The methylation status of 6 genes, including a candidate tumor suppressor gene (BLU), the cadherin 13 gene (CDH13), the fragile histidine triad gene (FHIT), the cell cycle control gene p16, the retinoic acid receptor beta gene (RARbeta), and the Ras association domain family 1 gene (RASSF1A), was examined in plasma samples, corresponding tumor tissues, and normal lung tissues from a group of 63 patients with lung cancer and in plasma samples from 36 cancer-free individuals.
Although the aberrant methylation of E-cadherin (CDH1) or H-cadherin (CDH13) genes has been reported in lung cancer, to the authors' knowledge, the relation between the concurrent hypermethylation in E-cadherin and H-cadherin has not been explored to date.
In conclusion, the frequency of p16INK4A or CDH13 hypermethylation in patient serum, together with evidence of their early occurrence in lung cancerogenesis and the total lack of methylation in serum from healthy individuals, offer a promising tool for non invasive early detection of lung cancer.
Methylation status of p16(INK4a), RASSF1A, APC, RARbeta, and CDH13, frequently methylated in lung cancer, was determined by methylation-specific PCR and the degree of methylation was defined as the methylation index.
Since the H-cadherin (CDH13) gene has been isolated and mapped to this common region of allelic loss, we have investigated this gene in human lung cancer.