Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel gene, designated UROC28, was identified by an agarose gel-based differential display technique, and it was found to be up-regulated in prostate, breast, and bladder cancer. Expression of UROC28 was also up-regulated in prostate cancer cells in the presence of androgens as demonstrated by relative quantitative reverse transcription-PCR. The elevated expression of this gene was observed to increase in surgically removed tissues concomitantly with rising Gleason grade and was most elevated in metastatic tissue. UROC28 protein was detected in serum by Western slot blot analyses, and a significant higher UROC28 protein level was found in sera of prostate cancer individuals compared with normal individuals and individuals with nonmalignant prostatic hyperplasia. Northern analyses in normal tissues showed that the UROC28 cDNA hybridizes to two mRNAs at about 2.1 and 2.5 kb. Nucleic acid sequence analyses indicated that these two alternatively spliced mRNA variants differ only at the 3' untranslated region. These two mRNAs encode the same protein with 135 amino acids. Bioinformation analyses suggest that there is a possible transmembrane domain from amino acid aa34 to aa50, three protein kinase-C phosphorylation sites at aa62 (SQK), aa89 (TMK), and aa94 (SMK), and one myristylation site at aa118 (GLECCL). Genomic Southern hybridization and chromosomal mapping demonstrated that UROC28 is encoded by a single copy of gene at chromosome 6q23-24. In situ hybridization and immunohistochemistry experiments further confirmed up-regulation of this gene in prostate and breast cancers with the expression localizing to the glandular epithelium. This gene did not demonstrate increased expression in lung and colon cancer tissues.
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PMID:Cloning and characterization of UROC28, a novel gene overexpressed in prostate, breast, and bladder cancers. 1115 5

Abnormal expression of bone morphogenic proteins (BMP) has been reported in prostate cancer as compared to benign prostatic tissue. Since aberrations in gene expression often result from alterations in gene copy number, we have investigated this possibility in patients with early prostate cancer. Probes for fluorescence in situ hybridization for the BMP, BMP5, BMP7, and UC28 gene loci were developed and applied to archival sections with areas of adjacent benign epithelium, high-grade prostatic intraepithelial neoplasia, and prostate carcinoma. Two hundred nuclei from each region were evaluated. No deletions of the gene loci examined were observed, but gain of BMP2, BMP5, BMP7, and UC28 occurred in 58, 50, 50, and 67% of tumor foci, respectively. These aberrations in copy number may be caused by early events in tumor development because they were also present in 10-30% of high-grade prostatic intraepithelial hyperplasia foci. In addition, one tumor demonstrated a tandem amplification of the UC28 gene locus. Approximately half of the prostate tumors displayed increased copy numbers of the BMP2, BMP5, BMP7, and UC28 gene loci, which may account for their abnormal gene expression patterns in neoplastic prostate tissue.
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PMID:Bone morphogenic factor gene dosage abnormalities in prostatic intraepithelial neoplasia and prostate cancer. 1765 61