TY - JOUR
T1 - Lifestyle and personal factors associated with having macroscopic residual disease after ovarian cancer primary cytoreductive surgery
AU - on behalf of the Ovarian Cancer Association Consortium
AU - Phung, Minh Tung
AU - Webb, Penelope M.
AU - DeFazio, Anna
AU - Fereday, Sian
AU - Lee, Alice W.
AU - Bowtell, David D.L.
AU - Fasching, Peter A.
AU - Goode, Ellen L.
AU - Goodman, Marc T.
AU - Karlan, Beth Y.
AU - Lester, Jenny
AU - Matsuo, Keitaro
AU - Modugno, Francesmary
AU - Brenton, James D.
AU - Van Gorp, Toon
AU - Pharoah, Paul D.P.
AU - Schildkraut, Joellen M.
AU - McLean, Karen
AU - Meza, Rafael
AU - Mukherjee, Bhramar
AU - Richardson, Jean
AU - Grout, Bronwyn
AU - Chase, Anne
AU - McKinnon Deurloo, Cindy
AU - Terry, Kathryn L.
AU - Hanley, Gillian E.
AU - Pike, Malcolm C.
AU - Berchuck, Andrew
AU - Ramus, Susan J.
AU - Pearce, Celeste Leigh
N1 - Funding Information:
We are grateful to the family and friends of Kathryn Sladek Smith for their generous support of the Ovarian Cancer Association Consortium through their donations to the Ovarian Cancer Research Fund. We thank the study participants, doctors, nurses, clinical and scientific collaborators, health care providers and health information sources who have contributed to the many studies contributing to this manuscript.
Funding Information:
TVG is a Senior Clinical Investigator of the Fund for Scientific Research-Flanders (FWO Vlaanderen 18B2921N ). SJR is supported by National Health and Medical Research Council of Australia (NHMRC) grant APP2009840 . PMW is supported by NHMRC GNT1173346 . MCP was supported in part through the NIH/NCI Support Grant P30 CA008748 to Memorial Sloan Kettering Cancer Center. CLP was supported in part by P30 CA046592. MCP, CLP and MTP were supported in part by W81XWH-16-2-0010. The contents of the published material are solely the responsibility of the authors and do not reflect the views of NHMRC, NIH and other funders.
Funding Information:
Funding for individual studies: AUS: The Australian Ovarian Cancer Study (AOCS) was supported by the U.S. Army Medical Research and Materiel Command ( DAMD17-01-1-0729 ), National Health & Medical Research Council of Australia ( 199600 , 400413 and 400281 ), Cancer Councils of New South Wales , Victoria, Queensland, South Australia and Tasmania and Cancer Foundation of Western Australia (Multi-State Applications 191, 211 and 182). AOCS gratefully acknowledges additional support from Ovarian Cancer Australia and the Peter MacCallum Foundation ; HAW: U.S. National Institutes of Health ( R01-CA58598 , N01-CN-55424 and N01-PC-67001 ); HOP: University of Pittsburgh School of Medicine Dean's Faculty Advancement Award (F. Modugno), Department of Defense ( DAMD17-02-1-0669 ) and NCI ( K07-CA080668 , R01-CA95023 , P50-CA159981 MO1-RR000056 R01-CA126841 ); LAX: American Cancer Society Early Detection Professorship ( SIOP-06-258-01-COUN ) and the National Center for Advancing Translational Sciences (NCATS), Grant UL1TR000124 ; MAYO: National Institutes of Health ( R01-CA122443 , P30-CA15083 , P50-CA136393 ); Mayo Foundation ; Minnesota Ovarian Cancer Alliance ; Fred C. and Katherine B. Andersen Foundation ; Fraternal Order of Eagles ; NEC: National Institutes of Health R01-CA54419 and P50-CA105009 and Department of Defense W81XWH-10-1-02802 ; OPL: National Health and Medical Research Council (NHMRC) of Australia ( GNT1025142 , GNT1120431 ).
Funding Information:
The Ovarian Cancer Association Consortium is supported by a grant from the Ovarian Cancer Research Fund thanks to donations by the family and friends of Kathryn Sladek Smith (PPD/RPCI.07). The scientific development and funding for this project were in part supported by the US National Cancer Institute GAME-ON Post-GWAS Initiative (U19-CA148112). This study made use of data generated by the Wellcome Trust Case Control consortium that was funded by the Wellcome Trust under award 076113. The results published here are in part based upon data generated by The Cancer Genome Atlas Pilot Project established by the National Cancer Institute and National Human Genome Research Institute (dbGap accession number phs000178.v8.p7).Funding for individual studies: AUS: The Australian Ovarian Cancer Study (AOCS) was supported by the U.S. Army Medical Research and Materiel Command (DAMD17-01-1-0729), National Health & Medical Research Council of Australia (199600, 400413 and 400281), Cancer Councils of New South Wales, Victoria, Queensland, South Australia and Tasmania and Cancer Foundation of Western Australia (Multi-State Applications 191, 211 and 182). AOCS gratefully acknowledges additional support from Ovarian Cancer Australia and the Peter MacCallum Foundation; HAW: U.S. National Institutes of Health (R01-CA58598, N01-CN-55424 and N01-PC-67001); HOP: University of Pittsburgh School of Medicine Dean's Faculty Advancement Award (F. Modugno), Department of Defense (DAMD17-02-1-0669) and NCI (K07-CA080668, R01-CA95023, P50-CA159981 MO1-RR000056 R01-CA126841); LAX: American Cancer Society Early Detection Professorship (SIOP-06-258-01-COUN) and the National Center for Advancing Translational Sciences (NCATS), Grant UL1TR000124; MAYO: National Institutes of Health (R01-CA122443, P30-CA15083, P50-CA136393); Mayo Foundation; Minnesota Ovarian Cancer Alliance; Fred C. and Katherine B. Andersen Foundation; Fraternal Order of Eagles; NEC: National Institutes of Health R01-CA54419 and P50-CA105009 and Department of Defense W81XWH-10-1-02802; OPL: National Health and Medical Research Council (NHMRC) of Australia (GNT1025142, GNT1120431).TVG is a Senior Clinical Investigator of the Fund for Scientific Research-Flanders (FWO Vlaanderen 18B2921N). SJR is supported by National Health and Medical Research Council of Australia (NHMRC) grant APP2009840. PMW is supported by NHMRC GNT1173346. MCP was supported in part through the NIH/NCI Support Grant P30 CA008748 to Memorial Sloan Kettering Cancer Center. CLP was supported in part by P30 CA046592. MCP, CLP and MTP were supported in part by W81XWH-16-2-0010. The contents of the published material are solely the responsibility of the authors and do not reflect the views of NHMRC, NIH and other funders.
