{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T05:30:30Z","timestamp":1780983030970,"version":"3.54.1"},"reference-count":23,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2006,7,17]],"date-time":"2006-07-17T00:00:00Z","timestamp":1153094400000},"content-version":"vor","delay-in-days":4735,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[1993,7,30]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Activation by point mutation of the H\u2010, K\u2010 and N\u2010ras genes is found in many tumors. However, no such mutation has yet been found in human esophageal carcinomas from various parts of the world. We have confirmed the absence of mutation at codons 12, 13 and 61 of K\u2010 and N\u2010ras and at codons 12 and 61 of H<jats:italic>\u2010ras<\/jats:italic> in 25 primary tumors obtained in France. In contrast, among 7 human esophageal carcinoma cell lines (TE1, TE2, TE3, TE8, TE9, TE TE10, TE 13) with different degrees of tumorigenicity in nude mice, 3 highly tumorigenic lines (TE1, TE2 and TE8) exhibited activation of <jats:italic>ras<\/jats:italic> oncogenes; 2 showed a G<jats:sup>35<\/jats:sup> to A<jats:sup>35<\/jats:sup> transition of K<jats:italic>\u2010ras<\/jats:italic> gene and one a H<jats:italic>\u2010ras<\/jats:italic> G<jats:sup>35<\/jats:sup> to T<jats:sup>35<\/jats:sup> transversion. Since these cell lines had been established from tumors of Japanese patients from Sendai, we examined 3 primary esophageal tumors from Tokyo and 19 from Sendai, including the primary tumors from which the TE cell lines had been derived. No <jats:italic>ras<\/jats:italic> mutation was detected, which suggests that the <jats:italic>ras<\/jats:italic> gene mutations in the TE cell lines are either due to their long\u2010term culture or that only a small portion of the original tumors contained such mutations. In order to directly examine the effect of <jats:italic>ras<\/jats:italic> gene mutation, one of the non\u2010tumorigenic cell lines, TE 13, was transfected with a plasmid coding for a mutated H<jats:italic>\u2010ras<\/jats:italic> gene (G<jats:sup>35<\/jats:sup> to T<jats:sup>35<\/jats:sup>). Transfected clones expressing high levels of mutated <jats:italic>ras<\/jats:italic> gene were able to induce tumors in nude mice. Thus, although no primary human esophageal tumor contained mutated <jats:italic>ras<\/jats:italic> genes, our studies do not exclude a significant role of mutated <jats:italic>ras<\/jats:italic> genes in cell proliferation and malignant transformation of human esophageal cells.<\/jats:p>","DOI":"10.1002\/ijc.2910540619","type":"journal-article","created":{"date-parts":[[2007,2,19]],"date-time":"2007-02-19T23:52:02Z","timestamp":1171929122000},"page":"978-982","source":"Crossref","is-referenced-by-count":13,"title":["Possible role of activated <i>ras<\/i> genes in human esophageal carcinogenesis"],"prefix":"10.1002","volume":"54","author":[{"given":"C.","family":"Galiana","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Fusco","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Martel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Nishihira","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Hirohashi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Yamasaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,7,17]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.56.070187.004023"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/12.12.2373"},{"key":"e_1_2_1_4_1","first-page":"1779","article-title":"Archival analysis of p53 genetic and protein alterations in Chinese esophageal cancer","volume":"6","author":"Bennett W. 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