Genetic factors in lung disease. Part II: Lung cancer and angiotensin converting enzyme gene.
The recent progress in molecular biology has led to the elucidation of pathogenesis of lung cancer. The development of a lung cancer requires multiple genetic changes, consisting of the activation of oncogenes, including the K-ras and myc genes, and of inactivation of tumour suppressor genes, including the Rb, p53 and CDKN2 genes. Knowing the specific genes undergoing such changes should be useful as biomarkers for the early detection of cells destined to become malignant. Moreover, such genetic changes could be targets of newly designed drugs and gene-based therapy. Although the angiotensin I-converting enzyme was originally discovered in equine plasma, it has been recognized in various organs and cells other than vascular endothelial cells. This enzyme is also known to have wide substrate specificity to many peptides. The definite roles of angiotensin converting enzyme (ACE) in the respiratory system are largely unknown. Recent progress in molecular biology of the ACE, however, gives us a good chance to look over the significance of ACE in respiratory diseases as well as cardiovascular disorders. In this review, we show the recent advances in the basic studies of the ACE and refer to its clinical application.
Kawakami
Y
Y
First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Yamaguchi
E
E
Munakata
M
M
Dosaka-Akita
H
H
Furuya
K
K
D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor / Q000276:immunology; D006801:Humans; D008175:Lung Neoplasms / Q000209:etiology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*
D007703:Peptidyl-Dipeptidase A