Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An autopsy case of Dubin-Johnson syndrome (DJS), associated with hepatocellular carcinoma (HCC), the third such case in Japanese literature, is reported. A 64-year-old man, known to have had jaundice from his childhood, was admitted because of weight loss. Close examination revealed that the patient had DJS with HCC and a right lobectomy of the liver was performed. He died, however, of metastasis of HCC about 36 months later. At autopsy, the liver was found to be brownish-black in color. Microscopic findings of the liver were those common to HCC and chronic active hepatitis, and the brown pigment seen in the hepatocytes was mainly confined to the centrilobular ares. After histochemical and electronmicroscopic study, a close relation between this pigment and lysosome is suspected.
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PMID:[Dubin-Johnson syndrome associated with hepatocellular carcinoma--report of an autopsy case]. 282 78

The pigment in the Dubin-Johnson syndrome (DJS) is shown unequivocally not to be a typical melanin or closely related polymer. In electron spin resonance (ESR) studies of DJS pigment from a hepatoma, it is shown that, unlike true melanins, the pigment associated with the DJS syndrome has no free radical in the absence of light. Exposure to even low levels of visible light over a broad frequency range induces a free radical in the DJS pigment. Previous studies did not appreciate the sensitivity to light of this pigment and therefore erroneously concluded that the DJS pigment had a permanent free radical. The light induced ESR signal in DJS tissue has spectroscopic properties that differ significantly from any known melanins. The pigment is not extracted by lipophilic solvents and is centrifuged down at 50,000g, but not at 5,000g.
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PMID:Further evidence that the pigment in the Dubin-Johnson syndrome is not melanin. 285 43

A 57-year-old man with hepatocellular carcinoma and liver cirrhosis combined with Dubin-Johnson syndrome was successfully treated by extensive right hepatic lobectomy. While the preoperative serum bilirubin level is one of the criteria in determining the indication for radical hepatic resection, it does not play a decisive role in the case of combined Dubin-Johnson syndrome.
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PMID:Hepatocellular carcinoma in a case of Dubin-Johnson syndrome treated successfully with right extended lobectomy. 626 Oct 27

A hepatocellular carcinoma which was predominately black was surgically excised from a noncirrhotic, asymptomatic 62-year-old white man. Brown-black, pigment granules, found only in the tumor cells, were histochemically and ultrastructurally identical to the hepatocellular pigment found in Dubin-Johnson syndrome. The latter pigment is thought to accumulate as a consequence of a genetically determined abnormality in the excretion of catecholamines and related substances. It is postulated that the pigment formation in this tumor developed via a similar, though epigenetic, mechanism. This occurrence has not been previously described. Unusual PAS-negative, globular cytoplasmic inclusions were also found in the tumor cells and these proved to be Mallory bodies by electron microscopy.
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PMID:A black hepatocellular carcinoma with Dubin-Johnson-like pigment and Mallory bodies: a histochemical and ultrastructural study. 628 73

The condition that the porphyrins are excreted into the urine due to impairment of bile excretion, is called as secondary porphyrinuria. The main porphyrin is coproporphyrin, there fore the condition is called as secondary coproporphyrinuria. Secondary porphyrinuria is associated with various disorders, such as hepatobiliary diseases, hereditary hyperbilirubinemia, intoxications, blood and metabolic diseases, but the etiology of secondary porphyrinuria is unclear. Coproporphyrin is divided into two isomers, one is coproporphyrin-I type and the other is coproporphyrin-III type. In normal human urine, coproporphyrin-III type is predominant, and the ratio of coproporphyrin-I to total coproporphyrin is 10-50% (% as isomer I), while in urines of hepatobiliary diseases, the ratio is 40-60%. In Dubin-Johnson syndrome, the ratio is 80-100%. Coproporphyrinuria in hepatocellular carcinoma and alcoholic liver disease may be different from that in hepatobiliary diseases, often associated with uroporphyrinuria as well as coproporphyrinuria. Coproporphyrinuria arising in blood and metabolic diseases must be taken into account of associated liver diseases.
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PMID:[Secondary porphyrinuria]. 761 71

We report herein the case of a 46-year-old man with Dubin-Johnson syndrome (DJS) who was referred to our hospital to undergo a right hepatic lobectomy for hepatocellular carcinoma. His complicated postoperative conjugated hyperbilirubinemia was successfully treated by hemopurification based on the increased level of serum hepatocyte growth factor (HGF). It is considered that hemopurification based on the early postoperative HGF levels has beneficial effects for patients with DJS; however, the specific role of hemopurification in the conjugated hyperbilirubinemia that develops postoperatively in these patients has not been determined.
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PMID:Postoperative management following massive hepatectomy in a patient with Dubin-Johnson syndrome: report of a case. 987 48

We report two cases of hepatocyte neoplasia with extensive deposition of Dubin-Johnson-like pigment in men without Dubin-Johnson syndrome. This pigment has previously been described in hepatocellular carcinoma but not in liver cell adenoma. The tumors of both patients showed some atypical cytologic features, but no frank histologic evidence of malignancy. Long-term follow up for several years showed no evidence of recurrence after limited surgical excision. We conclude that tumors with this structure may be cured by limited surgical excision and should be considered as pigmented liver cell adenomas.
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PMID:Pigmented liver cell adenoma in two male patients. 1102 7

