Megan E Buechel1, Danielle Enserro2, Robert A Burger3, Mark F Brady4, Katrina Wade5, Angeles Alvarez Secord6, Andrew B Nixon7, Seyedehnafiseh Mirniaharikandehei8, Hong Liu9, Bin Zheng10, David M O'Malley11, Heidi Gray12, Krishnansu S Tewari13, Robert S Mannel14, Michael J Birrer15, Kathleen N Moore16. 1. Stephenson Cancer Center, The University of Oklahoma Health Sciences Center, Section of Gynecologic Oncology, Oklahoma City, OK, United States of America. Electronic address: MEBuechel@gmail.com. 2. NRG Oncology SDMC, CTD Division, Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States of America. Electronic address: enserrod@nrgoncology.org. 3. University of Pennsylvania, Philadelphia, PA, United States of America. Electronic address: Robert.Burger@uphs.upenn.edu. 4. NRG Oncology SDMC, CTD Division, Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States of America. Electronic address: bradym@nrgoncology.org. 5. Oschner Medical Center, New Orleans, LA, United States of America. Electronic address: katrina.wade@ochsner.org. 6. Duke University, Division of Gynecologic Oncology, Durham, NC, United States of America. Electronic address: angeles.secord@duke.edu. 7. Duke University, Division of Medical Oncology, Durham, NC, United States of America. Electronic address: anixon@duke.edu. 8. University of Oklahoma, Department of Electrical and Computer Engineering, Norman, OK, United States of America. Electronic address: snmirna@ou.edu. 9. University of Oklahoma, Department of Electrical and Computer Engineering, Norman, OK, United States of America. Electronic address: liu@ou.edu. 10. University of Oklahoma, Department of Electrical and Computer Engineering, Norman, OK, United States of America. Electronic address: bin.zheng-1@ou.edu. 11. James Cancer Center at the Ohio State University, Columbus, OH, United States of America. Electronic address: omalley.46@osu.edu. 12. University of Washington, Seattle, WA, United States of America. Electronic address: hgray@uw.edu. 13. University of California, Irvine, CA, , United States of America. Electronic address: ktewari@uci.edu. 14. Stephenson Cancer Center, The University of Oklahoma Health Sciences Center, Section of Gynecologic Oncology, Oklahoma City, OK, United States of America. Electronic address: Robert-Mannel@ouhsc.edu. 15. University of Alabama, Birmingham, AL, United States of America. Electronic address: mbirrer@uabmc.edu. 16. Stephenson Cancer Center, The University of Oklahoma Health Sciences Center, Section of Gynecologic Oncology, Oklahoma City, OK, United States of America. Electronic address: Kathleen-Moore@ouhsc.edu.
Abstract
PURPOSE: Increasing measures of adiposity have been correlated with poor oncologic outcomes and a lack of response to anti-angiogenic therapies. Limited data exists on the impact of subcutaneous fat density (SFD) and visceral fat density (VFD) on oncologic outcomes. This ancillary analysis of GOG-218, evaluates whether imaging markers of adiposity were predictive biomarkers for bevacizumab (bev) use in epithelial ovarian cancer (EOC). PATIENTS AND METHODS: There were 1249 patients (67%) from GOG-218 with imaging measurements. SFD and VFD were calculated utilizing Hounsfield units (HU). Proportional hazards models were used to assess the association between SFD and VFD with overall survival (OS). RESULTS: Increased SFD and VFD showed an increased HR for death (HR per 1-SD increase 1.12, 95% CI:1.05-1.19 p = 0.0009 and 1.13, 95% CI: 1.05-1.20 p = 0.0006 respectively). In the predictive analysis for response to bev, high VFD showed an increased hazard for death in the placebo group (HR per 1-SD increase 1.22, 95% CI: 1.09-1.37; p = 0.025). However, in the bev group there was no effect seen (HR per 1-SD increase: 1.01, 95% CI: 0.90-1.14) Median OS was 45 vs 47 months in the VFD low groups and 36 vs 42 months in the VFD high groups on placebo versus bev, respectively. CONCLUSION: High VFD and SFD have a negative prognostic impact on patients with EOC. High VFD appears to be a predictive marker of bev response and patients with high VFD may be more likely to benefit from initial treatment with bev.
PURPOSE: Increasing measures of adiposity have been correlated with poor oncologic outcomes and a lack of response to anti-angiogenic therapies. Limited data exists on the impact of subcutaneous fat density (SFD) and visceral fat density (VFD) on oncologic outcomes. This ancillary analysis of GOG-218, evaluates whether imaging markers of adiposity were predictive biomarkers for bevacizumab (bev) use in epithelial ovarian cancer (EOC). PATIENTS AND METHODS: There were 1249 patients (67%) from GOG-218 with imaging measurements. SFD and VFD were calculated utilizing Hounsfield units (HU). Proportional hazards models were used to assess the association between SFD and VFD with overall survival (OS). RESULTS: Increased SFD and VFD showed an increased HR for death (HR per 1-SD increase 1.12, 95% CI:1.05-1.19 p = 0.0009 and 1.13, 95% CI: 1.05-1.20 p = 0.0006 respectively). In the predictive analysis for response to bev, high VFD showed an increased hazard for death in the placebo group (HR per 1-SD increase 1.22, 95% CI: 1.09-1.37; p = 0.025). However, in the bev group there was no effect seen (HR per 1-SD increase: 1.01, 95% CI: 0.90-1.14) Median OS was 45 vs 47 months in the VFD low groups and 36 vs 42 months in the VFD high groups on placebo versus bev, respectively. CONCLUSION: High VFD and SFD have a negative prognostic impact on patients with EOC. High VFD appears to be a predictive marker of bev response and patients with high VFD may be more likely to benefit from initial treatment with bev.
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