Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recurrence of disease following liver transplantation is emerging as a major area of concern. We retrospectively investigated for evidence of recurrent hepatitis B, hepatitis non-A, non-B (NANB), primary biliary cirrhosis (PBC) and malignancy in 106 transplant patients. Recurrence of hepatitis B was diagnosed in 11 of 14 (79%) patients who survived longer than 2 months posttransplant. The first histologic evidence of recurrence occurred at 4 to 64 weeks posttransplant (mean, 22.2 weeks). In two patients, progression to cirrhosis was documented histologically. Recurrence was diagnosed in three patients transplanted for fulminant hepatic necrosis due to hepatitis B. Administration of hepatitis B vaccine and hepatitis B immunoglobulin was ineffective in preventing recurrence. Recurrence of hepatitis NANB was diagnosed in only two of 23 patients transplanted for hepatitis NANB cirrhosis. Evidence of posttransplant hepatitis was also detected in one of 10 patients transplanted for fulminant hepatitic failure presumably caused by hepatitis NANB. Recurrence of PBC was not diagnosed in any of 15 patients, but the length of follow-up was too limited in most patients to allow definite conclusions to be made. Posttransplant antimitochondrial antibodies titers remained elevated in nine of 11 patients tested. Six of 13 patients transplanted for hepatocellular carcinoma (46%) developed recurrent tumor, and five died. The role of preoperative and postoperative chemotherapy is currently undefined.
 ...
PMID:Disease recurrence following liver transplantation. 210 46

Overexpression of a family of plasma membrane glycoproteins, known as P-glycoproteins, is commonly associated with multidrug resistance in animal cells. In rodents, three multidrug resistance (mdr or pgp) genes have been identified, but only two can confer the multidrug resistance phenotype upon transfection into animal cells. Using the RNase protection method, we demonstrated that the levels of three mdr gene transcripts differ among mouse tissues, confirming a previous report that the expression of these genes is tissue specific (J.M. Croop, M. Raymond, D. Huber, A. DeVault, R. J. Arceci, P. Gros, and D. E. Housman, Mol. Cell. Biol. 9:1346-1350, 1989). The levels of mdr transcripts were determined for mouse liver tumors spontaneously arising in both C3H/HeN and transgenic animals containing the hepatitis B virus envelope gene and for tumors induced by two different carcinogenic regimens in C57BL/6N and B6C3-F1 mice. The mdr3 gene was overexpressed in all 22 tumors tested. Our results demonstrate that overexpression of the mdr3 gene in mouse liver tumors does not require exposure of the animals to carcinogenic agents and suggest that its overexpression is associated with a general pathway of hepatic tumor development. The overexpression of the mdr3 gene, which is the homolog of human mdr1 gene, in hepatocellular carcinomas may be responsible for the poor response of these tumors to cancer chemotherapeutic agents.
 ...
PMID:Overexpression of the multidrug resistance gene mdr3 in spontaneous and chemically induced mouse hepatocellular carcinomas. 212 32

Hepatitis B virus transcripts and DNA from paired samples of neoplastic and nonneoplastic liver tissue of HBsAg seropositive patients were analyzed. The data obtained support the view that transcription of integrated DNA is frequent, both in neoplastic as well as in nonneoplastic liver tissue. In the case of one patient, integrated and free forms of hepatitis B virus DNA were detected in the tumor. Complete cycles of viral replication in this tumor were suggested by the following markers: (i) DNA and RNA intermediates expected to occur during replication of the viral genome, (ii) HBcAg and HBsAg, (iii) core and Dane particles. Viral DNA cloned from tumor tissue was proven to be replication competent in a transient replication assay. Five independent clones of viral DNA were established and found to be closely related at the nucleotide level. A preX open reading frame and a stop codon within preC were common features. In tissue surrounding the tumor, a nonreplicative state of virus infection prevailed, characterized by free viral DNA exclusively of the covalently closed, circular form. The replication of the viral DNA appeared to be blocked at the level of transcription.
 ...
PMID:Replication of hepatitis B virus in a hepatocellular carcinoma. 215 90

The Liver Cancer Study Group of Japan analyzed statistically 12,887 cases of primary liver cancer diagnosed from January 1, 1982 to December 31, 1985 in more than 500 institutes throughout the country. The study was based on the answers to 258 questions. There were 4354 cases of hepatocellular carcinoma, 256 cases of cholangiocellular carcinoma, 49 cases of mixed carcinoma, 22 cases of hepatoblastoma, 10 cases of sarcoma, and 74 other cases. The survey and analysis, based mainly on 4765 histologically proved cases, included gross anatomic and histologic features of the tumors, pathology of the noncancerous portion, distant metastases, past medical history, frequency of positive Hepatitis B surface antigen and Hepatitis B surface antibody, age distribution, various diagnostic procedures, surgical procedures, and survival rate in relation to operative curability and tumor stage.
 ...
PMID:Primary liver cancer in Japan. Clinicopathologic features and results of surgical treatment. 215 91

We assessed the frequency of silent (i.e., clinically asymptomatic) cirrhosis among 305 patients with hepatocellular carcinoma (HCC) and cirrhosis in relation to the patients' country of birth, the cause of the cirrhosis, clinical features, and hepatitis B surface antigen (HBsAg) status. Overall, 56% of the patients had silent cirrhosis, but this occurred significantly more frequently among those born in areas of the world where HCC is common (64% compared with 36%), those who were HBsAg-seropositive (75% compared with 25%), and those who had cryptogenic cirrhosis (71% compared with 29%). Previously recognized ("known") cirrhosis was more common among those from low-incidence areas (52% compared with 36%) and the cause of the cirrhosis was more often alcoholic (44% compared with 10%). The clinical features at the time of presentation with HCC did not differ between the two groups. During the 10-year period of the study (1978 to 1988), 448 patients with HCC were seen (including those without cirrhosis and those in whom the presence or absence of cirrhosis could not be determined). Overall, therefore, cirrhosis was recognized before presentation with tumor in only 30% of the patients. The screening of cirrhotic patients can only have a limited impact on the early detection of HCC.
 ...
PMID:Silent cirrhosis in patients with hepatocellular carcinoma. Implications for screening in high-incidence and low-incidence areas. 215

