TY - JOUR
T1 - Prognostic relevance of c-MYC gene amplification and polysomy for chromosome 8 in suboptimally-resected, advanced stage epithelial ovarian cancers
T2 - A Gynecologic Oncology Group study
AU - Darcy, Kathleen M.
AU - Brady, William E.
AU - Blancato, Jan K.
AU - Dickson, Robert B.
AU - Hoskins, William J.
AU - McGuire, William P.
AU - Birrer, Michael J.
N1 - Funding Information:
This study was supported by the National Cancer Institute grants of the Gynecologic Oncology Group Administrative Office (CA 27469) and the Gynecologic Oncology Group Statistical and Data Center (CA 37517), and the Intramural Research Program of the National Cancer Institute of the National Institute of Health. The following Gynecologic Oncology Group (GOG) institutions participated in this study: University of Alabama at Birmingham, Abington Memorial Hospital, University of Rochester Medical Center, Walter Reed Army Medical Center, Wayne State University, Colorado Gynecologic Oncology Group P.C., University of California at Los Angeles, University of Pennsylvania Cancer Center, Milton S. Hershey Medical Center, Georgetown University Medical Center, Wake Forest University School of Medicine, University of California Medical Center at Irvine, University of Kentucky, The Cleveland Clinic Foundation, Johns Hopkins Oncology Center, Eastern Pennsylvania Gyn/Onc Center, P.C., Cooper Hospital/University Medical Center, Columbus Cancer Council, University of Massachusetts Medical Center, and University of Oklahoma.
PY - 2009/9
Y1 - 2009/9
N2 - Objective: The Gynecologic Oncology Group (GOG) examined the prognostic relevance of c-MYC amplification and polysomy 8 in epithelial ovarian cancer (EOC). Methods: Women with suboptimally-resected, advanced stage EOC who participated in GOG-111, a multicenter randomized phase III trial of cyclophosphamide + cisplatin vs. paclitaxel + cisplatin, and who provided a tumor block through GOG-9404 were eligible. Fluorescence in situ hybridization (FISH) with probes for c-MYC and the centromere of chromosome 8 (CEP8) was used to examine c-MYC amplification (≥ 2 copies c-MYC/CEP8) and polysomy 8 (≥ 4 CEP8 copies). Results: c-MYC amplification, defined as ≥ 2 copies c-MYC/CEP8, was observed in 29% (28/97) of EOCs and levels were ranged from 2.0-3.3 copies of c-MYC/CEP8. c-MYC amplification was not associated with patient age, race, GOG performance status, stage, cell type, grade, measurable disease status following surgery, tumor response or disease status following platinum-based combination chemotherapy. Women with vs. without c-MYC amplification did not have an increased risk of disease progression (hazard ratio [HR] = 1.03; 95% confidence interval [CI] = 0.65-1.64; p = 0.884) or death (HR = 1.08; 95% CI = 0.68-1.72; p = 0.745). c-MYC amplification was not an independent prognostic factor for progression-free survival (HR = 1.03, 95% CI = 0.57-1.85; p = 0.922) or overall survival (HR = 1.01, 95% CI = 0.56-1.80; p = 0.982). Similar insignificant results were obtained for c-MYC amplification categorized as ≥ 1.5 copies c-MYC/CEP8. Polysomy 8 was observed in 22 patients without c-MYC amplification and 3 with c-MYC amplification, and was associated with age and measurable disease status, but not other clinical covariates or outcomes. Conclusions: c-MYC amplification and polysomy 8 have limited predictive or prognostic value in suboptimally-resected, advanced stage EOC treated with platinum-based combination chemotherapy.
AB - Objective: The Gynecologic Oncology Group (GOG) examined the prognostic relevance of c-MYC amplification and polysomy 8 in epithelial ovarian cancer (EOC). Methods: Women with suboptimally-resected, advanced stage EOC who participated in GOG-111, a multicenter randomized phase III trial of cyclophosphamide + cisplatin vs. paclitaxel + cisplatin, and who provided a tumor block through GOG-9404 were eligible. Fluorescence in situ hybridization (FISH) with probes for c-MYC and the centromere of chromosome 8 (CEP8) was used to examine c-MYC amplification (≥ 2 copies c-MYC/CEP8) and polysomy 8 (≥ 4 CEP8 copies). Results: c-MYC amplification, defined as ≥ 2 copies c-MYC/CEP8, was observed in 29% (28/97) of EOCs and levels were ranged from 2.0-3.3 copies of c-MYC/CEP8. c-MYC amplification was not associated with patient age, race, GOG performance status, stage, cell type, grade, measurable disease status following surgery, tumor response or disease status following platinum-based combination chemotherapy. Women with vs. without c-MYC amplification did not have an increased risk of disease progression (hazard ratio [HR] = 1.03; 95% confidence interval [CI] = 0.65-1.64; p = 0.884) or death (HR = 1.08; 95% CI = 0.68-1.72; p = 0.745). c-MYC amplification was not an independent prognostic factor for progression-free survival (HR = 1.03, 95% CI = 0.57-1.85; p = 0.922) or overall survival (HR = 1.01, 95% CI = 0.56-1.80; p = 0.982). Similar insignificant results were obtained for c-MYC amplification categorized as ≥ 1.5 copies c-MYC/CEP8. Polysomy 8 was observed in 22 patients without c-MYC amplification and 3 with c-MYC amplification, and was associated with age and measurable disease status, but not other clinical covariates or outcomes. Conclusions: c-MYC amplification and polysomy 8 have limited predictive or prognostic value in suboptimally-resected, advanced stage EOC treated with platinum-based combination chemotherapy.
KW - FISH
KW - Gene amplification
KW - Ovarian cancer
KW - Polysomy 8
KW - c-MYC
UR - http://www.scopus.com/inward/record.url?scp=67651225134&partnerID=8YFLogxK
U2 - 10.1016/j.ygyno.2009.05.012
DO - 10.1016/j.ygyno.2009.05.012
M3 - Article
C2 - 19524285
AN - SCOPUS:67651225134
SN - 0090-8258
VL - 114
SP - 472
EP - 479
JO - Gynecologic Oncology
JF - Gynecologic Oncology
IS - 3
ER -