Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the differential display method to analyze mRNA expression in hepatocellular carcinoma (HCC) and nontumor livers, we cloned a full-length cDNA of 2263 bp, which was designated GTR2-2 and was identical with MXR7. The MXR7 mRNA was detected in 143 of 191 (74.8%) primary and recurrent HCCs taken from 154 patients but only in 5 (3.2%) nontumor livers. MXR7 mRNA was detected in one of two hepatoblastomas but not in hepatocellular adenoma, cholangiocarcinoma, or metastatic carcinomas to the liver. In human cancer of other anatomical sites, MXR7 mRNA was detected in low levels in one Wilms' tumor and in 4 of 40 gastric adenocarcinomas but not in several other types of cancer and 21 nonhepatocellular human tumor cell lines examined. MXR7 mRNA was expressed in high levels in the placenta, fetal liver, lung, and kidney, but it was undetectable in adult liver and was expressed in very low levels in adult lung and kidney. Our observations suggest that the MXR7 gene is regulated developmentally and expressed preferentially in HCC. To study its potential biological significance, we selected 113 patients who had unicentric primary HCC and had been followed for more than 4 years for further analysis. The MXR7 mRNA expression correlated closely with elevated serum alpha-fetoprotein (AFP) levels (88 versus 55%; P = 0.0001) and with expression of AFP mRNA (87 versus 55%; P = 0.005) and CD24 mRNA in HCC (80 versus 50%; P < 0.04), high tumor grade (76 versus 56%; P = 0.05), and tumor invasion (76 versus 55%; P < 0.05), but not with patient outcome. In HCC < or =3 cm, the frequency (77%) of MXR7 mRNA expression was significantly higher than that of elevated serum AFP (43%; P < 0.007) and AFP mRNA expression in HCC (41%; P < 0.004). Thus, MXR7 may serve as a sensitive early tumor marker for HCC and warrants more study to better understand its biological function.
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PMID:Cloning and expression of a developmentally regulated transcript MXR7 in hepatocellular carcinoma: biological significance and temporospatial distribution. 937 21

Hepatic (hepatocellular) adenoma of the placenta is an extremely rare nontrophoblastic placental lesion of disputed histogenesis, four examples of which were diagnosed over a 10-year period. The lesions, which were incidental findings in women 21 to 30 years of age (mean, 25; median, 24.5), ranged from 0.3 to 1.0 cm in greatest dimension. Two were found within the villous parenchyma and two in subchronic locations. On cross section, two examples were tan to dark red nodules without necrosis or hemorrhagic foci, whereas two were not visible grossly. The lesions were composed of semidistinct lobules of cords and nests of polygonal epithelial cells resembling fetal liver. Extramedullary hematopoiesis was a constant feature. The lesional cells contained glycogen and were immunoreactive for cytokeratin, alpha-fetoprotein, alpha-1-antitrypsin, and carcinoembryonic antigen. Although the histogenesis of these lesions remains uncertain, an origin from displaced yolk sac elements with hepatocytic differentiation is the most likely hypothesis. It is important to distinguish hepatic adenoma of the placenta from placental cell island, heterotopic adrenocortical nodule, chorangioma, and placental metastasis of maternal and fetal malignancies.
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PMID:Hepatic (hepatocellular) adenoma of the placenta: a study of four cases. 965 20

