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Molecular cloning of human TAK1 and its mutational analysis in human lung cancer
Author(s) -
Kondo Masashi,
Osada Hirotaka,
Uchida Kosaku,
Yanagisawa Kiyoshi,
Masuda Akira,
Takagi Kenzo,
Takahashi Toshitada,
Takahashi Takashi
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19980209)75:4<559::aid-ijc11>3.0.co;2-4
Subject(s) - lung cancer , biology , cancer , somatic cell , cancer research , cdna library , gene isoform , positional cloning , gene , complementary dna , genetics , pathology , medicine , mutant
In previous reports, we described that DPC 4/ Smad 4 and Smad 2 are mutated in a fraction of human lung cancers and suggested possible roles of the downstream mediators of transforming growth factor‐β (TGF‐β)–elicited signals in the pathogenesis of this most common cancer. In the present study, we investigated whether another downstream mediator, human TGF‐β‐activated kinase 1 ( hTAK 1), also is altered in lung cancer. For this purpose, the hTAK 1 gene was cloned with the aid of an expression sequence tag database search and cDNA library screening, and hTAK 1 was found to be expressed ubiquitously in 2 distinct isoforms regulated in a tissue‐specific manner in fetal and adult normal tissues. Interestingly, hTAK 1 was assigned to the chromosome region 6q14‐21, which is deleted frequently in various human malignancies, including lung cancer. Despite our extensive search for alterations in 39 lung cancer specimens as well as in 16 lung cancer cell lines, somatic mutations of hTAK 1 were not identified, indicating that hTAK 1 itself is not a frequent target for genetic alterations in lung cancer. Int. J. Cancer 75:559–563, 1998. © 1998 Wiley‐Liss, Inc.