Meeting News

Chlamydia infection may double risk for ovarian cancer

Britton Trabert

An antibody present in the blood of women previously infected with chlamydia appeared to double the person’s risk for ovarian cancer, according to a study scheduled for presentation at the American Association for Cancer Research Annual Meeting.

“Ovarian cancer is a relatively rare cancer, but women who get it face poor survival rates,” Britton Trabert, PhD, MS, Earl Stadtman investigator in the division of cancer epidemiology and genetics at NCI, said in a press release. “We need to understand more about what causes ovarian cancer so that we can improve screening and treatment and, ultimately, improve survival.”

Chlamydia is the most commonly reported sexually transmitted bacterial infection in the United States.

“Pelvic inflammatory disease (PID) has been associated with ovarian cancer, and chlamydia infection is the leading cause of PID in the developed world,” Trabert said during a press conference. “Chlamydia infections are often asymptomatic and may persist for several months and/or years and as such, both the ascertainment of prior chlamydia infection and PID is challenging in epidemiological studies.

Trabert and colleagues analyzed data from two studies. One of them, conducted in Poland, included 279 women with ovarian cancer and 556 matched controls. The other, an NCI nested case-control study, included 160 women diagnosed with ovarian cancer during follow-up and 159 matched controls.

The researchers used blood tests to determine the presence of Pgp3 antibodies, an indicator of active or prior chlamydia infection.

In the study conducted in Poland, women with Pgp3 demonstrated an increased risk for ovarian cancer (OR = 1.63, 95% CI 1.2-2.22). When redefining chlamydia positivity at a higher titer, which represents chronic or persistent infection, risk for ovarian cancer increased (cutpoint 2 OR = 2; 95% CI 1.38-2.89; cutpoint 3 OR = 2.19; 95% CI, 1.29-3.73).

Researchers in the NCI study observed similar risk associations:

  • Laboratory cutpoint: OR = 1.43 (95% CI, 0.78-2.63);
  • Cutpoint 2: OR = 2.25 (95% CI, 1.07-4.71); and
  • Cutpoint 3: OR = 2.53 (95% CI, 0.63-10.08).

The presence of antibodies against HPV, herpes simplex virus, hepatitis B and hepatitis C did not appear associated with ovarian cancer risk in either study.

“Serologic markers of prior chlamydia infection were associated with increased ovarian cancer risk in two independent study populations, which lends further support to an association between PID and ovarian cancer,” Trabert said during the conference. “The null associations associated with the other infectious agents we measured further support the specificity of our findings. Replication of the results is necessary and if corroborated, support future study to evaluate the possibility of ovarian cancer risk reduction through treatment of chlamydia and PID.” – by Cassie Homer

 

Reference:

Trabert B, et al. Abstract 4942. Scheduled for presentation at: American Association for Cancer Research Annual Meeting; April 14-18, 2018; Chicago.

 

Disclosure: Trabert reports no relevant financial disclosures. Please see the abstract for all other authors’ relevant financial disclosures.

Britton Trabert

An antibody present in the blood of women previously infected with chlamydia appeared to double the person’s risk for ovarian cancer, according to a study scheduled for presentation at the American Association for Cancer Research Annual Meeting.

“Ovarian cancer is a relatively rare cancer, but women who get it face poor survival rates,” Britton Trabert, PhD, MS, Earl Stadtman investigator in the division of cancer epidemiology and genetics at NCI, said in a press release. “We need to understand more about what causes ovarian cancer so that we can improve screening and treatment and, ultimately, improve survival.”

Chlamydia is the most commonly reported sexually transmitted bacterial infection in the United States.

“Pelvic inflammatory disease (PID) has been associated with ovarian cancer, and chlamydia infection is the leading cause of PID in the developed world,” Trabert said during a press conference. “Chlamydia infections are often asymptomatic and may persist for several months and/or years and as such, both the ascertainment of prior chlamydia infection and PID is challenging in epidemiological studies.

Trabert and colleagues analyzed data from two studies. One of them, conducted in Poland, included 279 women with ovarian cancer and 556 matched controls. The other, an NCI nested case-control study, included 160 women diagnosed with ovarian cancer during follow-up and 159 matched controls.

The researchers used blood tests to determine the presence of Pgp3 antibodies, an indicator of active or prior chlamydia infection.

In the study conducted in Poland, women with Pgp3 demonstrated an increased risk for ovarian cancer (OR = 1.63, 95% CI 1.2-2.22). When redefining chlamydia positivity at a higher titer, which represents chronic or persistent infection, risk for ovarian cancer increased (cutpoint 2 OR = 2; 95% CI 1.38-2.89; cutpoint 3 OR = 2.19; 95% CI, 1.29-3.73).

Researchers in the NCI study observed similar risk associations:

  • Laboratory cutpoint: OR = 1.43 (95% CI, 0.78-2.63);
  • Cutpoint 2: OR = 2.25 (95% CI, 1.07-4.71); and
  • Cutpoint 3: OR = 2.53 (95% CI, 0.63-10.08).

The presence of antibodies against HPV, herpes simplex virus, hepatitis B and hepatitis C did not appear associated with ovarian cancer risk in either study.

“Serologic markers of prior chlamydia infection were associated with increased ovarian cancer risk in two independent study populations, which lends further support to an association between PID and ovarian cancer,” Trabert said during the conference. “The null associations associated with the other infectious agents we measured further support the specificity of our findings. Replication of the results is necessary and if corroborated, support future study to evaluate the possibility of ovarian cancer risk reduction through treatment of chlamydia and PID.” – by Cassie Homer

 

Reference:

Trabert B, et al. Abstract 4942. Scheduled for presentation at: American Association for Cancer Research Annual Meeting; April 14-18, 2018; Chicago.

 

Disclosure: Trabert reports no relevant financial disclosures. Please see the abstract for all other authors’ relevant financial disclosures.

    See more from American Association for Cancer Research Annual Meeting