Cyclin D1 is a possible predictor of sensitivity to chemoradiotherapy for esophageal squamous cell carcinoma.
BACKGROUND
Chemoradiotherapy is currently performed on patients with advanced esophageal squamous cell carcinoma (SCC). The preoperative administration revealed that the patients who responded well to chemoradiotherapy had favorable outcomes, whereas the poor responders conversely resulted in worse prognosis. The aim of this study was to identify molecular markers predicting sensitivity to chemoradiotherapy prior to this treatment.


METHODS
Our clinical protocol for chemoradiotherapy for esophageal SCC were enrolled in 34 patients comprising 20 patients who underwent surgery after neoadjuvant chemoradiotherapy and 14 patients who were treated chemoradiotherapy without surgery. The expressions of cyclin D1, p53 and Ki-67 were investigated immunohistochemically in biopsy specimens obtained before the treatment from all 34 patients. The immunoreactivities were compared with responsiveness to chemoradiotherapy as evaluated by macroscopic or microscopic method.


RESULTS
The mean rate of primary tumor reduction as estimated by esophagography was 75.3% in the cyclin D1 negative group whereas 42.7% reduction rate was observed in the cyclin D1 positive group. The difference in the reduction rate between cyclin D1 positive and negative groups was statistically significant (p = 0.0025). The immunoreactivities of p53 and Ki-67 did not show a significant correlation with responsiveness to chemoradiotherapy. In neoadjuvant group, patients with cyclin D1-positive tumors showed significantly worse overall survival than patients with cyclin D1-negative tumors (p = 0.0380).


CONCLUSIONS
Among 34 patients with esophageal SCC, differences in the responsiveness to chemoradiotherapy were correlated with cyclin D1 immunoreactivity assessed in the biopsy specimens. Thus the cyclin D1 protein may be a useful predictor of sensitivity to concurrent chemoradiotherapy for esophageal SCC.
Samejima
R
R
Department of Surgery, Saga Medical School, Japan.
Kitajima
Y
Y
Yunotani
S
S
Miyazaki
K
K
D000328:Adult; D000368:Aged; D014408:Biomarkers, Tumor / Q000096:biosynthesis* / Q000276:immunology; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy / Q000378:metabolism* / Q000532:radiotherapy / Q000601:surgery; D003131:Combined Modality Therapy; D019938:Cyclin D1 / Q000096:biosynthesis* / Q000276:immunology; D004938:Esophageal Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000532:radiotherapy / Q000601:surgery; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D016019:Survival Analysis; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
D014408:Biomarkers, Tumor; D019394:Ki-67 Antigen; D016159:Tumor Suppressor Protein p53; D019938:Cyclin D1