Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Point-mutational activation of the c-Ki-ras proto-oncogene has been shown to be rare in human hepatocellular carcinoma, the most common primary liver cancer and one usually associated with chronic viral infection. To reveal the association of c-Ki-ras activation with cholangiocarcinogenesis under different etiological backgrounds, the incidence of point mutation at codons 12 and 13 of the c-Ki-ras proto-oncogene was examined in three groups of human liver cancers with differentiation to biliary epithelial cells: Group 1, cholangiocellular carcinoma in Japanese with normal livers; Group 2, cholangiocellular carcinoma in Thais who had lived in an area where the liver fluke Opisthorchis viverrini is endemic; and Group 3, combined hepatocellular-cholangiocellular carcinoma, a rare type showing features of both hepatocellular and biliary epithelial differentiation, in Japanese with chronic viral hepatitis with or without cirrhosis. The polymerase chain reaction and direct sequencing of its product were used to detect the mutation. Point mutation at codon 12 of the c-Ki-ras gene was detected in five (56%) of nine cases in Group 1. In contrast, the mutation was not detected in any of the cases in Groups 2 and 3. Therefore, point-mutational activation of c-Ki-ras did not seem to be involved in the development of primary liver cancers associated with apparent chronic irritation of liver cells or biliary epithelial cells caused by exogenous liver-fluke or viral infection. On the other hand, point-mutational activation of the c-Ki-ras proto-oncogene may be involved in cholangiocarcinogenesis in liver without preexisting liver-fluke or viral infection.
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PMID:Cholangiocarcinomas in Japanese and Thai patients: difference in etiology and incidence of point mutation of the c-Ki-ras proto-oncogene. 133 66

Changes of nucleotide sequences and expressions of cellular oncogenes in human hepatoma cell lines, PLC/PRF/5, HCC-M and HCC-T cells, were examined by Southern and Northern blot analyses. The probes used are DNA fragment of myc, N-, H-, K-ras, fos, fms, raf, erb-A, erb-B, and erb-B2 genes and synthetic oligonucleotides corresponding to the part of N-, H-, K-ras genes. The results are as follows. DNA amplification and rearrangement were not detected in these three human hepatoma cell lines. Point mutations at codons 12, 13, and 61 in N- and K-ras genes were not demonstrated in these cell lines. N-, H-, K-ras and myc transcripts were detected in these three cell lines. However, fos gene transcript was detected only in PLC/PRF/5 and HCC-M cells which were derived from hepatitis B related hepatocellular carcinoma and having integrated hepatitis B virus (HBV) DNA. These data showed that there are no specific proto-oncogene expression into RNA except for myc and ras genes, nor DNA rearrangement in these 3 human hepatoma cell lines with regards to at least 10 different oncogenes examined and suggest the relationship between fos gene expression and integration of HBV DNA in host cell DNA.
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PMID:Proto-oncogene expression in three human hepatoma cell lines, HCC-M, HCC-T and PLC/PRF/5. 166 47

To elucidate the cell biological significance of ras oncogene, the expression of ras-p21 was analyzed in 53 cases of liver tissues including 34 cases of hepatocellular carcinoma (HCC), by using immunohistochemical method. In result, 22 (65%) cases of 34 HCC and 34 (79%) cases of 43 liver cirrhosis were positive for p21, whereas all of chronic hepatitis and normal livers were negative. Especially, comparative study between the expression of p21 and clinicopathological background of HCC revealed that p21 was prominently expressed in well differentiated form, nodular type, small liver cancer, and the cases showing AFP levels below 400 ng/ml. From these results, it was indicated that ras oncogene might play an important role in malignant transformation of hepatocytes or differentiation of HCC.
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PMID:[The expression of ras p21 product in hepatocellular carcinoma]. 170 Jan 76

Pathological diagnosis of hepatic tumors is sometimes difficult when performed with only routine examinations such as Hematoxylin and Eosin (H.E.) stain. The diagnostic usefulness of KM01 was compared to that of alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), CA19-9 and ras p21 in this immunohistochemical study. AFP was positive in about half of the cases of hepatocellular carcinoma and hepatoblastoma, and AFP-positive cells were frequently found at the periphery of acini in both diseases. Absorbed CEA stain was mostly negative in hepatocellular carcinoma, but was positive in the cells of mixed hepatocellular and cholangiocellular carcinoma (MHCC) and metastatic liver cancer, especially in their cytoplasm. CA19-9 immunostaining was completely negative, and was only 3% positive in hepatocellular carcinoma. KM01 stain was positive in about half of the cases of hepatocellular carcinoma, hepatoblastoma and MHCC. It was positive in proliferated bile ducts around the capsule in the former two diseases but positive in the tumor cell of both parts of the cytoplasm in the latter. The histological positivity of ras p21 was high in all tumor cells of these three types of tumors. Negative absorbed CEA and KM01 in pseudoglandular hepatocellular carcinoma differentiated from MHCC and metastatic liver cancer. However these tumor markers were occasionally positive and nonspecific in cancer-like lesions, implying no advantage for differential diagnosis between hepatocellular carcinoma and apparent cancer-like lesions. The above results demonstrate that AFP, CEA and KM01 are effective for differentiating hepatocellular carcinoma among various hepatic tumors.
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PMID:Immunohistochemical study on hepatic tumors--KM01 stains compared with AFP, CEA, CA19-9 and RAS P21. 171 40