A 65-year-old man presented with multiple liver tumours. Imaging techniques could not differentiate between adenomas and hepatocellular carcinomas. He had no relevant past medical history. Liver function tests were normal except for a 1.5-fold rise in GGT. AFP was normal. Viral markers were negative. During laparoscopy, numerous black tumours of different sizes were seen. These tumours were adenomas without malignant transformation. Tumoral hepatocytes contained a brown pigment in the canalicular area without evidence of cholestasis. This pigment was Fontana positive and looked like Dubin-Johnson pigment by electron microscopy. The expression of the canalicular multispecific organic anion transporter (cMOAT) was decreased in the tumours but normal in the non-tumoral liver ruling out the diagnosis of Dubin-Johnson syndrome. There was mild iron deposition possibly related to an homozygous H63D mutation in the HFE gene. Three years after their discovery, the size of the tumours remained stable. It is concluded that this male patient with multiple adenomas and mild iron overload is at risk of developing an hepatocellular carcinoma and that the black colour of adenomas is probably due to a partial defect in excretion of organic anions.
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PMID:Multiple black hepatocellular adenomas in a male patient. 1111 85

Hepatocellular carcinoma (HCC) is the most common malignant tumor of males in the world, with an incidence of 1,000,000 new cases a year. It is endemic in Southeast Asia and Sub-Saharan Africa. Risk factors include chronic infection with hepatitis B virus (HBV) and hepatitis C virus (HCV), Aflatoxin B1 uptake, hemochromatosis, and alpha1 -antitripsin deficiency. Epidemiological studies provide evidence for the association of HCC with HBV infection. The incidence of HCC is high in regions hyperendemic for HBV. Chronic carrier state and maternal-infant transmission are important factors in the development of HCC. Evidence of direct oncogenic effect of H BV is well established, HCCs contain viral DNA sequences integrated into hepatocyte DNA that act as random insertional mutagens, and these sites are near genes involved in the control of proliferation and differentiation. The mechanism of hepatitis C virus in hepatocarcinogenesis is still imprecise but a high percentage of cases are related to this virus. Chronic alcohol consumption and cirrhosis are cofactors that increase the development of HCC in patients with chronic viral infection. In experimental carcinogenesis a multipotential element called oval cell proliferates in the early stages. The cellular events are accompanied by increased expression of several growth factors that enhance the survival of carcinogen-activated cells by suppressing apoptosis and increasing elements entering the cell cycle. Hepatic carcinogenesis is a complex process associated with accumulation of genetic and epigenetic changes that run through steps of initiation, promotion and progression. Activation of oncogenes of the "ras" family and others has been detected during chemically-induced HCC in rodents, but there is little evidence of such activation in human tumors. The role of tumor supressor genes such as retinoblastoma (RB) and P53 genes has been documented. Aflatoxin B1 that contaminates foods in endemic areas has a clear role in hepatocarcinogenesis. Metabolites of this toxin promote apurinic sites and G to T mutations in chromosomal DNA, the third base of codon 249 of the P53 gene is preferentially targeted to form aducts with aflatoxin B1, and this mutation has been specifically identified in HBV infection. Histological and cytological criteria for the diagnosis of HCC are well established and are based in architectural and cytological changes. An important issue is the diagnosis of liver "nodules" detected by image, from which small biopsies or aspiration material is obtained. Special studies such as reticulin, CD34, cytokeratin profile, and MOC-31 can be very useful for the differential diagnosis of primary and metastatic tumors. Telomerase activity has been found in HCC and negative in pericancerous tissue. It is more pronounced in poorly differentiated tumors and correlates with factors of clinical importance, such as prognosis and recurrences. Cells of well-differentiated HCC have an ultrastructural appearance similar to normal hepatocytes. During the process of dedifferentiation, there is progressive loss of organization of intracellular organelles. The cell cohesion is lost, intercellular gaps with microvilli appear, the sinusoids become capillarized, and reparative changes are seen in the spaces of Disse. A variety of inclusions, such as Mallory bodies, granular material, secondary lysosomes, and Dubin-Johnson pigment, have been described. Fibrolamellar carcinoma has a characteristic histological picture and ultrastructurally oncocytic features. Neuroendocrine granules and combination of HCC with bile duct carcinoma are seen by electron microscopy.
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PMID:Hepatocellular carcinoma: an update. 1178 14

A 72-year-old woman with hepatocellular carcinoma and HCV cirrhosis combined with Dubin-Johnson syndrome was successfully treated by a central bilateral segmentectomy. While the preoperative serum bilirubin level is one of the established criteria for determining the indications for a hepatic resection, it is not effective for HCV cirrhosis cases associated with Dubin-Johnson syndrome. Postoperative hyperbilirubinemia may be cured without special treatment such as bilirubin absorption or plasma exchange, but such patients must be carefully observed to ensure that liver failure does not occur.
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PMID:Hepatocellular carcinoma in a case of Dubin-Johnson syndrome treated successfully with a central bilateral segmentectomy. 1514 28


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