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[Cancer Research 60, 4689-4692, September 1, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

Histological Type-selective, Tumor-predominant Expression of a Novel CHK1 Isoform and Infrequent in Vivo Somatic CHK2 Mutation in Small Cell Lung Cancer1

Nobuhiro Haruki, Hiroko Saito, Yoshio Tatematsu, Hiroyuki Konishi, Tomoko Harano, Akira Masuda, Hirotaka Osada, Yoshitaka Fujii and Takashi Takahashi2

Division of Molecular Oncology, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan [N. H., H. S., Y. T., H. K., T. H., A. M., H. O., T. T.], and Department of Surgery II, Nagoya City University Medical School, Nagoya 467-8601, Japan [N. H., Y. F.]

Inactivation of p53, which represents the most prevalent genetic alteration in lung cancer, has been shown to play a crucial role in the acquisition of genomic instability. We examined 44 lung cancer specimens to search for mutations in the CHK1 and CHK2 genes, which have been suggested to play roles in regulating p53 after DNA damage. We found that the CHK2 gene was somatically mutated in lung cancer in vivo, although at a low frequency, and that a previously undescribed shorter isoform of CHK1 was expressed preferentially in small cell lung cancer in a tumor-predominant manner. Additional studies are warranted to investigate the functional significance of these changes as well as the potential involvement of other components in this important pathway to maintain genomic stability.




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Copyright © 2000 by the American Association for Cancer Research.