Dominant-transforming oncogenes are frequently detected in mouse liver tumors, but are rare or inconsistently detected in rat liver tumors. Most of those that have been identified are members of the ras family. While altered expression of many oncogenes has been reported, an increase in the expression of the c-myc gene is consistently observed in both rat and mouse hepatocellular tumors. Both hepatocytes and liver epithelial cells have been immortalized or transformed with viral or cellular oncogenes. Immortalization of cells occurs without the loss of differentiated functions, while transformation induces the expression of many genes/gene products associated with liver cancer in vivo. Cells transformed with chemical carcinogens or oncogenes display a phenotype of growth factor independence or greatly reduced growth factor requirements. Transformation is frequently associated with a substantial decrease in the expression of the exogenous growth factor receptor in the hepatocellular tumors.
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PMID:Oncogene activation and hepatocarcinogenesis. 222 7

Chinese medicinal herbs with Jian Pi Li Qi action were tested for their effects in inhibiting the precancerous lesions, gamma-GT positive hepatocellular foci and the expression of oncogenes (N-ras, Ha-ras) in male SD rats. The rats were given one i.p. dose of initiator DEN within 24 hours after 2/3 partial hepatectomy. The livers of sacrificed rats were processed to gamma-GT histochemical staining and measuring of oncogenic expression. The results of these two parameters showed that Chinese medicinal herbs with Jian Pi Li Qi action are effective in inhibiting the precursory lesions of liver cancer in rats.
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PMID:[Inhibitory effects of jian pi li qi Chinese medicinal herbs on diethylnitrosamine (DEN)-induced hepatocarcinogenesis in rats]. 267 88

The transfection of NIH 3T3 cells was performed with DNAs from 2 duck primary hepatic carcinomas (DHC 40K, 9K) and 1 tumor-adjacent liver tissue (TAL, 9N). Transfectants were found from 40K, 9K and 9N DNAs. The secondary transfectants were obtained after transfection of RAT-1 cells with DNAs from primary transfectants. After hybridization with Ha-ras, Ki-ras, N-ras and mht oncogenes, it was found that duck mht (5.2 and 3.2 kb EcoRI fragments) and duck Ha-ras (3.4 kb EcoRI fragments) were present in all these transformants. This is the first report on transforming genes in duck primary hepatic cancer as well as tumor-adjacent liver tissue.
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PMID:Transforming genes in duck hepatic carcinoma--mht(raf) and Ha-ras. 285 57

Poly(A)+ RNA was isolated from 9 specimens of human primary hepatic carcinoma, 1 non-tumorous liver tissue adjacent to cancer and 1 normal liver tissue samples. The Oligo-dT cellulose-purified poly(A)+ RNAs were subjected to formaldehyde agarose gel electrophoresis, Northern transfer and hybridization with various oncogene probes. Two RNA species, 5.6 kb and 2.2 kb were identified by N-ras gene hybridization in 6 out of 9 mRNA samples from primary hepatic carcinoma specimen. N-ras specific mRNA was not detectable in mRNA samples from normal human liver and tumor surrounding cirrhotic tissue. No detectable hybridization of mRNA from hepatoma and normal liver with Ki-ras or Ha-ras was observed. As human N-ras gene has been identified in DNA of mouse transfectants transformed with PHC DNA, it strongly suggests that N-ras gene might be responsible for the transforming activity of part of cases of human liver cancer.
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PMID:Expression of N-ras gene in human primary hepatocarcinoma. 301 23

Using the human liver cancer DNA transfected NIH/3T3 cell line, the human N-ras oncogene and the over expression of the oncoprotein P21ras was demonstrated, BALB/C mice were immunized. The spleen cells from the immunized mice were fused with SP2/0 myeloma cells. After the HAT medium selection and screening, two hybridoma cell lines, SCI-Oncogema 1 and 2, were established. In the immunoprecipitation test, the molecular weight of the protein reacting to Oncogema 1 was 21,000. This M.W 21,000 protein possessed the capability to bind with GTP, i.e. the character of P21ras. These data indicate that the Oncogema 1 is the monoclonal antibody against P21ras. Using Oncogema 1, specimens from 6 liver cancer patients were studied by immunopathology. With ABC stain, it was observed that the malignant cells in all the samples showed dark staining; the P21ras revealed over expression. Although the staining was heterogeneous, it implied that the ras oncogene was involved in the carcinogenesis of these six samples. No over expression was seen in the normal liver cells even in those around the cancerous lesion. However, dysplastic cells were moderately stained which means that the ras oncogene was activated and P21ras over expressed in these cells. The results suggest that the ras oncogene and P21ras play an important role in the early stage of liver cancer carcinogenesis.
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PMID:[Localization of oncoprotein P21ras in the human liver cancer]. 330 83

Clinical evidence suggests that hepatitis C virus (HCV) is etiologically involved in hepatic cancer and liver cirrhosis. To investigate whether the HCV nonstructural protein NS3 has oncogenic activity, NIH 3T3 cells were transfected with an expression vector containing cDNA for the 5'- or 3'-half sequence of the HCV genome segment encoding NS3. Only cells transfected with the 5'-half cDNA rapidly proliferated, lost contact inhibition, grew anchorage independently in soft agar, and formed tumors in nude mice. PCR analysis confirmed the presence of the 5'-half DNA in the transfectants. These results suggest that the 5' region of the HCV genome segment encoding NS3 is involved in cell transformation.
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PMID:Hepatitis C virus nonstructural protein NS3 transforms NIH 3T3 cells. 774 41


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