作者: Maite Cazorla , Luis Hernández , Pedro L Fernández , Àngels Fabra , Miguel A Peinado
DOI: 10.1002/(SICI)1098-2744(199804)21:4<251::AID-MC4>3.0.CO;2-N
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摘要: Ki-ras and p53 genes are involved in human lung carcinogenesis; however, the role of these experimental tumors is not well known. In our study, CBA/J mouse strain was used to investigate presence alterations carcinogenesis spontaneous induced with high low doses urethane (ethyl carbamate). To study early stages very small tumors, restriction fragment length polymorphism single-strand conformation analyses were performed on polymerase chain reaction–amplified DNA from microdissected tumoral normal samples. gene mutations codons 12 61 detected all types lesions, even preneoplastic their incidence increased progression hyperplasias (18%) adenomas (75%) carcinomas (80%). Urethane exposure, both doses, especially adenomas. The urethane-induced absence among treated-group lesions may indicate that accelerates progression. No exons 5–8 any epithelium-derived tumors. Only one mutation exon 5 found a lymphoma. Therefore, do seem cooperate or represent an alternative molecular pathway murine carcinogenesis. Mol. Carcinog. 21:251–260, 1998. © 1998 Wiley-Liss, Inc.