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)

We studied the development of liver tumors in male transforming growth factor alpha (TGF-alpha) transgenic mice of the CD1 strain and examined the expression of the transgene by immunohistochemistry and in situ hybridization. Livers of 4-5-week-old transgenic mice contained areas of centribobular hypertrophy with low glucose-6-phosphatase activity. These areas progressively expanded, and hypertrophy and dysplasia became generalized in livers of mice at 10-12 months of age. The expression of the transgene, determined by either immunohistochemistry or in situ hybridization, was uneven in animals that were 10 weeks old or older. The positive hepatocytes formed patches with a predominant centrilobular distribution. We studied a total of 23 liver tumors (7 hepatocellular carcinomas and 16 adenomas) obtained from 11 mice at 13-15 months of age and from one 7-month-old animal which received zinc sulfate to induce the transgene. The carcinomas were well differentiated tumors, without glucose-6-phosphatase or gamma-glutamyltranspeptidase activity, that developed from the dysplastic parenchyma and occasionally within an adenoma. In all carcinomas and in 56% of the adenomas there was overexpression of the transgene in relationship to the surrounding tissue. The majority of the tumors that overexpressed TGF-alpha were alpha-fetoprotein positive, while alpha-fetoprotein staining was not detected in tumors (all adenomas) that did not show excessive transgene expression. We conclude that TGF-alpha functions as a promoter of liver carcinogenesis through its effect as an autocrine inducer of hepatocyte proliferation. Further, the data indicate that TGF-alpha overexpression may favor tumor progression.
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PMID:Development of liver tumors in transforming growth factor alpha transgenic mice. 132 2

The structure of 12 spontaneous hepatoblastomas found in old (average age 26.5 months) male mice is described. There were considerable strain differences in their incidence: 0.5% (1/194), 0.5% (1/194) and 5% (10/198) in strain C57B1, CBA and F1 (CBA X C57B1), respectively. This proves the importance of genetic factor the role of which in the development of human hepatoblastoma is not established so far. Mouse hepatoblastoma develops almost invariably within or adjacent to liver cell tumours (adenoma or carcinoma). There was a correlation between the incidence of liver cell tumours within a given strain treated with different doses of carcinogen but such correlation was absent in mice of different strains. Histologically and ultrastructurally, mouse hepatoblastoma corresponds to the anaplastic variant of human hepatoblastoma. As distinct from human tumour, mouse hepatoblastoma does not contain alpha-fetoprotein. One tumour was transplanted to the syngeneic host and passed 30 transplant generations retaining the structure of a primary tumour with areas of osteoid tissue and foci of squamous cell metaplasia. Mouse hepatoblastoma may be induced by carcinogens. Likewise, according to the literature, risk of hepatoblastoma is higher in children whose mothers were exposed to the potential carcinogens before or during the pregnancy.
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PMID:[Mouse hepatoblastoma: comparative aspects]. 165 92

We compared the clinical characteristics and histological classifications of young adult women with hepatocellular carcinoma with and without exposure to increased amounts of sex steroids in order to investigate the possibility that sex steroids changed the behavior of the tumor. Fifteen women were found to have a history of exposure to increased levels of sex steroids while 14 did not. One of the women in the exposed group had elements of adenoma next to her carcinoma, allowing speculation as to whether the malignancy arose from a previous adenoma. Statistically significant differences between the two groups were that the exposed group had a higher number of gravida (2.2 compared to 0.9, p = 0.013) and suffered tumor rupture with hemoperitoneum more frequently (4/15 compared to 0/4, p = 0.037). Trends worth noting were that the exposed group tended to survive longer, complain of pain and weight loss less frequently, and have lower alpha-fetoprotein levels. These findings indicate that exposure to sex steroids may change the clinical behavior of hepatocellular carcinoma, producing among other things a hypervascularity and tendency for hemoperitoneum.
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PMID:Clinical and pathological comparison of young adult women with hepatocellular carcinoma with and without exposure to oral contraceptives. 240 65

