These data suggest a role for the overexpression of c-MET oncogene in the pathogenesis and progression of thyroid tumors derived from the follicular epithelium.
Amplification of ERBB-2 was detected in 14 out of 63 (22%) cases of breast carcinoma, in 1 out of 23 patients with ovarian cancers, in 1 out of 19 cases of colon carcinoma and in 1 out of 27 patients with thyroid cancer.
Analysis by a reverse transcriptase-polymerase chain reaction method showed that the ret rearrangement-positive tumor contained the PTC/retTPC chimeric transcript, which was reported to be found specifically in thyroid tumors and adenomatous goiter.
Analysis by a reverse transcriptase-polymerase chain reaction method showed that the ret rearrangement-positive tumor contained the PTC/retTPC chimeric transcript, which was reported to be found specifically in thyroid tumors and adenomatous goiter.
Analysis by a reverse transcriptase-polymerase chain reaction method showed that the ret rearrangement-positive tumor contained the PTC/retTPC chimeric transcript, which was reported to be found specifically in thyroid tumors and adenomatous goiter.
Analysis by a reverse transcriptase-polymerase chain reaction method showed that the ret rearrangement-positive tumor contained the PTC/retTPC chimeric transcript, which was reported to be found specifically in thyroid tumors and adenomatous goiter.
Analysis by a reverse transcriptase-polymerase chain reaction method showed that the ret rearrangement-positive tumor contained the PTC/retTPC chimeric transcript, which was reported to be found specifically in thyroid tumors and adenomatous goiter.
The present study indicates the normal patterns of DNA and RNA hybridization in a variety of thyroid tissues and disease states, and demonstrates that pathologic thyroid samples, with the possible exception of thyroid cancer, were not associated with specific nucleotide abnormalities in the unique area of the TSH receptor that was studied.
Mutations that lead to constitutive activation of Gs alpha, the guanine nucleotide-binding regulatory protein that stimulates adenylyl cyclase activity, have been identified in a subset of human growth hormone-secreting pituitary tumors and human thyroid tumors.
The presence of two crossovers between MEN2A and MBL in these families indicates that a defect of MBL itself is not the cause of the hereditary thyroid cancer syndrome.
Thus the a4 and a2 alleles of c-Ha-ras-1 may perhaps be viewed as genetic markers of predisposition to lung, ovarian and thyroid cancer, respectively, in combination with other clinical parameters.
Using polymerase chain reaction and sequence-specific oligonucleotide hybridization, the frequency of three ras oncogene mutations (N-ras, Ha-ras, and K-ras) in thyroid tumors (25 adenomas, 16 follicular carcinomas, and 22 papillary carcinomas) was investigated in both iodide-deficient and iodide-sufficient areas.
These findings are the first report of MOS expression in any human tissue, and indicate that MOS oncogene activation might be important in the development of some thyroid tumours.