 1980s, which attenuated with improving availability and efficacy of ART during the 1990s and early 2000s. The breast cancer deficit was unrelated to CD4 count and other measures of immunity. In collaboration with prospective cohort studies of HIV-infected women in the U.S., we recently found that those who developed breast cancer were significantly less likely than control women to have HIV with tropism for the CXCR4 chemokine co-receptor. Our findings suggest that CXCR4-tropic HIV reduced breast cancer incidence by 80-90%, which is consistent with in vitro evidence that signaling of CXCR4 induces apoptosis of breast cancer cells. These findings suggest that CXCR4 could be an effective pharmacologic or immunologic target to reduce breast cancer for women in the general population.

Classical Kaposi sarcoma (KS) and KS-associated herpes virus (KSHV)

In 1994, the long sought infectious cause of KS was discovered to be a gamma herpesvirus, now known as KSHV or human herpesvirus 8 (HHV-8). KS is the major AIDS-related malignancy. Because both HIV and KSHV are highly prevalent in large areas of sub-Saharan Africa, KS has become the most common of all malignancies in several of these countries. In contrast, classical (non-AIDS) KS is rare, even in Mediterranean adult populations that have KSHV seroprevalence above 10 percent. To understand the epidemiology of KSHV and risk factors for classical KS, we have conducted several studies in Italy. In a case-control study of classical KS cases compared to KSHV seropositive controls, KS was significantly associated with infrequent bathing, topical corticosterioid use, asthma history, non-smoking. We conducted a randomized clinical trial that found topical nicotine to be safe but ineffective for classical KS. Field work on a second case-control study of classical KS conducted throughout Sicily was completed in 2006. In addition to validating, refuting, or refining the previous associations with classical KS, novel hypotheses related to specific plant and soil exposures are being explored. In collaboration with geneticists, the combined studies are being used to identify host genetic susceptibility.

Information for Journalists

To request an interview with a DCEG investigator, contact the NCI Office of Media Relations:

E-mail:
ncipressofficers@mail.nih.gov

Phone: 301-496-6641