For the evaluation of differential diagnostic parameters, hepatocellular carcinoma (HCC, n = 26), liver cell adenoma (n = 4), focal nodular hyperplasia (n = 8), and secondary liver tumors (n = 15) were studied with histologic and immunohistochemical methods. The study was performed on formalin-fixed, paraffin-embedded tissue sections, and, in some cases, also on frozen sections. The diagnostic contribution of the demonstration of alpha-fetoprotein, alpha-antitrypsin, hepatitis B surface antigen, carcinoembryonic antigen (CEA), and biliary glycoprotein I (BGPI), compared with routine hematoxylin-eosin and reticulin stains was evaluated. For the differentiation between HCC, adenoma, and focal nodular hyperplasia, immunohistochemistry contributed less than the strict application of histologic criteria. Immunohistochemistry of CEA and BGPI, however, appeared to be of help in differentiating between primary and secondary liver tumors as follows: CEA is consistently absent in liver cell tumors, while a bile canalicular staining pattern was seen in 80% of HCC due to the presence of BGPI reactivity.
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PMID:Hepatocellular carcinoma, adenoma, and focal nodular hyperplasia. Comparative histopathologic study with immunohistochemical parameters. 243 May 47

This paper reports an autopsy case of a 78-year-old male with multiple nodules in the liver developed after long-termed administration of phosphate diethylstilbestrol (PDES) for prostatic cancer. Large part of these nodules were suspected to be well differentiated hepatocellular carcinoma with high level of serum alpha-fetoprotein (AFP) up to 3,400 ng/ml, but a part of them was evaluated to be a borderline between hepatocellular carcinoma and adenoma with mild cellular atypism. The liver other than the nodules showed liver fibrosis associated with liver cell dysplasia and peliosis hepatis-like change. This is a unique autopsy case of hepatocellular carcinoma closely related to diethylstilbestrol (DES) therapy for prostatic cancer.
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PMID:Multicentric hepatocellular carcinoma following phosphate diethylstilbestrol therapy for prostatic cancer. 244 58

Unlike the proven causal association between oral contraceptive (OC) use and hepatic cell adenoma, the link between OCs and hepatocellular carcinoma remains speculative. The case history of a 53-year-old US woman suggests, however, that hepatic cell adenomas may transform into hepatocellular carcinoma. The patient, who had used Ovral continuously since 1966, presented in 1985 with vague abdominal pain and a palpable right upper quadrant mass. Computed tomography revealed a 12 x 8 cm mass in the right hepatic lobe and 2 small lesions in the left lobe. Serum alpha-fetoprotein and ferritin levels were normal and tests for hepatitis B were negative. A needle biopsy of the right lobe mass indicated benign hepatic adenoma. OC use was discontinued and the patient was examined at bimonthly intervals. Although she continued to report vague pain, there were no significant changes in radiologic findings or levels of alpha-fetoprotein over the next 18 months. At the 18-month follow-up visit, the alpha-fetoprotein level showed an increase to 227 mcg/L and had risen to 2300 mcg/L by the 30-month follow-up visit. At this time, computed tomography showed slight enlargement of the right lobe mass and inhomogeneity, while biopsy revealed sclerosing hepatocellular carcinoma. This is the 3rd case reported in the literature in which there is evidence of a transformation of hepatic cell adenomas into hepatocellular carcinoma in longterm OC users. Thus, the premalignant potential of hepatic cell carcinomas in OC users should be considered by physicians who follow such cases.
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PMID:Transformation of hepatic cell adenoma to hepatocellular carcinoma due to oral contraceptive use. 253 93

A 3-yr-old child underwent biopsy of a nonresectable liver cell adenoma. She was well thereafter, but at the age of 22 yr, she underwent orthotopic liver transplantation because the lesion had grown. The alpha-fetoprotein level was 4,300. The specimen showed poorly differentiated hepatocellular carcinoma in a noncirrhotic liver. At this writing, the patient is well 32 mo after transplantation.
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PMID:Liver cell adenoma at the age of 3 years and transplantation 19 years later after development of carcinoma: a case report. 768 80