Fibrolamellar carcinoma is a malignant hepatocellular tumor with distinct clinical and pathologic differences from hepatocellular carcinoma. It differs from hepatocellular carcinoma in demographics, condition of the affected liver, tumor markers, and prognosis. Fibrolamellar carcinoma characteristically manifests as a large hepatic mass in adolescents or young adults (without gender predominance). Cirrhosis; elevated alpha-fetoprotein levels; and typical risk factors for hepatocellular carcinoma such as viral hepatitis, alcohol abuse, and metabolic disease are typically absent. Fibrolamellar carcinoma is characterized pathologically by cords of tumor cells surrounded by abundant collagenous fibrous tissue arranged in a parallel or lamellar distribution. Fibrotic lamellae often coalesce to form a central scar. Fibrolamellar carcinoma characteristically appears on radiologic images as a lobulated heterogeneous mass with a central scar in an otherwise normal liver. Radiologic evidence of cirrhosis, vascular invasion, or multifocal disease--findings typical of hepatocellular carcinoma--is uncommon in fibrolamellar carcinoma. Imaging features of fibrolamellar carcinoma overlap with those of other scar-producing lesions including focal nodular hyperplasia (FNH), hepatocellular adenoma and carcinoma, hemangioma, metastases, and cholangiocarcinoma. FNH, in particular, may simulate fibrolamellar carcinoma, since both have similar demographic and clinical characteristics. Because some believe that radiologic diagnosis of FNH is possible, it is important to understand the imaging appearance of fibrolamellar carcinoma to avoid misdiagnosing this malignant tumor as a FNH.
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PMID:Fibrolamellar carcinoma of the liver: radiologic-pathologic correlation. 1019 90

The only hope of long-term survival for patients with hepatocellular carcinoma (HCC) is surgical resection or liver transplantation. However, recurrence or metastasis formation is common after surgery. We aim to assess whether surgical resection leads to hematogenous dissemination of malignant and nontumor hepatocytes and determine the quantity and timing of hepatocyte shedding into the circulation. Using semiquantitative reverse transcription-PCR for alpha-fetoprotein (afp) and albumin (alb) mRNAs, we measured the mass of malignant and nontumor hepatocytes in 53 peripheral blood samples collected preoperatively, intraoperatively, and postoperatively from 13 HCC patients. We compared these data with those in 54 control samples collected from 24 healthy subjects and patients with chronic hepatitis/cirrhosis and 10 hepatocellular adenoma patients who underwent resection. Clinicopathological information of HCC patients was obtained during 3-year follow-up. In 100% (23 of 23) of HCC and adenoma patients, alb mRNA levels increased 10-10(6)-fold intraoperatively and then markedly declined within 8 weeks after operation. Levels of afp mRNA increased 5-7600-fold preoperatively in 8% (1 of 13) and postoperatively in 70% (9 of 13) of HCC patients. All five HCC patients with persistently elevated afp mRNA levels died from intrahepatic/extrahepatic metastasis, liver recurrence, or persistent HCC within 1 year after surgery. The absence/clearance of afp mRNA in 75 % (six of eight) of survivors was strongly associated with the absence of metastasis/recurrence (P = 0.02). We present evidence that alb-expressing hepatocytes are released intraoperatively into the circulation, and afp-expressing tumor cells are disseminated mostly postoperatively that may potentially be the source of recurrence or metastasis. Sequential quantification of both alb and afp mRNAs may provide insights for risk assessment and prognostic indication.
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PMID:Hematogenous dissemination of hepatocytes and tumor cells after surgical resection of hepatocellular carcinoma: a quantitative analysis. 1063 34

Retro-differentiation of liver parenchyma during neoplastic processes is characterized by the expression of tumor antigens, such as alpha-fetoprotein and the placental isoenzyme of glutathione-S-transferase (GST-P). To investigate whether this may also affect a typical liver function such as bile acid secretion was the aim of this work. Rat hepatocarcinogenesis was induced by diethylnitrosamine (i.p., 200 mg/Kg body weight at day 0) and promoted by two-thirds partial hepatectomy (at day 21) plus 2-acetamidofluorene administration (50 mg/Kg body weight, subcutaneously, twice a week from day 14 to day 35). In order to carry out planimetric measurements of neoplastic tissue after immunohistochemical staining, a novel monoclonal antibody (MAb 14.1.3) against GST-P with no cross-reactivity against the major liver isoform of GST (GST-H) was raised. Analysis of total biliary bile acid output using the 3alpha-hydroxysteroid dehydrogenase method indicated that a significant reduction (-26%) occurred during the formation of GST-P-positive foci (12 wk). This was restored to normal values during adenoma formation (16-20 wk), but decreased again during carcinoma transformation (32 wk). These changes were not parallel to that observed in bile flow, which was progressively but slightly decreased throughout the whole period under study. HPLC analysis of bile samples collected for 1 h at different time points during hepatocarcinogenesis revealed that in contrast to what happens during cholestatic disease, a continuous and progressive increase in the cholic acid-to-chenodeoxycholic acid ratio (from 4.4+/-0.5 in control animals to 15.1+/-1.9 in rats with hepatocellular carcinoma) occurs. A significant and transient increase at 16 wk (+120%) in the proportion of bile acids amidated with glycine as compared to those conjugated with taurine was also observed. These results indicate that the mechanisms accounting for the secretion of major bile acids are modified differently at various steps of rat liver tumor development.
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PMID:Bile acid secretion during rat liver carcinogenesis. 1073 59

