Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cholangiocarcinoma is a low-prevalence neoplasia, but represents a great medical challenge in its diagnosis and treatment because of its insidious clinical manifestations. Its cellular origin has been associated to other hepatic tumors, and to multiple congenital or acquired factors (infections, drugs and other diseases). The most frequent histological type is the adenocarcinoma and the most common localization is the choledochal duct; local metastases are frequently found in autopsies. The usual clinical findings are pruritus, weight loss, anorexia, jaundice and hepatomegaly. The immunohistochemical advances related to oncogenes (ras & C-erb B-1) and tumor markers (Epidermal Growth Factor and Integrin among others) allow to make differential diagnosis with other hepatic cancers and will provide valuable information about its cell biology. The initial approach to patients with this disease is made by ultrasound (US), which can be associate to Doppler; Computed Axial Tomography and Nuclear Magnetic Resonance have similar sensitivity and specificity, so they are preferred to US in the elderly with history of weight loss. It's better to perform Percutaneous Transhepatic Cholangiography than Endoscopic Retrogrado Pancreatocholangiography when its possible because the first permits a comprehensive visualization of the biliary tree. The treatment includes resection and endoprosthesis placement. The combination of surgery, Chemotherapy and Radiotherapy allows to achieve the best survival rates, and opens a door to new strategies related to this malignancy.
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PMID:[Cholangiocarcinoma]. 856 79

A transgenic mouse line (Tg.AC) carrying an activated v-Ha-ras oncogene fused to the embryonic zeta-globin promoter develops an array of spontaneous epithelial and mesenchymal neoplasms. In this report we describe the morphological, immunophenotypic, and molecular features of a unique hematopoietic neoplasm in these mice. The cardinal lesion of this disease is marked hepatomegaly due to leukemic proliferation and infiltration. In the peripheral blood, there is a marked increase in the number of metarubricytes and other less differentiated erythroid progenitor cells. Leukemic cells stain positively with an erythroid-associated nuclear transcription factor (GATA-1). Using a reverse transcription polymerase chain reaction assay, co-expression of GATA-1 and endogenous zeta-globin genes is detected in hematopoietic tissues of nonleukemic transgenic and nontransgenic mice. ras transgene expression is, however, detected only in normal bone marrow and leukemic tissues of transgenic mice, and 5' mapping experiments using S1 protection analysis of total RNA from leukemic tissue indicates that transcription of the transgene mRNA is initiated from the natural zeta-globin promoter start site, supporting the belief that the zeta-globin promoter directs v-Ha-ras expression in erythroid progenitor cells, ultimately leading to leukemic transformation.
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PMID:Association of v-Ha-ras transgene expression with development of erythroleukemia in Tg.AC transgenic mice. 966 85

This retrospective study was carried out in the "Medecine Infantile 3 et Genetique" service at Brabois University Hospital in Nancy (France). We collected 14 cases of chronic hepatitis C following perinatal infection via mother to child transmission (group 1: 5 cases) and blood transfusion (group 2: 9 cases). The mean age of patients at the time of first serological screening test was 9.1+/-4.7 years. In 12 cases, the screening test was performed in view of the mother seropositivity or a personal history of perinatal blood transfusion. Only two patients presented with hepatomegaly. ELISA3 test was positive in all patients. With RIBA3 test, antibody to hepatitis C core antigen was absent in one patient while antibody anti-NS3 was present in all of the cases. The mean level of serum transaminase SGPT was 1.9+/-0.9 N in group 1 patients (mother to child transmission) versus 1.4+/-0.7 N in group 2 patients (blood transfusion). In 9 cases out of 14, hepatocytolysis was variable with SGPT levels around 2 N. Total mean Knodell was 3+/-4.1 in the group 1 versus 4.6 + 2.6 in group 2. Using the Metavir score, the mean activity was found to be 0.5+/-0.1 in group 1 versus 1+/-0.6 in group 2, while the mean level of fibrosis in the two groups was 0.3+/-0.5 and 0.7+/-0.1 respectively. On the whole, this study shows that chronic hepatitis C following perinatal infection is commonly asymptomatic, with mild histological changes not relating to the level of hepatocytolysis.
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PMID:[Chronic hepatitis C in children after perinatal infection]. 1577 49