Antibodies Against Chlamydia trachomatis and Ovarian Cancer Risk in Two Independent Populations
Pelvic inflammatory disease (PID) has been associated with ovarian cancer risk. To clarify the role of Chlamydia trachomatis and other infectious agents in the development of ovarian cancer, we evaluated the association of serologic markers with incident ovarian cancer using a staged approach in two...
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| Vydáno v: | JNCI : Journal of the National Cancer Institute Ročník 111; číslo 2; s. 129 |
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01.02.2019
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| Abstract | Pelvic inflammatory disease (PID) has been associated with ovarian cancer risk. To clarify the role of Chlamydia trachomatis and other infectious agents in the development of ovarian cancer, we evaluated the association of serologic markers with incident ovarian cancer using a staged approach in two independent populations.
Studies included: 1) a case-control study in Poland (244 ovarian cancers/556 control subjects) and 2) a prospective nested case-control study in the PLCO Cancer Screening Trial (160 ovarian cancers/159 control subjects). Associations of serologic marker levels with ovarian cancer risk at diagnostic as well as higher thresholds, identified in Poland and independently evaluated in PLCO, were estimated using multivariable adjusted logistic regression.
In the Polish study, antibodies (based on laboratory cut-point) against the chlamydia plasmid-encoded Pgp3 protein (serological gold standard) were associated with increased ovarian cancer risk (adjusted odds ratio [OR] = 1.63, 95% confidence interval [CI] = 1.20 to 2.22); when a positive result was redefined at higher levels, ovarian cancer risk was increased (cut-point 2: OR = 2.00, 95% CI = 1.38 to 2.89; cut-point 3 [max OR]: OR = 2.19, 95% CI = 1.29 to 3.73). In the prospective PLCO study, Pgp3 antibodies were associated with elevated risk at the laboratory cut-point (OR = 1.43, 95% CI = 0.78 to 2.63) and more stringent cut-points (cut-point 2: OR = 2.25, 95% CI = 1.07 to 4.71); cut-point 3: OR = 2.53, 95% CI = 0.63 to 10.08). In both studies, antibodies against other infectious agents measured were not associated with risk.
In two independent populations, antibodies against prior/current C. trachomatis (Pgp3) were associated with a doubling in ovarian cancer risk, whereas markers of other infectious agents were unrelated. These findings lend support for an association between PID and ovarian cancer. |
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| AbstractList | Pelvic inflammatory disease (PID) has been associated with ovarian cancer risk. To clarify the role of Chlamydia trachomatis and other infectious agents in the development of ovarian cancer, we evaluated the association of serologic markers with incident ovarian cancer using a staged approach in two independent populations.
Studies included: 1) a case-control study in Poland (244 ovarian cancers/556 control subjects) and 2) a prospective nested case-control study in the PLCO Cancer Screening Trial (160 ovarian cancers/159 control subjects). Associations of serologic marker levels with ovarian cancer risk at diagnostic as well as higher thresholds, identified in Poland and independently evaluated in PLCO, were estimated using multivariable adjusted logistic regression.
In the Polish study, antibodies (based on laboratory cut-point) against the chlamydia plasmid-encoded Pgp3 protein (serological gold standard) were associated with increased ovarian cancer risk (adjusted odds ratio [OR] = 1.63, 95% confidence interval [CI] = 1.20 to 2.22); when a positive result was redefined at higher levels, ovarian cancer risk was increased (cut-point 2: OR = 2.00, 95% CI = 1.38 to 2.89; cut-point 3 [max OR]: OR = 2.19, 95% CI = 1.29 to 3.73). In the prospective PLCO study, Pgp3 antibodies were associated with elevated risk at the laboratory cut-point (OR = 1.43, 95% CI = 0.78 to 2.63) and more stringent cut-points (cut-point 2: OR = 2.25, 95% CI = 1.07 to 4.71); cut-point 3: OR = 2.53, 95% CI = 0.63 to 10.08). In both studies, antibodies against other infectious agents measured were not associated with risk.