Early detection of recurrence is valuable for monitoring hepatocellular carcinoma (HCC) progression. By quantitative reverse transcriptase polymerase chain reaction (RT-PCR), we derived calibration curves for alpha-fetoprotein (afp) and albumin (alb) mRNAs using 40 matched tumors and non-tumor liver tissues from HCC/adenoma patients. We prospectively quantified tumor cells and non-tumor liver cells in 62 patients' blood samples before, during and after surgery. Expression of both mRNAs was heterogeneous (1-10(5)-fold) between tumors and HepG2 cell line. The alb-mRNA levels in non-tumor liver cells were 2-10-fold higher than in tumor cells. The afp-mRNA levels in HCC cells were 30-1000-fold higher than in non-tumor cells. The alb-mRNA level in blood may reflect the number of liver cells, whereas the afp-mRNA level may represent mostly the number of HCC cells. We found different ratios of circulating HCC cells to non-tumor liver cells during the clinical course of patients, in association with the subsequent development of recurrence/metastasis. This approach may prove useful for detecting and monitoring HCC progression.
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PMID:Quantitative comparison of alpha-fetoprotein and albumin mRNA levels in hepatocellular carcinoma/adenoma, non-tumor liver and blood: implications in cancer detection and monitoring. 1088 Jul 63

We report a unique, previously unreported pancreatic tumor with hepatoid differentiation associated with serous microcystic adenoma in a 70-year-old man. These two lesions localized, respectively, at the body and the tail of the pancreas, were found incidentally on abdominal ultrasonography. Serum alpha-fetoprotein was not increased and no hepatic lesion was displayed on computed tomography. A subtotal pancreatectomy with splenectomy was performed. The patient is alive and well 12 months after resection. Pathological examination showed a very unusual encapsulated solid tumor with hepatocytic differentiation, bile production and immunoreactivity for hepatocyte paraffin-1 antibody. The tumor cells were negative for endocrine (neuron-specific enolase, chromogranin A, synaptophysin) and acinar (amylase, trypsin) markers. Ultrastructurally, zymogen and neurosecretory granules were absent. The features of the tumor were almost indistinguishable from those of hepatocellular adenoma; therefore, we believe that this solid hepatoid tumor may represent a variant of pancreatic adenoma. Recognition of this entity is important because the only reported pancreatic hepatoid tumors to date have been malignant. The main differential diagnoses include hepatoid ductal adenocarcinoma, hepatoid acinar cell carcinoma, primitive hepatoid endocrine tumor, and metastatic hepatocellular carcinoma.
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PMID:Solid adenoma with exclusive hepatocellular differentiation: a new variant among pancreatic benign neoplasms? 1244 84

