Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three of 42 (7%) monkeys given aflatoxin B1 (AFB1) for longer than 2 years have developed primary malignant neoplasms of the liver. Liver biopsies performed at intervals during aflatoxin administration revealed that neoplasia was preceded by pathologic lesions of the liver, including toxic hepatitis, proliferation of pseudotubules, and hyperplastic nodules. Serum alpha-fetoprotein levels, monitored in one of the monkeys by radioimmunoassay, paralleled tumor growth and recurrence of the hepatocellular carcinoma. Normal serum alpha-fetoprotein levels were noted for a monkey with hemangioendothelial sarcoma. Our results implicate AFB1 as a liver carcinogen in monkeys and add additional support to the hypothesis that humans exposed to this substance may be at risk of developing liver cancer.
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PMID:Carcinogenicity of aflatoxin B1 in rhesus monkeys: two additional cases of primary liver cancer. 6 57

Serum alpha 1 antitrypsin, alpha 1 acid glycoprotein and beta 2 glycoprotein I concentrations were determined in 36 patients with malignant hepatocellularcarcinoma, 30 with cirrhosis and 35 with hepatitis by quantitative immunoelectrophoresis. Serum alpha 1 antitrypsin and alpha 1 acid glycoprotein levels were significantly higher in patients with hepatocellularcarcinoma than in those with cirrhosis (p less than 0.001) or hepatitis (p less than 0.001). Elevated levels of alpha 1 antitrypsin were found in 88.9% of patients with hepatoma compared to 23.3% of patients with cirrhosis and 28.6% of patients with hepatitis. Raised levels of alpha 1 acid glycoprotein were also found in 80.6% of patients with hepatoma compared to 20% of patients with cirrhosis and in only 5.7% of patients with hepatitis. beta 2 glycoprotein I levels were similar in the three conditions and therefore not useful for differential diagnosis. In monitoring the progress of tumor growth alpha 1 antitrypsin and alpha 1 acid glycoprotein levels were found to increase during the growth phase. Measurements of these two glycoproteins are suggested for differential diagnosis of these liver diseases, as tumor markers for the detection of hepatocarcinoma, and for the monitoring of the progress during treatment.
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PMID:Changes in serum alpha 1 antitrypsin, alpha1 acid glycoprotein and beta 2 glycoprotein I in patients with malignant hepatocellular carcinoma. 8 7

The growth characteristics and histological appearance of tumors resulting from transplantation of the tumor lines HEp-2 and SW480 into pathogen-free and mouse hepatitis virus infected athymic mice were studied. Subcutaneous or intraperitoneal implantation 1 x 10(6) neoplastic cells into pathogen-free animals resulted in tumor growth. Subcutaneous transplants grew locally, surrounded by a capsule of connective tissue. The fibrovascular stroma supporting the neoplastic tissue was minimal and infiltration of tumor capsule was observed. Intraperitoneal tumors grew in a multifocal pattern, were not encapsulated, showed marked invasiveness and metastasized. The same number of neoplastic cells (1 x 10(6)) transplanted into hepatitis-positive animals failed to develop into grossly visible tumors. When the number of transplanted cells was increased to 2 x 10(7), tumors appeared in a few animals. All tumors, regardless of the site of transplantation, were characterized by the presence of severe fibrohistiocytic reaction at the site of implantation that possibily influenced the tumor growth. No evidence supporting T-cell-mediated tumor rejection was observed. It is concluded that the state of health of the athymic mice is critical for the growth of human tumors and may account for the variations in reporting successful transplantation of such tumors in nude mice.
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PMID:Influence of the mouse hepatitis virus (MHV) infection on the growth of human tumors in the athymic mouse. 43 22

Hepatoblastoma differs from the adult type of hepatoma in clinical and pathologic features. The ratio of fucosylation of serum alpha-fetoprotein (AFP) was determined in seven patients with hepatoblastoma and in 21 infants and children with otherwise elevated serum AFP, using the improved technique of lentil agglutinin-affinity immunoelectrophoresis. The clinical data for the seven patients with hepatoblastoma were also reviewed. The ratio of fucosylation of AFP was significantly higher in all seven patients with hepatoblastoma, whereas it was minimal in all other cases of benign hepatic conditions such as neonatal hepatitis or biliary atresia, as well as in normal newborns. The ratio of fucosylation in hepatoblastoma, however, definitely decreased with the age of the patient at presentation. This finding suggests a correlation between fucosylation and a rapid rate of tumor growth, because all hepatoblastomas are believed to originate early in fetal life.
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PMID:The ratio of fucosylation of alpha-fetoprotein in hepatoblastoma. 247 Apr 90

Experimental procedures are described for the radiolocalization of human tumors by murine monoclonal antibodies (MAb) in animal model systems. Visualization of tumor xenografts was clearer in nude mice as compared to experimentally immunosuppressed mice due to the higher viability of the tumors in nude mice. MAb localization in tumor tissue was greatly enhanced when F(ab')2 fragments rather than intact antibody molecules were used. Although tumors could be visualized with either 131I-, 123I- or 111In-labeled MAb fragments without using background subtraction, tumor-to-background ratios of radioactivity were highest for 131I-labeled fragments. 131I-labeled F(ab')2 fragments of eight MAb against human colorectal carcinoma, melanoma or lung carcinoma localized specifically only in those tumors that bound the MAb in vitro and not in unrelated tumors. Radiolabeled fragments of MAb with other specificities (anti-hepatitis virus MAb) did not localize in tumors. All MAb that inhibited tumor growth in nude mice effectively localized these tumors by gamma-scintigraphy. On the other hand, some MAb were effective in localizing tumors but ineffective in inhibiting their growth. The ability of the specific radiolabeled F(ab')2 fragments to localize in tumor grafts correlated significantly with MAb binding affinity and density of antigenic sites on tumor cells together, but not with either in vitro binding parameter alone. Thus, Scatchard analysis of MAb binding to tumor cells may be an effective means to screen for MAb with tumor radiolocalization potential.
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PMID:Radioimmunodetection of human tumor xenografts by monoclonal antibody F(ab')2 fragments. 379 94

