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Query: UNIPROT:O76050 (neu)
 3,969 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Follicular neoplasms of oncocytic type in the thyroid gland frequently cause diagnostic problems and prognostic uncertainties. To identify numerical chromosomal aberrations of possible pathogenetic importance, we determined chromosome copy numbers in situ in interphase nuclei of 31 oncocytic adenomas and 25 oncocytic carcinomas. Archival formaldehyde-fixed, paraffin-embedded tumor samples and normal control thyroid tissues were arranged in arrays and analyzed by fluorescence in situ hybridization (FISH). We used pericentromeric or locus specific probes for chromosomes 1, 7, 8, 9, 11, 12, 17, 18, 22, and X as well as for the oncogenes Her2/neu, cyclin D1, N-myc, and c-myc. The average number of aneusomies per nucleus was significantly higher in carcinomas than in adenomas, and in both, monosomies were more frequent than polysomies. Loss of chromosome 22 was found in 8 of 21 (38%) carcinomas; in 5 cases, it was associated with chromosome 2 monosomy. Conversely, chromosome 2 aberrations were not found in adenomas. Monosomies for chromosome 8 and X were detected in most adenomas and carcinomas. The most common gains in adenomas and carcinomas were for chromosome 7 (13.8% and 32.0% of the cases, respectively), chromosome 12 (9.6% and 12.0%), and chromosome 17 (19.3% and 32.0%). None of the adenomas with trisomy 17 was associated with gains for chromosomes 7 and 12. None of the analyzed oncogenes was found to be amplified by FISH analysis. Our results indicate that numerical chromosomal aberrations in oncocytic follicular tumors of the thyroid gland are common findings and suggest that different patterns of aberrations may occur in these neoplasms.
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PMID:Interphase cytogenetics in oncocytic adenomas and carcinomas of the thyroid gland. 1092 24

Ovarian neoplasms display a wide range of phenotypic differentiation patterns. In the recent past, molecular genetic aberrations have been increasingly identified in various types of ovarian tumors. Granulosa cell tumors most often contain numeric chromosomal aberrations (monosomy 22, trisomy 12 and 14). Numeric changes can also be found in benign and borderline epithelial neoplasms, however without demonstrating specific patterns. K-ras mutations are characteristic for mucinous ovarian tumors and for serous borderline (LMP) tumors. In serous LMP tumors they are associated with low level microsatellite instability. Complex chromosomal aberrations are not detected in benign and borderline tumors. Invasive ovarian carcinomas show complex genetic changes. Chromosomal gains at 3q26, 8q24 and 20q13 apparently represent early lesions, whereas loss of material of chromosomes 4, 13, 16, 18 and X is associated with tumor progression and poor prognosis. The main targets of chromosomal changes are regulatory genes of cell proliferation and apoptosis (e.g. p16, cyclin D1, Rb, p53, myc, bcl-2) and members of the signaling cascade of tyrosine kinase receptors (e.g. Her-2/neu, dab-2, K-ras, PI3-K, PTEN). The genetic alterations of ovarian neoplasms described so far apparently correlate with the different level of aggressiveness. However, they do not fully explain the spectrum of phenotypic variability of these tumors.
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PMID:[Phenotype--genotype--correlation in ovarian neoplasia]. 1189 92