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Decreased expression of DFF45 /ICAD is correlated with a poor prognosis in patients with esophageal carcinoma
Author(s) -
Konishi Shigeru,
Ishiguro Hideyuki,
Shibata Yasuyuki,
Kudo Junzo,
Terashita Yukio,
Sugiura Hironori,
Koyama Hiroshi,
Kimura Masahiro,
Sato Atsushi,
Shinoda Noriyuki,
Kuwabara Yoshiyuki,
Fujii Yoshitaka
Publication year - 2002
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.10987
Subject(s) - medicine , icad , apoptosis , esophageal cancer , metastasis , messenger rna , carcinoma , pathology , gastroenterology , cancer , biology , biochemistry , gene
BACKGROUND DNA fragmentation factor 45 ( DFF45 )/inhibotor of caspase activated DNAse (ICAD) forms a complex with DFF40/CAD and inhibits its DNA cleaving function during apoptosis. DFF45 also functions as a chaperone for native DFF40 and is necessary for its function. It has been indicated that defects in the apoptotic pathway may exist in neoplastic cells. METHODS The authors investigated mRNA expression of DFF45 in a series of 46 esophageal squamous cell carcinoma (ESCC) specimens using polymerase chain reaction amplification. The results were correlated with the patients' clinicopathologic characteristics. RESULTS DFF45 mRNA expression was significantly lower in tumors with higher pathologic stage, higher tumor status (T status), lymph node metastasis, or more extensive lymphatic invasion. Patients who had low DFF45 mRNA expression (indicated by the ratio of DFF45 mRNA expression in tumor to DFF45 mRNA expression in normal esophageal mucosa [tumor:normal] < 1) had a significantly shorter survival after undergoing surgery compared with patients who had high DFF45 mRNA expression (tumor:normal > 1, P = 0.0006; log‐rank test, P = 0.0003; median follow‐up, 14.6 months). CONCLUSIONS Patients with ESCC with decreased DFF45 mRNA expression levels had a poor prognosis compared with patients who had high DFF45 mRNA expression levels. Cancer 2002;95:2473–8. © 2002 American Cancer Society. DOI 10.1002/cncr.10987