In two independent populations, antibodies against prior/current C. trachomatis (Pgp3) were associated with a doubling in ovarian cancer risk, whereas markers of other infectious agents were unrelated. These findings lend support for an association between PID and ovarian cancer. Pelvic inflammatory disease (PID) has been associated with ovarian cancer risk. To clarify the role of Chlamydia trachomatis and other infectious agents in the development of ovarian cancer, we evaluated the association of serologic markers with incident ovarian cancer using a staged approach in two independent populations.BACKGROUNDPelvic inflammatory disease (PID) has been associated with ovarian cancer risk. To clarify the role of Chlamydia trachomatis and other infectious agents in the development of ovarian cancer, we evaluated the association of serologic markers with incident ovarian cancer using a staged approach in two independent populations.Studies included: 1) a case-control study in Poland (244 ovarian cancers/556 control subjects) and 2) a prospective nested case-control study in the PLCO Cancer Screening Trial (160 ovarian cancers/159 control subjects). Associations of serologic marker levels with ovarian cancer risk at diagnostic as well as higher thresholds, identified in Poland and independently evaluated in PLCO, were estimated using multivariable adjusted logistic regression.METHODSStudies included: 1) a case-control study in Poland (244 ovarian cancers/556 control subjects) and 2) a prospective nested case-control study in the PLCO Cancer Screening Trial (160 ovarian cancers/159 control subjects). Associations of serologic marker levels with ovarian cancer risk at diagnostic as well as higher thresholds, identified in Poland and independently evaluated in PLCO, were estimated using multivariable adjusted logistic regression.In the Polish study, antibodies (based on laboratory cut-point) against the chlamydia plasmid-encoded Pgp3 protein (serological gold standard) were associated with increased ovarian cancer risk (adjusted odds ratio [OR] = 1.63, 95% confidence interval [CI] = 1.20 to 2.22); when a positive result was redefined at higher levels, ovarian cancer risk was increased (cut-point 2: OR = 2.00, 95% CI = 1.38 to 2.89; cut-point 3 [max OR]: OR = 2.19, 95% CI = 1.29 to 3.73). In the prospective PLCO study, Pgp3 antibodies were associated with elevated risk at the laboratory cut-point (OR = 1.43, 95% CI = 0.78 to 2.63) and more stringent cut-points (cut-point 2: OR = 2.25, 95% CI = 1.07 to 4.71); cut-point 3: OR = 2.53, 95% CI = 0.63 to 10.08). In both studies, antibodies against other infectious agents measured were not associated with risk.RESULTSIn the Polish study, antibodies (based on laboratory cut-point) against the chlamydia plasmid-encoded Pgp3 protein (serological gold standard) were associated with increased ovarian cancer risk (adjusted odds ratio [OR] = 1.63, 95% confidence interval [CI] = 1.20 to 2.22); when a positive result was redefined at higher levels, ovarian cancer risk was increased (cut-point 2: OR = 2.00, 95% CI = 1.38 to 2.89; cut-point 3 [max OR]: OR = 2.19, 95% CI = 1.29 to 3.73). In the prospective PLCO study, Pgp3 antibodies were associated with elevated risk at the laboratory cut-point (OR = 1.43, 95% CI = 0.78 to 2.63) and more stringent cut-points (cut-point 2: OR = 2.25, 95% CI = 1.07 to 4.71); cut-point 3: OR = 2.53, 95% CI = 0.63 to 10.08). In both studies, antibodies against other infectious agents measured were not associated with risk.In two independent populations, antibodies against prior/current C. trachomatis (Pgp3) were associated with a doubling in ovarian cancer risk, whereas markers of other infectious agents were unrelated. These findings lend support for an association between PID and ovarian cancer.CONCLUSIONSIn two independent populations, antibodies against prior/current C. trachomatis (Pgp3) were associated with a doubling in ovarian cancer risk, whereas markers of other infectious agents were unrelated. These findings lend support for an association between PID and ovarian cancer. |
