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Titolo:
Genetic alteration of the beta-catenin gene (CTNNB1) in human lung cancer and malignant mesothelioma and identification of a new 3p21.3 homozygous deletion
Autore:
Shigemitsu, K; Sekido, Y; Usami, N; Mori, S; Sato, M; Horio, Y; Hasegawa, Y; Bader, SA; Gazdar, AF; Minna, JD; Hida, T; Yoshioka, H; Imaizumi, M; Ueda, Y; Takahashi, M; Shimokata, K;
Indirizzi:
Nagoya Univ, Sch Med, Dept Clin Prevent Med, Nagoya, Aichi 4668550, Japan Nagoya Univ Nagoya Aichi Japan 4668550 Med, Nagoya, Aichi 4668550, Japan Nagoya Univ, Sch Med, Dept Thorac Surg, Nagoya, Aichi 4668550, Japan Nagoya Univ Nagoya Aichi Japan 4668550 Surg, Nagoya, Aichi 4668550, Japan Nagoya Univ, Sch Med, Dept Internal Med 1, Nagoya, Aichi 4668550, Japan Nagoya Univ Nagoya Aichi Japan 4668550 ed 1, Nagoya, Aichi 4668550, Japan Nagoya Univ, Sch Med, Dept Pathol 2, Nagoya, Aichi 4668550, Japan Nagoya Univ Nagoya Aichi Japan 4668550 ol 2, Nagoya, Aichi 4668550, Japan Hamon Ctr Therapeut Oncol Res, Dallas, TX 75235 USA Hamon Ctr Therapeut Oncol Res Dallas TX USA 75235 s, Dallas, TX 75235 USA Aichi Canc Ctr, Dept Internal Med, Chikusa Ku, Nagoya, Aichi 4648681, Japan Aichi Canc Ctr Nagoya Aichi Japan 4648681 u, Nagoya, Aichi 4648681, Japan
Titolo Testata:
ONCOGENE
fascicolo: 31, volume: 20, anno: 2001,
pagine: 4249 - 4257
SICI:
0950-9232(20010712)20:31<4249:GAOTBG>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-LINES; HEPATOCELLULAR CARCINOMAS; GROWTH SUPPRESSION; HUMAN SEMAPHORIN; E-CADHERIN; MUTATIONS; EXPRESSION; ACTIVATION; REGION; CHROMOSOME-3;
Keywords:
beta-catenin; lung cancer; malignant mesothelioma; chromosome 3; homozygous deletion; breakpoint cloning;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Sekido, Y Nagoya Univ, Sch Med, Dept Clin Prevent Med, Nagoya, Aichi 4668550, Japan Nagoya Univ Nagoya Aichi Japan 4668550 ya, Aichi 4668550, Japan
Citazione:
K. Shigemitsu et al., "Genetic alteration of the beta-catenin gene (CTNNB1) in human lung cancer and malignant mesothelioma and identification of a new 3p21.3 homozygous deletion", ONCOGENE, 20(31), 2001, pp. 4249-4257

Abstract

The beta -catenin gene (CTNNB1) has been shown to be genetically mutated in various human malignancies. To determine whether the beta -catenin gene is responsible for oncogenesis in thoracic malignancies, we searched for themutation in 166 lung cancers (90 primary tumors and 76 cell lines), one blastoma and 10 malignant mesotheliomas (two primary tumors and eight cell lines). Among the lung cancers, including 43 small cell lung cancers (SCLCs) and 123 non-small cell lung cancers (NSCLCs), we identified four alterations in exon 3, which is the target region of mutation for stabilizing beta -catenin. One primary adenocarcinoma had a somatic mutation from C to G, leading to an amino acid substitution from Ser to Cys at codon 37. Among the cell lines, SCLC NCI-H1092 had a mutation from A to G, leading to an Asp to Cry substitution at codon 6, NSCLC HCC15 had a mutation from C to T, leadingto a Ser to Phe substitution at codon 45, and NSCLC NCI-H358 had a mutation from A to G, leading to a Thr to Ala substitution at codon 75. One blastoma also had a somatic mutation from C to C, leading to a Ser to Cys substitution at codon 37. Among the 10 malignant mesotheliomas, we identified a homozygous deletion in the NCI-H28 cell line. Cloning of the rearranged fragment from NCI-H28 indicated that all the exons except exon 1 of the beta -catenin gene are deleted and that the deletion junction is 13 kb downstream from exon 1. Furthermore, Northern blot analysis of 26 lung cancer and eightmesothelioma cell line RNAs detected ubiquitous expression of the beta -catenin messages except NCI-H28, although Western blot analysis showed that relatively less amounts of protein products were expressed in some of lung cancer cell lines, Our findings suggest that the beta -catenin gene is infrequently mutated in lung cancer and that the NCI-H28 homozygous deletion of the beta -catenin gene might indicate the possibility of a new tumor suppressor gene residing in this region at 3p21.3, where various types of human cancers show frequent allelic loss.

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Documento generato il 31/03/20 alle ore 10:06:34