Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of nine oncogenes (c-myc, N-myc, N-ras, H-ras, k-ras, abl, fos, src, and raf) and two tumor suppressor genes (p53 and RB) were studied by northern blot hybridization in six human hepatocellular carcinoma or hepatoblastoma cell lines (PLC/PRF/5, Hep3B, Hep G2, 2.2.15, HLE, and HLF) and in a human embryonic lung fibroblast cell line (WI-38) to look for differences that might be associated with the presence (PLC/PRF/5, Hep3B, and 2.2.15) or absence (Hep G2, HLE, and HLF) of integrated hepatitis B virus (HBV) DNA. The levels of expression of the oncogenes and tumor suppressor genes were unrelated to the presence or absence of integrated HBV-DNA. Furthermore, the intensity of expression of these oncogenes was no greater in the 2.2.15 cell line (consisting of Hep G2 cells transfected with hepatitis B virus) than in untransfected Hep G2 cells.
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PMID:Expression of oncogenes and tumor suppressor genes in human hepatocellular carcinoma and hepatoblastoma cell lines. 133 79

The expression of oncogene N-ras mRNA and c-myc mRNA in paraffin embedded liver tissues from patients with hepatitis B virus (HBV) infection had been studied by in situ hybridization with biotin labeled probes. The results showed that the detection rates of N-ras mRNA and c-myc mRNA were 37.5% (24/64) and 29.7% (19/64) respectively in the liver tissues of 64 hepatitis B patients, 44.4% (16/36) and 47.2% (17/36) respectively in the liver tissues of 36 hepatocellular carcinoma (HCC) patients with HBV infection, and they were detected each in one of 6 normal liver tissue samples. No significant differences were observed among the three groups (P > 0.05). However, in HCC group, 11 out of 36 patients (30.5%) were positive for N-ras mRNA and c-myc mRNA simultaneously, which was higher than that in hepatitis B group (14.1%) (P < 0.05). None of the normal liver samples were N-ras mRNA and c-myc mRNA positive simultaneously. Further more, in the hepatitis group it was noticed that the detection rate of c-myc mRNA in HBV DNA positive cases (by in situ hybridization) was significantly higher than that in HBV DNA negative cases (P < 0.025).
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PMID:[Study on the expression of oncogenes in hepatocytes with hepatitis B virus infection]. 133 70

30 cases of hepatocellular carcinoma and pericancerous nontumor samples were studied by examining the serial sections for immunohistochemical detection of P21 product accompanying identification of N-ras mRNA by in situ hybridization with biotinylated N-ras cDNA probe and a significant correlation was noticed between the results obtained (P less than 0.02). It was suggested that immunohistochemical detection of ras oncogene P21 product may indicate the expression of ras oncogene. The higher expression of N-ras mRNA of the carcinoma and the non-tumor tissue peripheral to the cancer by in situ hybridization were 53.33% and 28.57% respectively. The positive ratio of P21 were 96.67% and 90.48%.
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PMID:[A comparison study of immunohistochemical detection of ras P21 and N-ras mRNA in situ hybridization in hepatocellular carcinoma and pericancerous nontumor liver tissue]. 164 55

A comparative study on HBV status and ets-2, IGF-II, C-myc and N-ras expression in 12 pairs of human primary hepatocellular carcinoma (PHC) and adjacent non-tumorous tissues (NT) showed that integrated forms of HBV DNA were present in 91.5% PHC and 75% NT. No specific integration sites were detected. Three PHC and 4 NT were found to have free forms of HBV DNA, which were defective in 2 PHC and 3 NT, i. e., being able to replicate but not to be secreted into the blood. At least one of four oncogenes studied was overexpressed in the 12 pairs of samples. IGF-II was expressed as 5.0 and 2.0 Kb fetal transcripts in 3 pairs of samples and 1 NT. Six NT had more than one of the four oncogenes that was expressed higher than PHC. This was commonly encountered in tissues with free forms of HBV DNA. The relation between HBV status, expression of ets-2, IGF-II, C-myc and N-ras and carcinogenesis of PHC is discussed.
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PMID:[HBV status and expression of ets-2, IGF-II, C-myc and N-ras in human hepatocellular carcinoma and adjacent nontumorous tissues--a comparative study]. 165 92

