FROM THE AACR ANNUAL MEETING

Pelvic inflammatory disease caused by chlamydia appears to significantly increase the risk of ovarian cancer, according to research to be presented at the annual meeting of the American Association for Cancer Research.

The finding, replicated in two large databases, suggests that promptly treating the infection might reduce the lifetime risk of developing ovarian cancer, Britton Trabert, PhD , said during a press briefing held in advance of the meeting.

“Although these findings need to be replicated, they suggest potential ovarian cancer risk reduction through targeted treatment of chlamydia infections,” said Dr. Trabert, the Earl Stadtman Investigator at the National Cancer Institute.

The study portends both promise and challenge, according to Elaine R. Mardis, PhD , who comoderated the session.

“Ovarian cancer is typically diagnosed at a late stage and therefore has a poor prognosis,” said Dr. Mardis of The Nationwide Hospital, Columbus, Ohio. “Chlamydia will be an important point of study here, both because of the frequency of this infection, and because it is quite difficult to detect, due to its asymptomatic nature. But the most important take-home point is that we might be able to go a long way in terms of preventing ovarian cancer by routinely screening for infective agents.”

Pelvic inflammatory disease is known to be associated with ovarian cancer, and chlamydia is a leading cause of the disease, noted Dr. Trabert. “But chlamydia infections can be asymptomatic and persist for months or even years, so ascertainment of past chlamydia infections is challenging.”

To investigate the potential link between these infections and ovarian cancer, Dr. Trabert and her colleagues examined associations between antibodies to several infectious agents, including chlamydia, in two large ovarian cancer databases: a population-based case/control study in Poland and a case-control study nested into the U.S. Prostate, Lung, Colorectal, and Ovarian ( PLCO ) Cancer Screening Trial.

The researchers screened for antibodies to chlamydia, Mycoplasma genitalium, Epstein-Barre virus, human papillomavirus, herpes simplex virus-1 and -2, polyomavirus, hepatitis B and C, and cytomegalovirus. The chlamydia antibody selected was plasmid-encoded Pgp3 protein, considered the gold standard measurement for prior or existing chlamydia infections.

The patient cohorts comprised 278 cases vs. 556 controls from the Polish study, and 160 cases vs. 159 controls from the PLCO study. Serum samples were collected at the time of ovarian cancer diagnosis in the Polish cohort, and before diagnosis in the PLCO cohort.

Dr. Trabert presented odds ratios for a Pgp3 antibody titer cut point indicative of past chlamydia infection, and a “more stringent” higher cut point indicative of current or chronic infection. She and her colleagues found statistically significant associations for each cut point in both studies.

In the Polish cohort, the lower Pgp3 cut point was associated with a 63% increased risk of ovarian cancer (odds ratio, 1.63). The higher cut point was associated with a doubling of risk (OR, 2.0).

In the PLCO cohort, the lower cut point was associated with a 43% increased risk (OR, 1.43). The higher cut point more than doubled the risk of ovarian cancer (OR, 2.25).

Neither cohort showed any significant association of ovarian cancer with any of the other antibodies, Dr. Trabert said.

The NCI Intramural Research Program supported the study. Dr. Trabert and her colleagues declared no conflicts of interest.

msullivan@frontlinemedcom.com

SOURCE: Trabert et al. Abstract 4942.

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