1. Infrequent Inactivation ofDCCGene in Replication Error-Positive Colorectal Cancers
- Author
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Fumio Itoh, Masanobu Kusano, Kohzoh Imai, Yuji Hinoda, Yukinari Yoshida, and Hiroyuki Yamamoto
- Subjects
endocrine system ,Deleted in Colorectal Cancer ,Biophysics ,Loss of Heterozygosity ,Locus (genetics) ,Biology ,medicine.disease_cause ,Polymerase Chain Reaction ,Biochemistry ,Metastasis ,Genotype-phenotype distinction ,medicine ,Humans ,RNA, Messenger ,RNA, Neoplasm ,Molecular Biology ,Gene ,Neoplasm Staging ,Sequence Deletion ,Genetics ,fungi ,nutritional and metabolic diseases ,Replication Error ,Cell Biology ,Reference Standards ,medicine.disease ,Gene Expression Regulation, Neoplastic ,Genes, DCC ,DNA Transposable Elements ,Cancer research ,Colorectal Neoplasms ,Carcinogenesis ,human activities ,Allelic loss ,Microsatellite Repeats - Abstract
Colorectal cancers with and without the replication error (RER) exhibit fundamental differences in genotype and phenotype. While alterations in APC, p53 , and K-ras genes have been characterized between RER+ and RER− colorectal cancers, the status of deleted in colorectal carcinomas (DCC) gene has not been yet. Alterations of DCC gene were analyzed in stage-matched two panels of 30 RER+ and 30 RER− colorectal cancers using semiquantitative reverse transcription-PCR and PCR-LOH analyses. Loss or reduction of DCC mRNA expression and allelic loss at the DCC locus were significantly less frequent in RER+ cancers than in RER− cancers. Interestingly, reduced DCC mRNA expression was observed in all 5 RER− cancers with liver metastasis. Our results support the concept that RER+ and RER− colorectal cancers represent different pathways of carcinogenesis and may give a hint for clarifying the specific mechanism of DCC inactivation in RER− colorectal cancers.
- Published
- 1998
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