Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012872 (DNA marker)
 929 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is now widely accepted that human neoplasms arise as a result of a sequence of mutations affecting the structure of genes involved in growth control. In humans, indirect measurements based on age dependent tumor incidence predict that, on average, the accumulation of 5 to 6 different steps is needed to initiate tumor formation. These mutations do not appear to be random, in that certain neoplasms show prediction for structural aberrations in specific genes. In thyroid tumors, some of gene abnormalities were found. The point mutations of ras oncogenes, predominantly H-ras codon 12, are found in 20-25% of follicular adenomas and papillary carcinomas. Recently, the gene rearrangements of the oncogenes trk and ret were identified in the DNA from papillary carcinomas. About 25% of papillary carcinomas contained an introchromosomal (10q) gene rearrangement involving the tyrosine kinase domain of the ret oncogene with an unknown amino-terminal sequence. The mutations of trk and/or ret were not observed in other thyroid neoplastic phenotypes. In medullary thyroid carcinoma, which is a tumor of the parafollicular, calcitonin-secreting C cell of the thyroid, approximately 20% of patients have autosomal dominant inherited forms. Germ line abnormalities on chromosome 10 are linked to at least one type of genetic medullary thyroid carcinoma (MEN type 2a). In the present time, the person who has the abnormality of gene causing MEN type 2a is able to detect by using DNA marker before the onset of tumor.
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PMID:[Thyroid carcinoma]. 198 98

Multiple endocrine neoplasia types 2A and 2B (MEN 2A and MEN 2B) and familial medullary thyroid carcinoma (FMTC) are dominantly inherited cancers that have in common the clinical feature of medullary thyroid carcinoma (MTC). We have performed both genomic long-range restriction mapping and yeast artificial chromosome (YAC) contig assembly and restriction mapping to establish physical linkage, order, and distances between six loci in 10q11.2 near the genes responsible for these hereditary cancers. RET, D10S94, D10S182, and D10S102 have been mapped in genomic DNA. RET, D10S94, D10S182, D10F38S3, and the 10q11.2 sequences detected by DNA marker DM124 are encompassed by a 1-Mb YAC contig. Six physically linked loci are within 1.4 Mb and have an order and orientation of 10cen, D10F38S3, DM124, RET, D10S94, D10S182, D10S102, 10qter. Mutations in the RET proto-oncogene have recently been demonstrated to be associated with MEN 2A and FMTC. RET is located within a genetically defined MEN2A candidate interval between D10S141 and D10S94; MEN2B has been mapped to a larger, overlapping region between D10S141 and a more distal locus, RBP3. Both our genomic physical map and our YAC contig span the entire MEN2A candidate region and overlap with that of MEN2B. These maps will facilitate the identification of genes that can be considered candidates for MEN2B and the identification of tumor-specific alterations important in sporadic MTC.
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PMID:Genomic and yeast artificial chromosome long-range physical maps linking six loci in 10q11.2 and spanning the multiple endocrine neoplasia type 2A (MEN2A) region. 790 24