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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A variety of neoplasms and nonneoplastic hepatic lesions have been noted in winter flounder, Pseudopleuronectes americanus, from Boston Harbor, Massachusetts. Inflammatory lesions include cholangiitis, pericholangiitis, pericholangial fibrosis, hepatitis, and pancreatitis. Necrotic lesions consist essentially of focal coagulative necrosis and a distinctive vacuolated cell lesion of the hepatic parenchyma. The most conspicuous and numerous proliferative lesion is macrophage aggregate hyperplasia and hypertrophy. Preneoplastic lesions include principally basophilic foci of cellular alteration and hepatocellular adenoma. Carcinomas consist of several morphologic varieties: hepatocarcinoma, cholangiocarcinoma, and anaplastic adenocarcinoma. The pathogenesis of the lesions observed is discussed with respect to anthropogenically introduced chemical contaminants and the resistant hepatocyte model of hepatocarcinogenesis. This study, and others of bottom-living food fish with enzootic neoplastic disease, warrants further evaluation, particularly with respect to possible bioaccumulation of chemical contaminants in edible tissues.
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PMID:Neoplasms and nonneoplastic liver lesions in winter flounder, Pseudopleuronectes americanus, from Boston Harbor, Massachusetts. 164 9

Benign liver tumors occurring in young women were rarely reported in the medical literature before the introduction of oral contraceptives in the early 1960s. Subsequently, there were numerous case reports from the U.S. and other countries of liver tumors in women who used combined oral contraceptives. These reports, coupled with data from two U.S. case-control studies, indicate that the risk of hepatocellular adenoma increases sharply with increasing duration of oral contraceptive use. Case reports suggest that there may be a similar effect on the risk of focal nodular hyperplasia, but this is not established because there have been no case-control studies of the lesion. The incidence of benign liver disease attributable to oral contraceptive use in the U.S. is small because of the very low incidence of the disease. There have also been numerous case reports of malignant liver tumors in young women who used oral contraceptives. Seven case-control studies have been conducted--two in Great Britain, two in the U.S., one in Italy, one in several developing countries (conducted by the World Health Organization (WHO)), and one in South Africa. Data from the first five studies, all conducted in low risk populations, indicated an association of hepatocellular carcinoma (largely in the absence of liver cirrhosis) with oral contraceptive use. Because of small numbers estimates were unstable, but the risk did not appear to be increased appreciably for durations of use less than about five years. For longer durations, the risk appeared increased by five- to tenfold or more. There was little evidence of hepatitis B infection in the cases, but systematic determinations were not carried out. An increased risk of cholangiocarcinoma was not established, but few of these lesions were studied. Because the incidence of primary liver cancer in Northern Europe and the U.S. is low, the incidence attributable to oral contraceptive use is also likely to be low. The WHO study was carried out in eight countries, most of which have a high incidence of liver cancer and a high prevalence of a predisposing factor, hepatitis B infection. Similarly, the South African study was carried out among black women, and virtually all of the cases had serological evidence of hepatitis B infection. Both studies indicated no association of short-term oral contraceptive use with risk of hepatocellular carcinoma, and the WHO study indicated a lack of association with cholangiocarcinoma.
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PMID:The risk of liver neoplasia in relation to combined oral contraceptive use. 165 Dec 5

The benign tumors hepatic adenoma and focal nodular hyperplasia are compared in their etiology, differential diagnosis, risk of transformation, and management. Hepatic adenomas range in size from 1-30 cm, averaged 8-10 cm in diameter, contain vacuoles and glycogen, but no Kupfer cells or bile ducts. Adenoma is usually symptomatic, causing pressure or hemorrhage. The risk of developing adenoma is increased with duration of oral contraceptive use, and chance of a larger tumor, a hemorrhage and mortality during pregnancy or surgery is also increased in pill users. Adenoma also occurs in people with Type Ia glycogen storage disease, and is associated with insulin-dependent diabetes. Often stopping oral contraceptives will cause an adenoma to regress. If not, It is best managed by elective resection, with 1% mortality, rather than 5-10% mortality due to spontaneous rupture. Adenomas can progress to adenomatosis, which are inoperable, or malignant transformation. Focal nodular hyperplasia is marked by a stellate scar, sometimes accompanied by hemangioma, but is asymptomatic. It is not increased in oral contraceptive users, but occurs in older women. It can transform to fibrolamellar hepatocellular carcinoma. The 2 benign lesions can be distinguished by radionuclide scanning and angiography. Only fine needle aspiration is advised for biopsy, because of the risk of hemorrhage with adenoma. Focal nodular hyperplasia takes up radionuclide, stains intensely on angiography, and is safe to biopsy percutaneously.
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PMID:Hepatic adenoma and focal nodular hyperplasia. 165 55

