It is known that no restriction endonuclease cleavage site exists at 12 codon in N-ras gene and at 12 and 13 codon in K-ras gene.Amismatched base was incorporated at the 3' end primer to creat a kind of restriction endonuclease cleavage site.Then it was possible for us to analyze the point mutation of the above mentioned codons with the polymerase chain reaction-restriction fragment length polymorphism.In this paper,the study of the point mutation at 12 and 61 codon in c-Ha-ras,at 12 codon in N-ras,and at 12 and 13 codon in K-ras was reported.

Objective To evaluate the feasibility in early diagnosis, predicting therapeutic effect, recurrence monitoring by examining promoter hypermethylation for cancer-associated genes E-cadherin in cancer tissue and peripheral blood of breast cancer patients. Methods The tumor tissue, paracancer- tissue and the paired plasma were examined for aberrant methylation of E-cadherin gene by methylation-specific PCR in 42 cases of breast cancer and 10 cases of breast benign diseases. Results The incidence of promoter hypermethylation of E-cadherin in tumor tissues was 52.4% and the paired plasma were 33.3%. E-cadherin hypermethylation in plasma samples and tumor samples significantly correlated with each other ( P

Both genetic and epigenetic events have been implicated in the stepwise histological progression involving adenoma-carcinoma and hyperplastic polyp/serrated adenoma-carcinoma sequences in the development of colorectal cancer. Genetic changes have been observed at each step in the initiation and progression of polyps to adenocarcinomas. Epigenetic changes also occur at each step in the pathogenesis of colorectal cancers and include CpG island DNA hypermethylation in the promoter region of genes resulting in transcriptional silencing through associated changes in chromatin structure and effects on binding of transcription factors, and DNA global hypomethylation which leads to chromosomal instability. Recent studies on MLH1 and APC genes indicate that epigenetic and genetic changes cooperate to facilitate tumor initiation and progression. Since aberrant CGI DNA promoter hypermethylation can be detected not only in colorectal polyps and cancers, but also in sera and stool, hypermethylated genes may serve as molecular markers for early detection, risk assessment and diagnosis. In addition, silenced genes caused by CGI DNA promoter hypermethylation can be reactivated by demethylating agents and also by both the inhibitors of DNA methyltransferases and histone deacetylases. Therefore, these epigenetically acting drugs should be evaluated for their chemopreventive and therapeutic potential for colorectal cancers.
Adenocarcinoma ; Chromatin ; Chromosomal Instability ; Colorectal Neoplasms ; CpG Islands ; Diagnosis ; DNA Methylation ; DNA* ; Epigenomics* ; Genes, APC ; Histone Deacetylases ; Methyltransferases ; Polyps ; Promoter Regions, Genetic ; Risk Assessment ; Transcription Factors