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Prognostic significance of cyclin D1 in esophageal squamous cell carcinoma patients treated with surgery alone or combined therapy modalities
Author(s) -
Sarbia Mario,
Stahl Michael,
Fink Ulrich,
Heep Hansjörg,
Dutkowski Philipp,
Willers Rainhart,
Seeber Siegfried,
Gabbert Helmut E.
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990219)84:1<86::aid-ijc16>3.0.co;2-7
Subject(s) - esophagus , medicine , cyclin d1 , carcinoma , esophageal cancer , immunohistochemistry , chemotherapy , cancer , oncology , univariate analysis , gastroenterology , pathology , multivariate analysis , cell cycle
In the present study, the expression of cyclin D1, as detected by immunohistochemistry, was compared with other prognostic variables and its prognostic impact was evaluated in a group of 172 patients with squamous cell carcinoma (SCC) of the esophagus who underwent potentially curative resection therapy and in a second group of 38 patients with SCC of the esophagus who were treated by combined modality therapy (radiochemotherapy ± surgery). Expression of cyclin D1 in surgically treated carcinomas correlated negatively with tumor differentiation ( p = 0.026) but positively with mitotic activity ( p = 0.0199) and nodal status ( p = 0.040). There were no significant correlations with pT category. Patients with cyclin D1‐positive carcinomas showed significantly worse overall survival than patients with cyclin D1‐negative carcinomas, both in univariate ( p = 0.0016) and in multivariate survival analyses ( p = 0.0038). Expression of cyclin D1 in carcinomas with multimodal treatment was correlated with poor response to chemotherapy ( p = 0.026) but not with overall survival. We thus consider expression of cyclin D1 to be an important parameter, predicting an unfavorable overall survival of surgically treated esophageal cancer patients. Int. J. Cancer (Pred. Oncol.) 84:86–91, 1999. © 1999 Wiley‐Liss, Inc.