| Author | Pawlita, Michael Hufnagel, Katrin Brinton, Louise A Brenner, Nicole Sherman, Mark E Coburn, Sally B Waterboer, Tim Wentzensen, Nicolas Inturrisi, Federica Lissowska, Jolanta Mentzer, Alexander Peplonska, Beata Wills, Gillian S Idahl, Annika Butt, Julia Hartge, Patricia Woodhall, Sarah C Trabert, Britton |
| Author_xml | – sequence: 1 givenname: Britton surname: Trabert fullname: Trabert, Britton organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD – sequence: 2 givenname: Tim surname: Waterboer fullname: Waterboer, Tim organization: Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany – sequence: 3 givenname: Annika surname: Idahl fullname: Idahl, Annika organization: Department of Clinical Science, Obstetrics and Gynecology, Umeå University, Umeå, Sweden – sequence: 4 givenname: Nicole surname: Brenner fullname: Brenner, Nicole organization: Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany – sequence: 5 givenname: Louise A surname: Brinton fullname: Brinton, Louise A organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD – sequence: 6 givenname: Julia surname: Butt fullname: Butt, Julia organization: Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany – sequence: 7 givenname: Sally B surname: Coburn fullname: Coburn, Sally B organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD – sequence: 8 givenname: Patricia surname: Hartge fullname: Hartge, Patricia organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD – sequence: 9 givenname: Katrin surname: Hufnagel fullname: Hufnagel, Katrin organization: Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany – sequence: 10 givenname: Federica surname: Inturrisi fullname: Inturrisi, Federica organization: Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany – sequence: 11 givenname: Jolanta surname: Lissowska fullname: Lissowska, Jolanta organization: Department of Epidemiology and Cancer Prevention, Cancer Center and M. Sklodowska-Curie Institute of Oncology, Warsaw, Poland – sequence: 12 givenname: Alexander surname: Mentzer fullname: Mentzer, Alexander organization: Wellcome Centre for Human Genetics, Oxford, UK – sequence: 13 givenname: Beata surname: Peplonska fullname: Peplonska, Beata organization: Department of Environmental Epidemiology, Nofer Institute of Occupational Medicine, Lodz, Poland – sequence: 14 givenname: Mark E surname: Sherman fullname: Sherman, Mark E organization: Department of Pulmonary Medicine, Mayo Clinic, Jacksonville, FL – sequence: 15 givenname: Gillian S surname: Wills fullname: Wills, Gillian S organization: Jefferiss Research Trust Laboratories, Imperial College London, St Mary's Campus, London, UK – sequence: 16 givenname: Sarah C surname: Woodhall fullname: Woodhall, Sarah C organization: Gloucestershire Hospitals NHS Foundation Trust, Cheltenham, UK – sequence: 17 givenname: Michael surname: Pawlita fullname: Pawlita, Michael organization: Molecular Diagnostics of Oncogenic Infections Division, German Cancer Research Center (DKFZ), Heidelberg, Germany – sequence: 18 givenname: Nicolas surname: Wentzensen fullname: Wentzensen, Nicolas organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD |
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| SubjectTerms | Adult Aged Antibodies, Bacterial - blood Antibodies, Bacterial - immunology Antigens, Bacterial - immunology Bacterial Proteins - immunology Case-Control Studies Chlamydia Infections - complications Chlamydia Infections - immunology Chlamydia trachomatis - immunology Female Follow-Up Studies Humans Middle Aged Ovarian Neoplasms - epidemiology Ovarian Neoplasms - etiology Ovarian Neoplasms - pathology Poland - epidemiology Prognosis Prospective Studies Risk Factors United States - epidemiology Young Adult |
| Title | Antibodies Against Chlamydia trachomatis and Ovarian Cancer Risk in Two Independent Populations |
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