In March 1989, ultrasonography revealed a hepatic mass in a 40 year old nulliparous woman who was then referred to the University of Southern California--Los Angeles (UCLA) Liver Unit. She exhibited no symptoms of a liver condition. From 19-28 years old, she took the combined oral contraceptive (OC) Ovulen 21 for irregular menses. After a brief period of taking Ortho Novum 1/80, she took Demulen 1/35-24 between ages 28-34. Her physician diagnoses endometriosis at 34. He stopped OC therapy and prescribed the progestin Norlutate. She had no history of hepatitis, toxin exposure, and previous liver disease. Further no one in her family had had liver disease or neoplasms. Computer tomography identified a 6.5 cm x 3.5 cm mass in the right lobe of the liver which matched a cold defect on a liver scan using technetium Tc 99m sulfur colloid. The mass selectively took up gallium. Arteriography revealed the mass to be a vascular tumor, but it did not exhibit a typical vascular pattern of an adenoma or the neovascularity of hepatocellular carcinoma. Physicians at UCLA used peritoneoscopy to take percutaneous needle biopsies of the right lobe which confirmed a hepatic adenoma. they then removed the right lobe of the liver. The remaining part of the liver was normal. Histologic examinations of the removed section showed features of a well differentiated hepatocellular carcinoma. Further tumor cells had invaded normal hepatic parenchyma. The physicians believed that hepatic adenoma was in the process of transforming into hepatocellular carcinoma in this patient. They thought that long term OC use, and possibly long term progestin use, may have contributed to the formation of the liver neoplasms. They emphasized the need for a pilot study to develop guidelines on surveillance ultrasonography of women taking OCs over a long period.
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PMID:Hepatocellular carcinoma coexisting with hepatic adenoma. Incidental discovery after long-term oral contraceptive use. 166 98

Focal nodular hyperplasia (FNH) is a rare benign hepatocellular tumor occurring in noncirrhotic patients, mostly females, 20-50 years of age. It is usually asymptomatic. The authors took the lead from 5 cases of FNH studied over last year to analyze the different patterns exhibited by the condition on the various imaging techniques currently available. At scintigraphy with 99mTc DISIDA or with TcSC, FNH can be hyper, normal, or hypocaptating. On US scans, the lesion is often homogeneous and isoechoic, but it can also be hyper/hypoechoic. With Doppler US, high-flow signals can be observed. On unenhanced CT scans the lesion is solid, well-demarcated, isodense or slightly hyperdense; sometimes it shows a central hypodense area corresponding to fibrovascular scar. On postcontrast scans it appears hyper/isodense. At dynamic CT the lesion density, which is high during the arterial phase, decreases quickly in the parenchymal and the venous phases and reaches equal/inferior values to surrounding liver parenchyma. On liver angio-CT it is sometimes possible to visualize the bile ducts in the central scar. At angiography, FNH is hypervascular and homogeneous. On MR scans, in T1-weighted SE sequences, the condition is isointense or slightly hypointense, whereas on T2-weighted pulse sequences it is slightly hyperintense; the central scar is hypointense on T1, and hyperintense on T2, weighted scans. As we have no pathognomonic patterns but only orientative ones, a reliable differential diagnosis with hepatocellular adenoma (HA) and fibrolamellar hepatocellular carcinoma (FL-HCC) must be based on biopsy or cytology or, even better, histology. The differential diagnosis is nevertheless necessary because, while FNH does not usually require a surgical approach but only a radiological follow-up, both HA (due to possible bleeding and degeneration) and FL-HCC require surgery.
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PMID:[The imaging diagnosis of hepatic focal nodular hyperplasia]. 166 64

The connective tissue content of four different human liver tumors (Fibrolamellar carcinoma, FLC; hepatocellular carcinoma, HCC; focal nodular hyerplasia, FNH and hepatocellular adenoma, HCA) was investigated by computer aided morphometry. A significantly higher connective tissue content was found in FNH and FLC as compared to HCA and HCC. The distribution of the connective tissue was homogeneous in the cases of FNH, HCA and HCC, while a highly unhomogeneous distribution was observed in FLC cases.
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PMID:Connective tissue content of fibrolamellar carcinoma and other human liver tumors. 166

The connective tissue content of four different human liver tumors (Fibrolamellar carcinoma, FLC; hepatocellular carcinoma, HCC; focal nodular hyperplasia, FNH and hepatocellular adenoma, HCA) was investigated by computer aided morphometry. A significantly higher connective tissue content was found in FNH and FLC as compared to HCA and HCC. The distribution of the connective tissue was homogeneous in the cases of FNH, HCA and HCC, while a highly unhomogeneous distribution was observed in FLC cases.
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PMID:Connective tissue content of fibrolamellar carcinoma and other human liver tumors. 166 1

