Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of cellular oncogenes was examined in human thyroid tissue. Four thyroid adenomas and three thyroid carcinomas expressed c-myc oncogene mRNA transcripts, which were not expressed in normal thyroid tissues. Agarose gel electrophoresis of poly(A) RNA extracts of adenoma tissues followed by hybridization with v-myc DNA yielded two distinct c-myc mRNA species [2.1 and 4.0 kilobases (kb)]. Thyroid cancer tissue poly(A) RNA revealed a predominant larger c-myc mRNA species (approximately 6 kb) and a smaller 2.1-kb species. After enzymatic dispersion of thyroid adenoma cells, cytoplasmic dot blot hybridization of immobilized thyroid adenoma RNA extracts with the v-myc cDNA probe showed stimulation of c-myc mRNA expression by TSH in a dose- and time-dependent manner. After 72-h pretreatment with serum-free medium, the quiescent adenoma cells yielded a negligible hybridization signal which was stimulated by TSH (10 mU/ml) after 6 h of treatment. Although normal cultured thyroid cells did not contain detectable c-myc mRNA, TSH also stimulated the myc protooncogene expression in a time-dependent manner in normal thyroid cells. These results demonstrate the expression of c-myc mRNA in human thyroid tumors and the in vitro induction of c-myc mRNA in both normal and adenoma thyroid cell cultures by TSH.
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PMID:Expression of the myc cellular proto-oncogene in human thyroid tissue. 376 Jan 17

We have investigated by restriction fragment analysis genomic abnormalities involving the c-myc gene in DNA isolated from adenomas and hepatocellular carcinomas (HCCs). Adenomas and HCCs were induced by the "resistant hepatocyte" protocol in diethylnitrosamine-initiated male F344 rats. Southern-blot analysis of EcoRI-restricted DNA from normal liver, early and late adenomas, 12 weeks (EAs) and 30 weeks (LAs) after initiation, and HCCs, showed 2 bands of 18 and 3.2 kb hybridizing with c-myc, in all tissues. c-myc amplification occurred in almost all HCCs, and in the majority of EAs and LAs. These results were confirmed by dilution analysis. c-myc amplification was also seen in adenomas and HCCs by Southern analysis with HindIII-restricted DNA, and in HCCs by differential PCR. c-myc mRNA increase occurred in all adenomas and HCCs, but it was higher in the lesions showing gene amplification. Moreover, a 13-kb DNA extraband, hybridizing with c-myc, was found in the HindIII-restricted DNA from HCCs, but not in normal liver and adenomas, and a 7.1-kb extra band was present in EcoRI-digested DNA from one LA. EcoRI-restricted DNA from some adenomas exhibited a decrease in intensity of the 18-kb fragment, and an increase in intensity of the 3.2-kb fragment. No alteration in banding pattern occurred in the beta-actin gene in adenomas. These results provide evidence of amplification and some other rearrangements involving the c-myc gene, in pre-malignant and malignant liver lesions, induced by the RH protocol, and suggest a role of c-myc rearrangement in the progression of adenomas to malignancy.
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PMID:c-myc amplification in pre-malignant and malignant lesions induced in rat liver by the resistant hepatocyte model. 889 54

Identification of gene products exclusively or abundantly expressed in cancer may yield novel tumour markers. We recently isolated a number of cDNA clones, including alpha-prothymosin, from rat hepatocellular carcinoma (HCC) using a subtraction-enhanced display technique. Alpha-Prothymosin is involved in cell proliferation and is regulated by the oncogene c-myc in vitro. In the present study, we analysed alpha-prothymosin gene expression and its correlation with c-myc in patients with HCC, cirrhosis and adenoma and in normal controls. Hepatic alpha-prothymosin messenger RNA (mRNA) levels were two- to 9.2-fold higher in tumoral tissues than in adjacent non-tumoral tissues in 14 of 17 patients with HCC, regardless of coexisting cirrhosis and viral hepatitis. No marked difference in alpha-prothymosin mRNA levels was present in patients with adenoma and hepatic cirrhosis and in healthy controls. The c-myc mRNA amounts were two- to fivefold increased in 11 of 17 patients with HCC and correlated significantly with those of alpha-prothymosin (P < 0.001). In situ hybridization revealed that increased alpha-prothymosin mRNA was localized in the tumour nodules of the patients with HCC. These data suggest that overexpression of alpha-prothymosin in HCC patients, correlated with c-myc, is possibly involved in the tumorigenic process and may be a novel molecular marker for human HCC.
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PMID:Overexpression of hepatic prothymosin alpha, a novel marker for human hepatocellular carcinoma. 936 69

Serum ferritin is elevated in many cancers. Using the subtraction-enhanced display technique, we isolated several cDNA clones including ferritin-H which is overexpressed in rat hepatocellular carcinoma (HCC) induced by diethylnitrosamine. We investigated hepatic messenger RNA (mRNA) levels of ferritin-H in patients with HCC, adenoma, cirrhosis and healthy controls in relation to those of oncogene c-myc. Ferritin-H mRNA levels were 2-12 fold higher in tumor tissues than in adjacent non-tumor tissues in 12 of 17 patients with HCC, irrespective of coexisting cirrhosis or viral hepatitis. However, no difference in ferritin-H mRNA levels was found in patients with adenoma, cirrhosis and healthy controls. c-myc mRNA levels were 2-5 ford increased in 11 of 17 HCC patients, and correlated significantly with those of ferritin-H (p<0.001). In situ hybridization showed that the overexpressed ferritin-H mRNA was restricted to the tumor nodules in HCC livers. These findings suggest that overexpression of ferritin-fl in HCC patients, correlated with c-myc, is phenotypically associated with HCC, and could become a useful molecular indicator for human HCC.
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PMID:Increased hepatic ferritin-H messenger RNA levels correlate with those of c-myc in human hepatocellular carcinoma. 2152

The expression of the carbohydrate antigen sialyl-Le(x) and of the oncogenes c-myc and Ki-ras increases after malignant transformation of the colorectum. Since the overexpression of these two oncogenes may affect O- or N-linked carbohydrate chain synthesis, we investigated if this is the case for sialyl-Le(x). In parallel sections from 11 adenomas and 9 colorectal carcinomas Ki-ras and c-myc mRNAs were detected by in situ hybridization and sialyl-Le(x) by immunohistochemistry. The moderate to high overexpression of sialyl-Le(x) found in 64% of adenomas and in 89% of carcinomas is a sharply delineated process, closely related to the local stage of tissue transformation. By contrast, the moderate to high overexpression of c-myc mRNA detected in 27% of adenomas and in 78% of carcinomas affects the whole adenomatous or carcinomatous tissue in a homogeneous manner. The Ki-ras mRNA was moderately and homogeneously overexpressed in 18% of adenomas and in 11% of carcinomas, but its expression level did not differ in adenoma and carcinoma of the same specimen. The independence of the three alterations was confirmed in HT-29 cells and its subclones 16.2 and 15.2, in which the relative amounts of total sialyl-Le(x) epitope were 100%: 67%: 38% while the amounts of c-myc mRNA or Ki-ras mRNA determined by Northern blotting did not vary. These data indicate that in human colon the expression of sialyl-Le(x) is independent from c-myc or Ki-ras oncogenes. It occurs more frequently in the early stage of transformation and is more consistently associated with the malignant process than the overexpression of either oncogene.
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PMID:The overexpression of the sialyl-lewis(x) moiety is an independent and a more consistent marker of colon carcinogenesis than the overexpression of C-myc and ki-ras oncogenes. 2156 12