The biodistribution of iodine-labelled alpha-fetoprotein ( I-AFP) in experimental mammary tumours was studied. C3H mice with subcutaneously transplanted mammary adenocarcinoma and Sprague-Dawley rats treated with -methyl- -nitrosourea for mammary adenoma induction were used as animal models. The accumulation of labelled I-AFP in mouse mammary adenocarcinoma was significantly higher than that in rat mammary adenoma. The tumour/muscle radioactivity ratios increased with time and, 48 h after intravenous injection, were estimated as 23.4 and 6.7, respectively. For experiments, extracts from both mammary tumours were prepared. The extracts were subjected to sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE), transferred to polyvinylidene difluoride (PVDF) membranes and incubated with I-AFP. A single major AFP-binding protein with a molecular weight of about 30 kDa was detected in both extracts. The amount of AFP-binding protein was clearly higher for adenocarcinoma than for adenoma. In the presence of cross-linking reagent, I-AFP formed a complex (about 100 kDa) with adenocarcinoma proteins.
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PMID:Uptake of radiolabelled alpha-fetoprotein by experimental mammary adenocarcinoma and adenoma: in vivo and in vitro studies. 1261 71

Expression profiling of hepatocellular carcinoma has demonstrated that glypican 3 (GPC3), a heparan sulfate proteoglycan anchored to the membrane, is expressed at a markedly elevated level in hepatocellular carcinoma. In this paper, two monoclonal antibodies against GPC3, GPC3-C02 and A1836A, were confirmed to specifically recognize GPC3 molecule in cells from hepatocellular carcinoma and hepatoblastoma cell lines by immunoblotting, and both were confirmed to recognize different epitopes of the GPC3 molecule by epitope mapping. Then, we evaluated the feasibility of GPC3-immunohistochemistry in the pathological diagnosis of benign and malignant hepatocellular lesions by applying these monoclonal antibodies to formalin-fixed and paraffin-embedded specimens. The immunoreactivity turned out to be identical in the two monoclonal antibodies and was thus confirmed to represent the actual expression of the GPC3 molecule. The expression was observed in the fetal liver, but not in normal adult liver, liver cirrhosis or hepatitis except for a tiny focus of a regenerative nodule of fulminant hepatitis. Diffusely positive staining of GPC3 was observed in malignant hepatocytes in hepatoblastomas and in hepatocellular carcinomas (47/56, 84%). GPC3 expression was independent of the differentiation and size of the hepatocellular carcinoma. On the other hand, there was only weak and focal staining in low-grade (2/8) and high-grade dysplastic nodules (6/8). GPC3 immunoreactivity was detected in only one of 23 metastatic lesions of colorectal carcinoma, and its expression was entirely absent in the liver cell adenoma (0/7), carcinoid tumor (0/1), and cholangiocellular carcinoma (0/16). When compared with immunohistochemistry of hepatocyte antigen and alpha-fetoprotein, GPC3-immunohistochemistry was significantly much more specific and sensitive for hepatocellular carcinomas. Thus, GPC3 was confirmed to be one of the oncofetal proteins now attracting attention for their promise both as markers of hepatocellular carcinoma in routine histological examination and as targets in monoclonal antibody-based hepatocellular carcinoma therapy.
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PMID:The glypican 3 oncofetal protein is a promising diagnostic marker for hepatocellular carcinoma. 1592 May 46

Only 7 cases of pancreatic tumor with hepatocytic differentiation have been reported in the literature, including 6 cases of hepatoid carcinoma and one case of hepatoid adenoma. Diagnosis of hepatoid carcinoma depends on recognition of characteristic histological features, supported by other evidence linked to hepatic lineage including alpha-fetoprotein production, positive immunoreactivity to liver synthesized proteins, and in situ hybridization detection of albumin mRNA. In addition, a synchronous focus of carcinoma arising in pancreatic ducts, islet cells, or acinar cells is essential. We report a unique case of pancreatic tumor with exclusive hepatocytic differentiation. In this tumor, we were unable to find a synchronous focus of carcinoma arising in pancreatic ducts, islet cells, or acinar cells, ruling out the possibility of its being hepatoid carcinoma. Long term follow-up can help to determine whether this tumor is benign or malignant. The patterns of reticulin staining and immunohistochemical staining are suggestive of malignancy, but mitotic activity is low and nuclear pleomorphism is minimal.
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PMID:A unique pancreatic tumor with exclusive hepatocytic differentiation. 1668 22


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