Funding Information:
The Ovarian Cancer Association Consortium is supported by a grant from the Ovarian Cancer Research Fund thanks to donations by the family and friends of Kathryn Sladek Smith ( PPD/RPCI.07 ). The scientific development and funding for this project were in part supported by the US National Cancer Institute GAME-ON Post-GWAS Initiative ( U19-CA148112 ). This study made use of data generated by the Wellcome Trust Case Control consortium that was funded by the Wellcome Trust under award 076113 . The results published here are in part based upon data generated by The Cancer Genome Atlas Pilot Project established by the National Cancer Institute and National Human Genome Research Institute (dbGap accession number phs000178.v8.p7).
Publisher Copyright:
© 2022 Elsevier Inc.
PY - 2023/1
Y1 - 2023/1
N2 - Objective: The presence of macroscopic residual disease after primary cytoreductive surgery (PCS) is an important factor influencing survival for patients with high-grade serous ovarian cancer (HGSC). More research is needed to identify factors associated with having macroscopic residual disease. We analyzed 12 lifestyle and personal exposures known to be related to ovarian cancer risk or inflammation to identify those associated with having residual disease after surgery. Methods: This analysis used data on 2054 patients with advanced stage HGSC from the Ovarian Cancer Association Consortium. The exposures were body mass index, breastfeeding, oral contraceptive use, depot-medroxyprogesterone acetate use, endometriosis, first-degree family history of ovarian cancer, incomplete pregnancy, menopausal hormone therapy use, menopausal status, parity, smoking, and tubal ligation. Logistic regression models were fit to assess the association between these exposures and having residual disease following PCS. Results: Menopausal estrogen-only therapy (ET) use was associated with 33% lower odds of having macroscopic residual disease compared to never use (OR = 0.67, 95%CI 0.46–0.97, p = 0.033). Compared to nulliparous women, parous women who did not breastfeed had 36% lower odds of having residual disease (OR = 0.64, 95%CI 0.43–0.94, p = 0.022), while there was no association among parous women who breastfed (OR = 0.90, 95%CI 0.65–1.25, p = 0.53). Conclusions: The association between ET and having no macroscopic residual disease is plausible given a strong underlying biologic hypothesis between this exposure and diagnosis with HGSC. If this or the parity finding is replicated, these factors could be included in risk stratification models to determine whether HGSC patients should receive PCS or neoadjuvant chemotherapy.
AB - Objective: The presence of macroscopic residual disease after primary cytoreductive surgery (PCS) is an important factor influencing survival for patients with high-grade serous ovarian cancer (HGSC). More research is needed to identify factors associated with having macroscopic residual disease. We analyzed 12 lifestyle and personal exposures known to be related to ovarian cancer risk or inflammation to identify those associated with having residual disease after surgery. Methods: This analysis used data on 2054 patients with advanced stage HGSC from the Ovarian Cancer Association Consortium. The exposures were body mass index, breastfeeding, oral contraceptive use, depot-medroxyprogesterone acetate use, endometriosis, first-degree family history of ovarian cancer, incomplete pregnancy, menopausal hormone therapy use, menopausal status, parity, smoking, and tubal ligation. Logistic regression models were fit to assess the association between these exposures and having residual disease following PCS. Results: Menopausal estrogen-only therapy (ET) use was associated with 33% lower odds of having macroscopic residual disease compared to never use (OR = 0.67, 95%CI 0.46–0.97, p = 0.033). Compared to nulliparous women, parous women who did not breastfeed had 36% lower odds of having residual disease (OR = 0.64, 95%CI 0.43–0.94, p = 0.022), while there was no association among parous women who breastfed (OR = 0.90, 95%CI 0.65–1.25, p = 0.53). Conclusions: The association between ET and having no macroscopic residual disease is plausible given a strong underlying biologic hypothesis between this exposure and diagnosis with HGSC. If this or the parity finding is replicated, these factors could be included in risk stratification models to determine whether HGSC patients should receive PCS or neoadjuvant chemotherapy.
KW - Lifestyle
KW - Ovarian cancer
KW - Primary cytoreductive surgery
KW - Residual disease
UR - http://www.scopus.com/inward/record.url?scp=85141998158&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85141998158&partnerID=8YFLogxK
U2 - 10.1016/j.ygyno.2022.10.018
DO - 10.1016/j.ygyno.2022.10.018
M3 - Article
C2 - 36401943
AN - SCOPUS:85141998158
SN - 0090-8258
VL - 168
SP - 68
EP - 75
JO - Gynecologic oncology
JF - Gynecologic oncology
ER -