From January 1976 to May 1990, 1673 patients with a liver mass or masses detected by imaging techniques underwent percutaneous fine-needle aspiration biopsy of the liver. Of these, 99 were diagnosed cytologically as "hepatocellular carcinoma" and 9 as "consistent with liver cell adenoma." The cytologic diagnoses were confirmed in the follow-up of all cases. Among the 99 patients with hepatocellular carcinoma, 3 had taken oral contraceptives for a period of 10, 11, and 12 years, respectively. The nine patients with liver cell adenoma were all users of oral contraceptives over a period ranging from 5 to 10 years. Of these, two who had taken oral contraceptives for a period of 8 and 10 years, respectively, had foci or areas of liver cell dysplasia within the adenomas. The cytologic criteria for the diagnosis of liver cell dysplasia included cytoplasmic and nuclear enlargement, nuclear pleomorphism together with prominent nucleoli, hyperchromasia and multinucleation. The cytologic features of liver cell dysplasia strikingly mimic hepatocellular carcinoma. From this study, the foci or areas of liver cell dysplasia arising within the liver cell adenomas appear to be the missing link responsible for the transformation of liver cell adenoma to carcinoma. It is believed that liver cell adenomas are not premalignant and may undergo reversible change after withdrawal of causative agents, whereas liver cell dysplasia is an irreversible, premalignant change and will eventually progress to hepatocellular carcinoma.
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PMID:Oral contraceptive-associated liver cell adenoma and hepatocellular carcinoma. Cytomorphology and mechanism of malignant transformation. 171 64

Adrenal imaging was performed using magnetic resonance (MR) was in 100 patients who had no clinical or biochemical evidence of adrenal abnormality and in 19 patients with 24 adrenal lesions (adenoma in 5, hyperplasia in 2, metastasis in 5, (lung cancer in 1, hepatoma in 4) adrenal cancer in 1, pheochromocytoma in 3, neuroblastoma in 3). Normal adrenal glands showed intermediate intensity between muscle and liver, and were detected in over 90% of cases on T1-weighted images (T1-weighted SE, inversion recovery). Adenomas and hyperplasias had the same intensity as normal glands. Medullary masses showed extreme hyperintensity on T2-weighted images and could be differentiated from cortical masses. Neuroblastomas were detected as hyperintense tumors with intratumoral hemorrhage and necrosis on T2-weighted MR images. Metastatic adrenal tumors from lung cancer were hyperintense on T2-weighted images, while metastasis from hepatoma showed low intensity on the same pulse sequence. In diagnosing adrenal metastasis, we must compare and contrast the tumor intensity and structure with those of the primary lesions. MR is considered a useful modality in characterizing adrenal tissue.
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PMID:[Magnetic resonance imaging of the adrenal gland]. 179 51

Plutonium-239 or 241Am administered intravenously in the monomeric citrate form was initially deposited in beagle livers principally in the hepatocytes and to a much lesser extent in the sinusoidal macrophages and connective tissues. The initial distribution was quite uniform throughout the hepatic parenchyma; however, at later postinjection intervals, depending on the amount of injected activity, the liver burden became increasingly more focal due to: (1) a progressive shift of the radionuclide from the hepatic epithelium to the macrophages; (2) the movement of such macrophages toward the portal or central regions of the lobule; and (3) the displacement of the older more radioactive tissue by regenerating hepatocytes, which generally have a much lower radionuclide content. The hepatic lesions produced by Pu or Am included: (1) necrosis and degenerative changes that were clinically serious or fatal in some of the animals injected with approximately 107 kBq kg-1; (2) marked structural and circulatory changes resulting from necrosis and focal hepatocyte hyperplasia; (3) a significant incidence of both benign and malignant primary liver tumors. In both Pu- and Am-treated dogs, the most frequently appearing neoplasm was the bile duct adenoma, followed by the cholangiocarcinoma. The most obvious difference between Pu- and Am-induced liver neoplasia was the greater frequency of fibrosarcomas and mast cell sarcomas in the Am-treated groups. Hepatomas were of relatively low frequency in animals with Pu or Am burdens. Although the incidence of bone neoplasia was high among the dogs in these studies, the risk of liver tumors, especially in the Am-treated animals, exceeded that of the skeleton in some of the lower dosage levels where the survival times were long. A risk coefficient of approximately 1200 fatal liver malignancies (10(4) beagle Gy)-1, derived from the dosage groups with long survival times, was calculated for combined Pu and Am animals. The prominence of the liver syndromes in beagles with burdens of Pu or Am indicates that humans with body burdens of 239Pu, 241Am, or other actinide elements may be at risk from radiation effects in the liver, including neoplasia development.
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PMID:Plutonium- or americium-induced liver tumors and lesions in beagles. 188 23


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