Abstract
Exons 1-3 of the p16/CDKN2 gene and exons 4-9 of the p53 gene were screened for mutations by single-strand conformation polymorphism (SSCP) analysis and direct sequencing of PCR-amplified DNA from human primary thyroid carcinomas and thyroid carcinoma cell lines. The samples included 21 papillary carcinomas, 2 undifferentiated carcinomas, 1 follicular carcinoma, 1 medullary carcinoma and 2 cell lines originating from thyroid undifferentiated carcinomas. No homozygous deletions and mutations in the p16/CDKN2 were observed in any of the primary tumors or cell lined. In contrast, one of the two undifferentiated carcinomas an both cell lines demonstrated point mutations in the p53 gene. These results that p16/CDKN2 gene alteration is not required for malignant transformation in the thyroid, while p53 gene mutations may play a role in the progression from differentiated to undifferentiated carcinoma.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenocarcinoma, Follicular / chemistry
-
Adenocarcinoma, Follicular / genetics
-
Adenocarcinoma, Follicular / pathology
-
Adult
-
Aged
-
Aged, 80 and over
-
Base Sequence
-
Carcinoma / chemistry
-
Carcinoma / genetics
-
Carcinoma / pathology
-
Carcinoma, Medullary / chemistry
-
Carcinoma, Medullary / genetics
-
Carcinoma, Medullary / pathology
-
Carcinoma, Papillary / chemistry
-
Carcinoma, Papillary / genetics
-
Carcinoma, Papillary / pathology
-
Carrier Proteins / analysis
-
Carrier Proteins / genetics
-
Child
-
Cyclin-Dependent Kinase Inhibitor p16
-
Female
-
Gene Deletion*
-
Genes, Tumor Suppressor / genetics*
-
Genes, p53 / genetics
-
Humans
-
Male
-
Middle Aged
-
Molecular Sequence Data
-
Oligonucleotide Probes / chemistry
-
Thyroid Neoplasms / chemistry
-
Thyroid Neoplasms / genetics*
-
Thyroid Neoplasms / pathology
-
Tumor Suppressor Protein p53 / analysis
-
Tumor Suppressor Protein p53 / genetics
Substances
-
Carrier Proteins
-
Cyclin-Dependent Kinase Inhibitor p16
-
Oligonucleotide Probes
-
Tumor Suppressor Protein p53