Details

Autor(en) / Beteiligte

• FARLEY, John
• SMITH, Leia M
• DARCY, Kathleen M
• SOBEL, Eugene
• O'CONNOR, Dennis
• HENDERSON, Benita
• MORRISON, Larry E
• BIRRER, Michael J

Titel

Cyclin E expression is a significant predictor of survival in advanced, suboptimally debulked ovarian epithelial cancers: A Gynecologic Oncology Group study

Ist Teil von

• Cancer research (Chicago, Ill.), 2003-03, Vol.63 (6), p.1235-1241

Ort / Verlag

Philadelphia, PA: American Association for Cancer Research

Erscheinungsjahr

2003

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• Cyclin E is a key regulator of the G(1)-S transition. Abnormalities in cyclin E expression have been related to survival in a variety of cancers. This study evaluated the prognostic relevance of cyclin E in human ovarian cancer. Immunohistochemical expression of cyclin E was evaluated in 139 advanced, suboptimally debulked epithelial ovarian cancer specimens from patients treated on Gynecologic Oncology Group protocol 111. High cyclin E protein expression (> or =40% cyclin E positive tumor cells) was seen in 62 (45%) of the advanced, suboptimally debulked ovarian cancer patients. Expression of cyclin E was not associated with age, race, stage, grade, cell type, or amount of residual disease. High verses low cyclin E expression was associated with a shorter median survival (29 +/- 2 versus 35 +/- 3 months) and worse overall survival (P < 0.05). Univariate and multivariate regression analyses revealed that high relative to low cyclin E was associated with a 40-50% increase in the risk of death (hazard rate, P < or = 0.05). Fluorescence in situ hybridization was used in a subset of 20 cases to examine cyclin E gene amplification. Eight of 10 cases with high cyclin E expression exhibited amplification of the cyclin E gene, whereas only 1 of 10 cases with low expression displayed gene amplification (P < 0.006). High cyclin E expression was an independent poor prognostic factor for patients with advanced ovarian cancer, and it was associated with amplification of the cyclin E gene.