Open AccessAbsence of ras Family Point Mutations at Codons 12, 13 and 61 in N‐Ethyl‐N‐hydroxyethylnitrosamine‐ or N‐Nitrosomorpholine‐induced Renal Cell Tumors in Rats
Author(s) -
Matsumoto Kazuyuki,
Tsuda Hiroyuki,
Iwase Teruhiko,
Ito Mitsuya,
Nishida Yoshihisa,
Oyama Fumitaka,
Titani Koiti,
Ushijima Toshikazu,
Nagao Minako,
Hirono Iwao
Publication year - 1992
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1992.tb02003.x
Subject(s) - point mutation , mutation , exon , microbiology and biotechnology , kidney , polymerase chain reaction , biology , oligonucleotide , gene , cancer research , pathology , genetics , medicine
The prevalence of Ki‐ ras , Ha‐ ras and N‐ ras point mutation within exons 1 and 2 was studied in 17 cases of renal cell tumors (8 carcinomas and 9 adenomas) induced by N‐ethyl‐N‐hydroxyethylnitrosamine or N‐nitrosomorpholine. DNA samples prepared from acetone‐fixed, paraffin‐embedded tissues were amplified by means of the polymerase chain reaction, and point mutations at codons 12, 13 and 61 were analyzed by direct sequence methods with oligonucleotide primers. No mutations were detected in any of the renal tumors. The results thus indicated that ras family point mutation is not necessary for kidney tumor development in rats, supporting the view that ras mutations may not be generally relevant to neoplastic development in various organs in different species.