In situ hybridization revealed an apparently higher expression of N-ras and c-fos in human hepatoma than in its adjacent liver tissue. When the isolated nuclei were partially digested with micrococcal nuclease followed by DNA extraction, gel electrophoresis and hybridization with labelled probes, it was shown that in hepatoma the c-fos and N-ras DNA sequences were mainly distributed on the nucleosomes of lower order structures, while these gene sequences in the adjacent liver tissue were found mainly on the nucleosomes of higher order structures. These results clearly indicate a close correlation between gene expression and chromatin conformation of c-fos and N-ras.
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PMID:Correlation between gene expression and chromatin conformation of c-fos and N-ras in human liver and hepatoma. 166 52

LEC (Long-Evans with a cinnamon-like coat color) rats develop hepatocellular carcinomas (HCCs) spontaneously. We examined mutations of codons 12, 13, and 61 of the Ha-ras, Ki-ras, and N-ras genes in four HCCs by the polymerase chain reaction (PCR)-single-stranded DNA direct sequencing method. No ras gene mutations were observed, suggesting that ras activation is not involved in spontaneous hepatocarcinogenesis in LEC rats. The expression of mRNAs for c-myc, Ha-ras, c-raf, and the protein phosphatase 2A alpha gene (PP-2A alpha) was also examined in the four HCCs by northern blot analysis. Three of the four HCCs had c-myc expression levels approximately 30-fold higher than that in the liver of control Long-Evans rats with an agouti coat color (LEA), a sibling line of LEC rats, while the remaining HCC had an expression level sevenfold higher than that of control. In contrast, the expression levels of the Ha-ras, c-raf, and PP-2A alpha genes were the same as those in the livers of control rats. Studies of c-myc expression and mitotic index in five other HCCs, two hyperplastic nodules, and two nontumorous portions of livers of HCC-bearing LEC rats that had chronic-phase hepatitis suggested that the high level of c-myc gene expression was not due only to increased cell proliferation but might possibly be more integrally involved in hepatocarcinogenesis.
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PMID:Possible involvement of c-myc but not ras genes in hepatocellular carcinomas developing after spontaneous hepatitis in LEC rats. 171 40

With dot blot and cytoplasmic hybridization techniques we found that the c-Ha-ras, c-Ki-ras, c-N-ras, c-myc and c-fos oncogenes were over-expressed in human hepatocellular carcinoma cell line BEL 7402 cells. The mRNA expression of c-Ha-ras, c-Ki-ras, c-N-ras and c-myc oncogenes could be inhibited by 2 mmol/L sodium butyrate treatment, but this had no effect on the expression of c-fos. However, the mRNA expression of c-Ha-ras, c-N-Ras and c-myc oncogenes was enhanced by 4 mmol/L sodium butyrate treatment, while the expression of c-Ki-ras and c-fos remained unchanged. No significant effect on the expression of carbamyl phosphate synthetase I, a tissue-specific enzyme associated with the differentiation of liver cells, was observed by 2 mmol/L or 4 mmol/L sodium butyrate treatment of the hepatoma cells.
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PMID:[Expression of cellular oncogenes in human hepatocellular carcinoma cell line BEL 7402 and the effect of sodium butyrate on the expression of cellular oncogenes]. 196 12

We have studied the expressions of nine proto-oncogenes (c-myc, N-myc, c-fos, C-jun, p53, H-ras, N-ras, c-raf, hst) and two other genes (PCNA, GST-P) during the spontaneous development of hepatocellular carcinomas (HCCs) in LEC rats. Expression of c-myc, H-ras, N-ras, C-raf, p53 and PCNA genes was detected, but this did not significantly change during the development of HCCs in LEC rats. Expression of N-myc and hst genes was not detectable. Expression of c-fos gene was detected in one HCC case out of four. Significantly increased expression of c-jun gene was observed in the liver tissues of LEC rats aged 8 months. This high expression was decreased with the development of HCCs. On the other hand, the expression of GST-P gene increased in parallel with the clinical course of the development of HCCs in LEC rats. The pattern of c-jun mRNA augmentation was different from that of GST-P mRNA. These observations suggest that c-jun gene may play a role in the spontaneous development of HCCs in LEC rats.
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PMID:Increased expression of c-jun gene during spontaneous hepatocarcinogenesis in LEC rats. 197 34

