Expression of pancreatic secretory trypsin inhibitor gene in neoplastic tissues

AbstractExpression of the human pancreatic secretory trypsin inhibitor (PSTI) gene was examined in 24 cases of neoplastic tissues by Northern blot analyses. In three cases of lung adenocarcinoma and one case of sigmoid colon polyp, we detected transcripts which hybridized to the human PSTI cDNA probe. cDNA libraries were constructed using mRNAs of the two PSTI-positive tumor tissues. Two PSTI cDNA clones were obtained from each sample. Sequencing analyses showed that they were completely identical with that of pancreatic PSTI cDNA which had been reported [(1985) Biochem. Biophys. Res. Commun. 132, 605–612]. Southern blot analyses showed that the elevated expression of PSTI in neoplastic tissues was accompanied by neither PSTI gene amplification nor rearrangements

Studies of Multiple Endocrine Neoplasia Type 2A Syndrome: Linkage Analyses and Comparison of Constitutional and Tumor Genotypes

Linkage analyses were carried out in nine Japanese kindreds with multiple endocrine neoplasia type 2A (MEN-2A) using polymorphic classical markers and DNA markers. We excluded close linkage of the MEN-2A gene (MEN2A) locus with Gm, JK, PGMl, and a DNA segment, D20S5, which is assigned to band 12 of the short arm of chromosome 20 (20p12.2). Assuming that MEN2A is recessive at the cellular level as in retinoblastoma (RB) and Wilms\u27 tumor (WT). comparison of constitutional and tumor genotypes may be useful in the search for the MEN2A locus. When DNA samples from 12 patients with medullary thyroid carcinoma (MTC) were compared with 15 polymorphic DNA markers including two assigned to chromosome 20, the results were negative. Both the negative linkage data and the failure to find loss of heterozygosity in MTC with chromosome 20 probes suggest that MEN2A may not be at 20p12.2, which was previously suggested as the site of an inherited chromosomal deletion in MEN-2A

Allele Loss on Chromosome 10 and Point Mutation of ras Oncogenes are Infrequent in Tumors of MEN 2 A

The multiple endocrine neoplasia type 2A (MEN 2A) gene has been mapped to the centromeric region of chromosome 10 by linkage analysis. We examined 36 medullary thyroid carcinomas (MTCs) (16 hereditary and 20 sporadic) and ten pheochromocytomas (eight hereditary and two sporadic) to detect loss of alleles on chromosome 10 using seven polymorphic DNA markers mapped to this chromosome. Of 20 informative cases, only one (5%) sporadic MTC showed loss of heterozygosity at the locus RBP3. Allele loss at the RBP3 locus was not found in pheochromocytomas from six heterozy gates. All tumors retained constitutional heterozygosity at six other loci on chromosome 10 (D10S17, D10S34, D10S24 on the short arm, D10S15 in the pericentromeric region, D10S20, and D10S4 on the long arm). Our findings suggest that the second hit for tumorigenesis in MEN 2 A may not be loss of function of the normal allele at the homologous locus on the other copy of chromosome 10. Mutated ras oncogene was found only in one of 18 MTCs at the codon 61 of H-ras