How Infection and Inflammation Can Lead to Cancer

New research is emerging that suggests a link between infection-related diseases and risk of cancer, according to findings presented here at the American Association for Cancer Research 101st Annual Meeting 2010.

“Chronic or recurrent inflammatory conditions appear to contribute to the development of a diverse array of cancers, and tackling these conditions early could be an avenue for prevention,” said William G. Nelson V, M.D., Ph.D., professor and director of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University.

Nelson will host a press conference on Infection, Inflammation and Cancer at the Annual Meeting in room 142 of the Walter E. Washington Convention Center on Monday, April 19, 2010, at 1:00 p.m. ET.

Reporters who cannot attend in person can call in using the following information:

U.S. and Canada: (888) 282-7404
International: (706) 679-5207
Access Code: 59333854

According to Nelson, the emerging data on the relationship between infections and cancer suggest a need for synergy between the cancer and infectious disease research communities.

“How we alter the bacteria levels in our body is a complex issue, but there is a potential to develop cancer prevention strategies,” said Nelson.

The following abstracts will be presented at the press conference:

5353. Identification of a subset of AIDS related lymphoma (ARL) containing HIV infected macrophages that is immunophenotypically distinct from EBV positive ARL

Researchers at the University of California, San Francisco, have identified HIV-infected macrophages that are associated with more than half of AIDS-related lymphoma (ARL) in the post-highly active antiretroviral therapy (HAART) era.

“The frequency of this type of tumor is double that from the pre-HAART era and it is present in all subtypes of lymphoma,” said Leanne C. Huysentruyt, Ph.D., assistant research scientist at the University of California, San Francisco.

The risk of developing non-Hodgkin lymphoma is 60 times greater in patients with HIV, despite the initiation of HAART — an aggressive treatment regimen of at least three anti-retroviral drugs that attack different parts of HIV to suppress viral replication.

Using specimen data from the AIDS and Cancer Specimen Resource (from 1982 to 2007), Huysentruyt and colleagues investigated the incidence of HIV-infected lymphomas in the pre- and post-HAART eras to determine if HIV-positive lymphomas have a specific immunophenotype.

In the current study, the researchers evaluated tissue microarrays containing more than 150 ARLs for the presence of HIV.

“In the case of cells already infected, such as macrophage viral reservoirs, HAART has little or no effect. This suggests that HIV-infected macrophages in ARLs must be relatively long-lived and unaffected by anti-retroviral therapy,” she said. “Therefore, targeting HIV-infected macrophages for drug development may be an effective adjunct to current anti-lymphoma therapies.”