Journal Article

How many tumor suppressor genes are involved in human lung carcinogenesis?

Takashi Kohno and Jun Yokota1

in Carcinogenesis

Volume 20, issue 8, pages 1403-1410
Published in print August 1999 | ISSN: 0143-3334
Published online August 1999 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/20.8.1403
How many tumor suppressor genes are involved in human lung carcinogenesis?

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To date, only a limited number of tumor suppressor genes have been identified as being inactivated in lung cancer. The p53 and RB genes are frequently inactivated by genetic alterations such as chromosomal deletions and loss-of-function mutations, while the p16 gene is inactivated not only by genetic alterations but also by transcriptional silencing due to hypermethylation. Recently, it was shown that the FHIT gene encompassing the chromosomal fragile site, FRA3B, is also inactivated in a large proportion of lung cancers. Several lines of evidence indicate the presence of additional tumor suppressor genes involved in lung carcinogenesis. Lung cancer cells often show deletions at multiple chromosomal regions, and deletion mapping studies have defined more than 30 regions dispersed on 21 different chromosome arms as candidate tumor suppressor loci. Several chromosomal regions hypermethylated in lung cancer cells and a number of chromosomal fragile sites have been mapped to the regions deleted in lung cancer. These chromosomal loci can harbor unknown tumor suppressor genes inactivated in lung cancer. Studies on the inherited susceptibility to lung cancer in mice have also indicated the presence of additional tumor suppressor genes for lung cancer. Further analyses of these loci should elucidate how many tumor suppressor genes are involved in human lung carcinogenesis. Molecular and functional analyses of those genes will make it possible to fully understand the molecular mechanism of lung carcinogenesis.

Keywords: LOH, loss of heterozygosity; NSCLC, non-small cell lung carcinoma; SCLC, small cell lung carcinoma

Journal Article.  7293 words. 

Subjects: Clinical Cytogenetics and Molecular Genetics

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