Hutch News Stories

More sexual partners = more prostate cancer

magnified human papilloma virus
Electron micrograph of human papilloma virus magnified 50,000 times. Dr. Janet Stanford, whose recent study found a link between prostate cancer and number of sexual partners, will collaborate with Dr. Denise Galloway on a study to examine an association between HPV status and prostate-cancer risk. SLIDE COURTESY OF GREG WIPF

Risk of prostate cancer - the most frequently diagnosed cancer among men in the United States - increases with the number of lifetime sexual partners, according to recently published Hutch research.

Results of the study, conducted by Public Health Sciences Division investigators Drs. Janet Stanford and Kristine Wicklund with Dr. Karin Rosenblatt of the University of Illinois, support the existence of an infectious component that contributes to risk of disease.

"Studies done in the 1970s indicated an association of sexual factors or sexual history with risk of prostate cancer," said Stanford, who is head of the Hutch's Prostate Cancer Research Program and a professor of epidemiology at the University of Washington.

"Some of the research suggested an increased risk with increasing numbers of sexual partners or early age of first intercourse. But none of these studies considered multiple sexual factors at the same time, while ours did. When we considered all factors together, the number of lifetime sexual partners emerged as an important variable for cancer risk."

The study evaluated 753 King County men aged 40 to 64 who had been diagnosed with prostate cancer between 1993 and 1996 and compared them with 703 age-matched controls. Men were questioned about sexual behavior, medical history, including sexually transmitted diseases, and other demographic factors.

Researchers found an increased risk of prostate cancer in men who had multiple lifetime female sexual partners, with greater than twice the risk in men who had 30 or more partners.

A modest increase in risk was observed in men who had suffered from gonorrheal infections, and non-significant increases in risk were observed with increasing number of sexually transmitted diseases.

Research challenge

The challenge, Stanford said, is to figure out if physiological factors such as male hormone levels, which have been associated with risk of prostate cancer, are correlated with aspects of sexual behavior such as multiple partners or earlier ages of first intercourse.

"We don't fully understand the relationship between a man's androgen profile and his lifetime pattern of sexual behavior," she said. "If men with higher androgen levels also have more sexual partners, our finding of an elevated risk in men with multiple partners could be confounded by hormone status.

"Our study did not measure androgen levels, and even if we had, it may be that the level of androgen during adolescence or early adulthood, some years before the study was conducted, would be more relevant in terms of lifetime sexual behavior."

The observation of an increased prostate cancer risk with increasing number of lifetime sexual partners suggests that an infectious agent may contribute, at least in part, to disease development.

Most human cancers have no known infectious origin. Exceptions include several anogenital cancers, most notably cervical cancer, in which specific strains of human papilloma virus (HPV) are the cause.

Stanford said studies have disagreed on whether or not HPV infection is linked to prostate-cancer incidence. She will collaborate with Dr. Denise Galloway, an investigator in the Human Biology Division, on a study recently funded by the National Institutes of Health to examine the association between HPV status and prostate cancer risk.

Conflicting studies

"Using stored serum that we collected at the time of the study, we'll be looking for antibodies to HPV-16 and HPV-18," Stanford said. "The reason for doing this is that there have been suggestive but conflicting studies on the role of these two types of HPV infection in relation to the occurrence of prostate cancer.

"There have been positive and negative serological studies and pathology studies looking for evidence of the virus in prostate tumor tissue. While the results were variable, there is evidence that HPV may play a role. We think it is important to follow up and find out."

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