A mouse monoclonal antibody directed against the protein product of the hepatitis B virus X open reading frame was prepared. This antibody was used to screen liver tissue sections from patients with chronic hepatitis (CH) and patients with liver cell carcinoma (LCC). Reactive antigen was detected by immunohistochemistry in about 30% auf the samples from CH patients and in about 80% of the samples from LCC patients regardless of whether tumor or surrounding nontumor tissue was analyzed. A predominant localization of the antigen in the cytoplasm was observed. In liver sections of CH patients the presence of HBx or HBx-related protein appeared to correlate with the presence of the classical viral antigens HBs- and/or HBcAg. A similar correlation was not found in liver or tumor tissue samples from LCC patients. The occurrence of X-monoclonal-antibody-reactive protein (Xarp) at a low frequency in liver tissue from patients without hepatitis B virus related disease suggests that Xarp in some cases may not be identical with the putative viral X antigen.
 ...
PMID:Mouse monoclonal antibody directed against hepatitis B virus X protein synthesized in Escherichia coli: detection of reactive antigen in liver cell carcinoma and chronic hepatitis. 215 3

Because of the various neoplastic manifestations of human immunodeficiency virus (HIV) and the variable period between HIV infection and the development of tumors related to acquired immunodeficiency syndrome (AIDS), it is possible that certain behaviors, toxins, genes, or infectious agents--particularly viruses--may act as cofactors in the pathogenesis of AIDS-related neoplasms. Most epidemiologic and laboratory investigations of possible cofactors have been directed toward Kaposi's sarcoma (KS), by far the most common AIDS-related tumor and one closely associated with male homosexual lifestyle in the U.S. Nonetheless, epidemiologic investigations of putative associations have not demonstrated any clear association between KS and particular viruses. Furthermore, laboratory investigations, both serologic and molecular/genetic, have failed to definitively implicate as cofactors for KS these viruses: cytomegalovirus, Epstein-Barr virus (EBV), herpes simplex viruses, pathogenic human papillomaviruses, or human herpes virus type 6. Investigations of a suggested association between EBV and AIDS-associated non-Hodgkin's (B cell) lymphomas (NHLs) have also been inconclusive. However, HIV may act as a cofactor in accelerating the development of hepatitis B-associated hepatocellular carcinoma. In summary, viral or other cofactors have not been definitely identified as cofactors in AIDS-related tumors.
 ...
PMID:Possible cofactors for the development of AIDS-related neoplasms. 216 69

Loss of heterozygosity on chromosome 16 is a common genetic alteration in human hepatocellular carcinoma (HCC). To clarify the pathogenetic significance of allele loss on chromosome 16, we performed restriction fragment length polymorphism analysis of 70 surgically resected tumors by using 15 polymorphic DNA markers for chromosome 16. Loss of heterozygosity on chromosome 16 was detected in 36 (52%) of 69 informative cases, and the common region of allele loss in these 36 tumors was located between the HP locus (16q22.1) and the CTRB locus (16q22.3-q23.2). These losses occurred more frequently in HCCs of poor differentiation, of larger size, and with metastasis, whereas they were not detected in HCC at the earliest stage. In addition, these losses were not associated with presence or absence of hepatitis B virus DNA integration or hepatitis C virus infection. These results show that loss of heterozygosity on chromosome 16 is a late event occurring after hepatocarcinogenesis and strongly suggest that this phenomenon is involved in enhancement of tumor aggressiveness during progression of HCC.
 ...
PMID:Allele loss on chromosome 16 associated with progression of human hepatocellular carcinoma. 216 60

One patient with the fibrolamellar variant of hepatocellular carcinoma was found to be seropositive for HBsAg and anti-HBe. DNA from tumor and nontumor areas of the liver was examined by molecular hybridization for hepatitis B virus DNA sequences. Undigested DNA from the tumor gave a high-molecular-weight smear, and restriction-enzyme analysis indicated a single instance of integration. Nontumor liver tissue was analyzed from three separate areas. Hepatitis B virus DNA was detected in two of these; restriction-enzyme digestion suggested they contained different sites of viral integration. As with the typical hepatitis B virus-related hepatocellular carcinoma, analysis of hepatitis B virus DNA from nontumorous liver yielded a different pattern of high-molecular-weight bands, indicating that the virus genome had integrated at different chromosomal locations than that seen in the tumor. The finding of integrated hepatitis B virus DNA, especially in tumorous but also in nontumorous liver, would be consistent with an oncogenic role for hepatitis B virus in certain instances of fibrolamellar tumors and in the more typical hepatitis B virus-related hepatocellular carcinoma.
 ...
PMID:HBV-DNA sequences in tumor and nontumor tissue in a patient with the fibrolamellar variant of hepatocellular carcinoma. 217 Feb 66

We have examined several tumors from South African patients with hepatitis B virus (HBV)-associated hepatocellular carcinoma for the presence of integrated viral DNA. In contrast with our findings in patients from Taiwan, few copies of the viral genome were integrated in each tumor. Furthermore, Southern hybridization showed similarities in integration patterns between different tumors. We are presently constructing genomic libraries from selected single-copy tumors in order to make a more detailed analysis of HBV DNA integration at the molecular level.
 ...
PMID:Hepatitis B virus-associated hepatocellular carcinoma in African patients. 217 68


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>