The C57BL/6 x C3H F1 (hereafter called B6C3F1) mouse is an important animal model for long-term carcinogenesis studies. Maintained under normal laboratory conditions, these mice develop various types of spontaneous tumors during their lifetime. Activated Ha-ras genes have been detected in 66% of spontaneous hepatocellular tumors in the B6C3F1 mouse [Reynolds et al., Science (Washington DC), 237:1309, 1988]. In this study 49 spontaneous non-liver tumors were investigated for oncogene activation by DNA transfection techniques. Of the 49 tumor DNAs analyzed, only 5 yielded multiple foci in the NIH 3T3 focus assay: 2 of 10 pulmonary adenocarcinomas; 0 of 25 lymphomas; 2 of 2 Harderian gland adenomas; 0 of 1 adenocarcinoma of the small intestine; 1 of 6 malignant skin tumors; 0 of 4 hemangiosarcomas; and 0 of 1 lung metastasis of a hepatocellular carcinoma. DNA from six lymphomas which were negative in the NIH 3T3 focus assay were further analyzed for transforming genes by the nude mouse tumorigenicity assay. One of the five lymphomas tested positive with this assay. Southern blot analysis identified five activated ras genes: H-ras in two Harderian gland adenomas; K-ras in one pulmonary adenocarcinoma and in one s.c. adenocarcinoma; and N-ras in one lymphoma. The mutations involved were CG to AT and AT to TA in codon 61 of the Ha-ras genes, GC to AT or TA in codon 12 of the K-ras genes, and a GC to AT mutation in codon 12 of the N-ras gene. Transformant DNA from a pulmonary adenocarcinoma which yielded multiple foci in the transfection assay did not hybridize to DNA probes specific for the K-, H-, and N-ras, raf, neu, and met genes. Thirteen additional tumor DNAs yielded a single focus in the NIH 3T3 transfection assay. The transformant DNAs retransmitted in a second cycle transfection assay. Rearranged and/or amplified raf genes were detected in six of the transformant DNAs. At present we do not know whether these activated raf genes were present in the original tumor DNA. The other seven transformant DNAs did not hybridize with any of the above mentioned specific DNA probes utilized in Southern blot analysis. Unlike liver tumors, the activation of ras protooncogenes is not a frequent event in the development of spontaneous non-liver tumors of the B6C3F1 mouse. The results from this study should aid in understanding the neoplastic development associated with exposure to chemical carcinogens in the B6C3F1 mouse.
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PMID:Activation of protooncogenes in spontaneously occurring non-liver tumors from C57BL/6 x C3H F1 mice. 199 58

With RNA-DNA hybridization techniques, the mRNA expression of c-Ha-ras, c-Ki-ras, N-ras, and c-fos oncogenes in rat liver with neoplastic nodules or hepatocellular carcinoma induced by DENA was found to be higher than that in normal liver. No significant difference of c-myc expression was observed between normal liver and liver with neoplastic nodules or hepatocellular carcinoma. In the initiation stage of hepatocarcinogenesis in DENA+AAF+PH+PB and AAF+PH+PB model systems, the expression of c-myc increased markedly, and that of N-ras was remarkably stimulated under the action of AAF. It appears that a cooperative action between the c-myc and N-ras oncogenes was involved in the initiation of hepatocarcinogenesis. In the promotion stage, the expression of c-myc and N-ras returned to a normal level. The expression of c-fos decreased progressively in both the initiation and promotion stages, while that of c-Ha-ras and c-Ki-ras was not much changed. The significance of these results is briefly discussed.
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PMID:[Expression of cellular oncogenes during hepatocarcinogenesis in rats]. 214 11


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