{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,9,12]],"date-time":"2024-09-12T13:14:57Z","timestamp":1726146897673},"reference-count":25,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2006,7,20]],"date-time":"2006-07-20T00:00:00Z","timestamp":1153353600000},"content-version":"vor","delay-in-days":5679,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[1991,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The DNA sequences for Ha\u2010, Ki\u2010, and N\u2010<jats:italic>ras<\/jats:italic> were determined in six cell lines derived from independent rat hereditary renal cell carcinomas (RCC). Genomic regions encompassing codons 12, 13, and 61 of Ha\u2010<jats:italic>ras<\/jats:italic>, Ki\u2010<jats:italic>ras<\/jats:italic>, and N\u2010<jats:italic>ras<\/jats:italic>, and codon 117 of Ha\u2010<jats:italic>ras<\/jats:italic> were PCR amplified and directly sequenced. The DNA sequences of Ha\u2010<jats:italic>ras<\/jats:italic> and Ki\u2010<jats:italic>ras<\/jats:italic> were normal in all lines tested, as were the codon 12 and 61 sequences of N\u2010<jats:italic>ras<\/jats:italic>. However, DNA sequence variations that could code for amino acid substitutions were observed in codons 13, 14, and 18 of N\u2010<jats:italic>ras<\/jats:italic> in all the lines. The codon 13 Gly\u2192Val alteration observed was consistent with activating N\u2010<jats:italic>ras<\/jats:italic> mutations previously reported. When normal kidney DNA from rats with the hereditary tumor syndrome was sequenced, the same N\u2010<jats:italic>ras<\/jats:italic> sequence variations observed in the tumor lines were found. DNA from outbred Long\u2010Evans and inbred Fischer rats also had the altered N\u2010<jats:italic>ras<\/jats:italic> sequences. The variant N\u2010<jats:italic>ras<\/jats:italic> sequence was not observed in PCR\u2010amplified N\u2010<jats:italic>ras<\/jats:italic> cDNA from the RCC lines. Thus, tumor\u2010associated activation of <jats:italic>ras<\/jats:italic> oncogene appears to be an infrequent event in spontaneous rat RCC. In addition, these data indicate that rats contain an N\u2010<jats:italic>ras<\/jats:italic> DNA polymorphism that appears to be a species\u2010specific anomaly.<\/jats:p>","DOI":"10.1002\/mc.2940040504","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T20:15:31Z","timestamp":1172088931000},"page":"350-353","source":"Crossref","is-referenced-by-count":12,"title":["Analysis of <i>ras<\/i> DNA sequences in rat renal cell carcinoma"],"prefix":"10.1002","volume":"4","author":[{"given":"Leslie","family":"Recio","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven C.","family":"Lane","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julie","family":"Ginsler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cheryl","family":"Walker","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,20]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/189858b0"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0272-0590(84)90227-6"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1177\/019262338601400204"},{"key":"e_1_2_1_5_2","first-page":"99","article-title":"Hereditary renal adenomas and adenocarcinomas in rats","volume":"4","author":"Eker R","year":"1981","journal-title":"Diagnostic Histopathology"},{"key":"e_1_2_1_6_2","unstructured":"BarrettJC HuffJCellular and molecular mechanisms of chemically induced renal carcinogenesis. 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