Literature DB >> 2185686

C-myc, N-myc, N-ras, and c-erb-B: lack of amplification or rearrangement in human medullary thyroid carcinoma and a derivative cell line.

K P Yang1, S G Castillo, C V Nguyen, R C Hickey, N A Samaan.   

Abstract

We investigated the copy number and possible rearrangement of the four protooncogenes, c-myc, N-myc, N-ras, and c-erb-B, in DNA from seven untreated primary cancers or metastases of medullary thyroid carcinoma and an established human medullary thyroid carcinoma cell line, TT, using the Southern blotting technique. The purpose of this study was two-fold: 1) to examine whether protooncogene perturbations in medullary thyroid carcinoma could be considered as a prognostic marker; and 2) to determine whether the protooncogenes could have a possible role in medullary thyroid tumorigenesis. Neither amplification nor rearrangement of the protooncogenes was detectable in the DNA from any tumor samples or in the cell line. Our results suggest that DNA-evident amplification and rearrangement of the c-myc, N-myc, N-ras, and c-erb-B oncogenes may not be mechanisms through which these oncogenes become activated in this malignancy.

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Year:  1990        PMID: 2185686

Source DB:  PubMed          Journal:  Anticancer Res        ISSN: 0250-7005            Impact factor:   2.480


  2 in total

1.  Somatic RAS mutations occur in a large proportion of sporadic RET-negative medullary thyroid carcinomas and extend to a previously unidentified exon.

Authors:  A Boichard; L Croux; A Al Ghuzlan; S Broutin; C Dupuy; S Leboulleux; M Schlumberger; J M Bidart; L Lacroix
Journal:  J Clin Endocrinol Metab       Date:  2012-08-03       Impact factor: 5.958

2.  Point mutations of ras and Gs alpha subunit genes in thyroid tumors.

Authors:  H Horie; Y Yokogoshi; M Tsuyuguchi; S Saito
Journal:  Jpn J Cancer Res       Date:  1995-08
  2 in total

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