New research is emerging that suggests a link between infection-related diseases and risk of cancer, according to findings presented at the American Association for Cancer Research 101st annual meeting.
“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, MD, PhD, professor and director of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University.
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 research will be presented at the American Association for Cancer Research meeting:
Abstract 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, PhD, 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.”
The frequency of the Epstein-Barr virus, another cancer-causing virus of the herpes family that was previously associated with ARL, did not change after the introduction of HAART.
Abstract 5746. Circulating cytokine levels, EBV and risk of AIDS-related non-Hodgkin lymphoma
Patients with AIDS are 100 times more likely to get non-Hodgkin lymphoma than the general population, and researchers have uncovered new information that suggests circulating cytokine levels may be playing a role in this increased risk.
“Although medicines that fight AIDS are becoming more effective, cancer remains a real risk among these patients. We need to keep working toward understanding the mechanisms that predispose people to certain cancers,” said Charles S. Rabkin, MD, senior investigator at the National Cancer Institute.
Cancer was one of the first clues that led researchers to identify AIDS in the early 1980s. Since then, researchers have been working to discover why patients with AIDS are at greater risk of cancer than the general population.
For the current study, Rabkin and colleagues used prospective cohort studies to examine prediagnostic blood samples from 66 patients with AIDS and non-Hodgkin lymphoma and 186 lymphoma-free controls. These patient groups had similar ages, racial composition and gender.
The researchers measured 30 separate cytokines and found that nine of them had significantly higher levels in patients who subsequently developed lymphoma.
Researchers also examined the link between Epstein-Barr virus (EBV), a cancer-causing virus of the herpes family, and non-Hodgkin lymphoma but found no association.
“If these findings are confirmed, the next step would be to try to determine if we can modify cytokine levels in some way to make lymphoma prevention more effective in this population,” said Rabkin.