Forty-one patients (16 females and 25 males) over 10 years of age from five different European centres were studied retrospectively. Of those patients 19 were below the 3rd percentile for height. Hypoglycaemia was still reported in 6 patients. Hepatomegaly was present in 39 out of 40, while 11 out of 27 reported patients had marked hepatomegaly (> 10 cm below the costal margin in the midclavicular line). Adenomas were detected in 11 out of 39 patients, alpha-1-fetoprotein was reported to be within normal limits in a total of 22 patients of whom 6 had adenomas. Blood cholesterol concentration was elevated in 31 out of 38 patients, in 7 greater than 10.0 mmol/l. Blood triglycerides were elevated in 29 out of 34 patients, in 8 patients greater than 4.0 mmol/l. Blood uric acid concentration was elevated in 19 out of 35 patients, 12 of them being treated with allopurinol. Mental development was reported to be normal in 32 out of 37 patients. Since limited information on treatment was available no significant differences between treatment groups could be detected. In order to evaluate the effect of treatment, 20 patients (10 females and 10 males) of one centre were studied before and after at least 5 years of treatment. This treatment consisted of frequent feedings during the day together with nocturnal gastric drip feeding. Patients were divided into responders (n = 16) and non-responders (n = 4) depending on their (change in) SDS (standard deviation score) for height. Liver adenomas were detected in 3 patients, of which one was a non-responder. Alpha-fetoprotein was normal in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The long-term outcome of patients with glycogen storage disease type Ia. 831 26

Two well circumscribed tumors, oncocytic and non-oncocytic, were removed from the non-cirrhotic liver of a 67 year old male. The large oncocytic tumor (OCT), occupying the entire left lobe, was multilobulated with focal coagulation necrosis and areas of hemorrhage. Light microscopy revealed that it consisted of exclusively large, granular oxyphilic cells with moderate nuclear atypia and occasional mitotic figures, which were trabecular and/or pseudoglandular in structure, but no lamellar fibrosis was seen. Characteristically, the OCT cells included numerous globular hyaline bodies (GHB) of various sizes which were stained red with acid fuchsin and deep blue or magenta with phosphotungstic acid hematoxylin (PTAH), but negative for periodic acid Schiff (PAS), orcein, rhodamine and Grimelius methods. Immunohistochemically, alpha-fetoprotein (AFP), alpha-1-antitrypsin, alpha-1-antichymotrypsin, fibrinogen and ferritin were all negative. On ultrastructural examination, tumor cells were mitochondria-rich, including electron dense, ovoid or polyhedral inclusions, with the delineated membrane identical with that of the GHB. In contrast, the small tumor in the right lobe (Segment 7) was a solid adenoma with no oncocytic transition. Based on these findings, it was postulated that OCT consists of heterogenous proliferation of mitochondria-rich hepatocytes which tend to induce lysosomal GHB closely associated with mitochondrial abnormalities.
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PMID:Oncocytic hepatocellular carcinoma with numerous globular hyaline bodies. 872 53

In the present study the establishment and characterization of a nontumorigenic liver epithelial cell line (HACL-1) derived from a human hepatocellular adenoma is described. The HACL-1 cells have a finite life span (i.e., they proliferate for a period of 2 months and then senesce), show cell-cell contact inhibition, do not grow in soft agar, are not tumorigenic when injected in nude mice, and possess a normal diploid karyotype. The cultured cells resemble hepatocytes, but exhibit some features of dedifferentiation. At the ultrastructural level the cells are endowed with round or oval nuclei, abundant cytoplasmic organelles, and varying amounts of glycogen. The rough endoplasmic reticulum is disorganized, while peroxisomes and matrix granules within mitochondria are lacking. HACL-1 cells are cytokeratin 18-positive as well as (transiently) albumin- and alpha-fetoprotein-positive, but do not express cytokeratin 19. Furthermore, no mutations were observed in exons 5-8 of the tumor suppressor gene p53. Taken together these results show that HACL-1 cells are nontumorigenic proliferating liver epithelial cells, which might prove to be of great value in future studies on diverse aspects of human liver cell biology and carcinogenesis.
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PMID:Establishment and characterization of a nontumorigenic cell line derived from a human hepatocellular adenoma expressing hepatocyte-specific markers. 936 26


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