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Titolo:
KI-RAS ONCOGENE ACTIVATION IN TRANSPLANTABLE RAT-THYROID CARCINOMA INDUCED BY N-BIS(2-HYDROXYPROPYL)NITROSAMINE
Autore:
HIASA Y; KITAHORI Y; NAKAHASHI K; YANE K; KONISHI N; LIN JC; OKAICHI K; OHNISHI T;
Indirizzi:
NARA MED UNIV,DEPT PATHOL 2,840 SHIJO CHO KASHIHARA NARA 634 JAPAN NARA MED UNIV,DEPT BIOL KASHIHARA NARA 634 JAPAN CTR DIS CONTROL & PREVENT,DIV HIV AIDS,HEMATOL DIS BRANCH,MOLEC BIOL SECT ATLANTA GA 30333
Titolo Testata:
Cancer letters
fascicolo: 1-2, volume: 83, anno: 1994,
pagine: 209 - 214
SICI:
0304-3835(1994)83:1-2<209:KOAITR>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
POINT MUTATION; HA-RAS; CARCINOGENESIS; TUMOR; TUMORIGENESIS; MOUSE; AMPLIFICATION; PROTOONCOGENE; PROGRESSION; MUTAGENESIS;
Keywords:
THYROID CARCINOMA; N-BIS(2-HYDROXYPROPYL)-NITROSAMINE; KI-RAS ONCOGENE; CODON 63; POINT MUTATION; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
23
Recensione:
Indirizzi per estratti:
Citazione:
Y. Hiasa et al., "KI-RAS ONCOGENE ACTIVATION IN TRANSPLANTABLE RAT-THYROID CARCINOMA INDUCED BY N-BIS(2-HYDROXYPROPYL)NITROSAMINE", Cancer letters, 83(1-2), 1994, pp. 209-214

Abstract

We have established 17 transplantable rat thyroid carcinoma cell lines from primary thyroid tumors of rats induced by N-bis(2-hydroxypropyl)nitrosamine (DHPN) (Cancer Res. (1993) 53, 4408-4412). The present study was designed to evaluate point mutations in the murine c-Ki-ras gene of these carcinoma cell lines. Using PCR amplification and direct sequencing, we found that the activated form of the Ki-ras oncogene waspresent in 4 (23%) of a total of 17 cell lines, all the Ki-ras gene mutations being GC --> AT transitions. In three of the cell lines, the mutations occurred in codon 12 (GTP-binding domain), and in the remaining one the first nucleotide of codon 63 was affected. Histologically,three of the carcinomas with Ki-ras mutation were diagnosed as well-differentiated carcinomas, and the other as poorly differentiated carcinoma. Mutations of the ras gene are relatively uncommon in tumors of these histological types. From these experimental results, we suggest that the mutation induced by DHPN is due to damage to guanine in cellular DNA. In addition, Ki-ras activation may play an important role in the initiation of thyroid carcinogenesis.

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Documento generato il 28/09/20 alle ore 11:27:17