The results of nonspecific immunotherapy with BCG vaccine in 98 cases of melanoma, breast cancer and other malignancies were used in evaluating the frequency and degree of side-effects and complications arising in cancer patients during this treatment. The procedure proved to be safe irrespective of patients' age. Prevention and treatment of side-effects such as fever, water-salt disorders, anorexia, interstitial hepatitis and promotion of tumor growth are discussed.
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PMID:[Treatment of the complications occurring in BCG vaccine immunotherapy of patients with malignant neoplasms]. 646 96

131I-labeled F(ab')2 fragments of murine monoclonal antibody (MAb) 425 specific to the epidermal growth factor receptor expressed on human gliomas were used in experimental human malignant glioma immunotherapy. Two injections of 150 microCi 131I-labeled 425 F(ab')2 achieved growth inhibition of U-87MG human malignant glioma xenografts in nude mice. This radiolabeled specific MAb F(ab')2 was significantly superior to radiolabeled fragments of an anti-hepatitis virus control MAb A5C3 in influencing tumor growth. However, similar treatment of established human malignant glioma xenografts did not inhibit progressive tumor growth significantly. No clear tumor inhibition was produced by unlabeled MAb 425 F(ab')2. These studies suggest that 131I-labeled MAbs have a significant antitumor effect where unmodified antibody is ineffective. Multiple doses of antibody may achieve an increase in labeled MAb concentration in tumors.
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PMID:Experimental radioimmunotherapy of a xenografted human glioma using 131I-labeled monoclonal antibody to epidermal growth factor receptor. 750 99

Biliary glycoproteins (BGPs) are members of the carcinoembryonic antigen (CEA) family. These glycoproteins function in vitro as intercellular adhesion molecules and, in vitro as intercellular adhesion molecules and, in the mouse, serve as receptors for the mouse hepatitis viruses. In previous studies, BGP expression has been reported to be generally downregulated in colon and liver carcinomas of human, rat and mouse origins. We now demonstrate that introduction of murine Bgp1 cDNA isoforms into a mouse colonic carcinoma cell line, negative for endogenous Bgpl expression, significantly alters the growth properties of these cells. Cells bearing two Bgp1 isoforms were growth-retarded and exhibited a reduced ability to form colonies in an in vitro transformation assay, when compared to parental or control neor cells. Furthermore, tumor formation was inhibited by 80% when cells bearing a full-length Bgp1 isoform were injected into BALB/c syngeneic mice, while cells expressing a Bgp1 isoform lacking most of the intracytoplasmic domain produced tumors as readily as the parental cells. There results indicate that a biliary glycoprotein isoform is involved in negative regulation of colonic tumor cell growth, by a process which requires its intracytoplasmic domain. The precise mechanisms causing Bgp-dependent tumor growth inhibition remain, however, to be defined.
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PMID:Inhibition of colonic tumor cell growth by biliary glycoprotein. 857 Jan 89

Surgical resection has been the standard approach for primary and metastatic liver tumors. Long-term survival, however, is limited because of recurrence or hepatic decompensation. Failure of chemotherapeutic regimens or liver transplantation (OLT) to prevent recurrence has resulted in the need for multimodality therapies. We report our experience with preoperative hepatic arterial chemoembolization (CET) followed by OLT in highly select patients. Over a 33-month period, 23 of 41 patients (56%) referred with primary (n = 16) or metastatic neuroendocrine (n = 7) liver tumors met eligibility requirements. Despite mild, self-limited chemical hepatitis, CET was well tolerated in all but three elderly patients who succumbed to liver failure. Four of five patients ultimately received OLT. Three are alive and free of disease at a mean followup of 17 months, one died of recurrent hepatocellular carcinoma, and one (NET) remains well at 33 months with elevated glucagon levels but no measurable disease. All NET patients are alive with resolution of hormonal symptoms. Four of five noncirrhotic patients died of disease, and one has progressive tumor growth. Although OLT following CET achieves superior survival, its application is limited to a minority of patients with such tumors. Careful pretreatment staging and patient selection combined with caution in the use of CET in elderly cirrhotic patients is critical to the success of such therapies.
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PMID:Intrahepatic arterial chemoembolization for hepatocellular carcinoma and metastatic neuroendocrine tumors in the era of liver transplantation. 875 63

Histamine is a classical, but still interesting inflammatory mediator. Many people have long believed that histamine is derived from mast cells or basophils alone. However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF). HDC is induced even in mast-cell-deficient mice. The histamine newly formed via the induction of HDC is released immediately and may be involved in a variety of immune responses. Reviewing our work and that of Schayer and Kahlson, the pioneers in this field, lead us to the conclusion that nowadays we need to understand that histamine can be produced via the induction of HDC by a mechanism coupled with the cytokine network. We call this histamine "neohistamine", to distinguish it from the classical histamine derived from mast cells or basophils. Neohistamine is involved in physiological reactions, inflammation, immune responses and a variety of diseases such as periodontitis, muscle fatigue (or temporomandibular disorders), stress- or drug-induced gastric ulcers, rheumatoid arthritis, complications in diabetes, hepatitis, allograft rejection, allergic reactions, tumor growth, and inflammatory side effects of aminobisphosphonates.
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PMID:[Induction of histidine decarboxylase in inflammation and immune responses]. 1149 27


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