Cases reported "Liver Neoplasms"

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21/56. Rapidly progressing budd-chiari syndrome complicated by hepatocellular carcinoma.

    budd-chiari syndrome (BCS) is a disorder caused by occlusion of the hepatic vein or inferior vena cava. The clinical presentation include abdominal pain, hepatomegaly, ascites, leg edema, collateral venous dilatation of the body trunk, and portal hypertension. In addition, BCS can cause hepatocellular carcinoma (HCC) in some patients, although its pathogenesis is not yet completely understood. The average reported time lag from diagnosis of BCS to full-blown HCC ranges from several years to several decades. Hepatic carcinogenesis in patients with BCS perhaps reflects a prolonged and persistent liver injury in that it occurs in the primary inferior vena cava obstruction rather than the primary hepatic vein thrombosis. Among patients with BCS, membranous obstruction of the vena cava (MOVC) usually presents an insidious and chronic illness, whereas primary hepatic vein thrombosis presents an acute or subacute illness. We experienced a case of a patient with BCS, which progressed rapidly that HCC developed only nine months after the diagnosis of BCS. The factors causing this rapid progression are still unclear and remain to be investigated.
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ranking = 1
keywords = carcinogenesis
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22/56. Nuclear accumulation of beta-catenin without an additional somatic mutation in coding region of the APC gene in hepatoblastoma from a familial adenomatous polyposis patient.

    The APC (adenomatous polyposis coli) gene status in a familial adenomatous polyposis (FAP) patient who developed hepatoblastoma was analyzed by the yeast color assay. Although a single base insertion at codon 462 resulting in truncation of its product was documented in hepatoblastoma cells, no additional somatic mutation was detectable in the whole coding sequence of the APC gene. The nuclear accumulation of beta-catenin without mutation in the exons 2-4 of the beta-catenin gene, however, was observed in the tumor cells by immunohistochemistry. The similar nuclear accumulation of beta-catenin without an additional somatic mutation in its gene, in the absence of somatic mutation in cluster region of the APC gene, has been previously reported in the single FAP case. Moreover, review in the hepatoblastoma cases in the FAP families showed a relatively later onset of the disease when compared with the sporadic cases. These observations suggest that accumulation of beta-catenin without an additional somatic mutation in the APC gene might be a possible mechanism for tumorigenesis of hepatoblastoma in the FAP families.
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ranking = 0.9979838364387
keywords = tumorigenesis
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23/56. A novel missense mutation of the MEN1 gene in a multiple endocrine neoplasia type 1 patient associated with carcinoid syndrome.

    We report a multiple endocrine neoplasia type 1 (MEN1) patient associated with carcinoid syndrome. A 50-year-old woman had parathyroid hyperplasia with primary hyperparathyroidism, a pancreatic tumor and carcinoid tumors in the liver and duodenum. The primary lesion of the carcinoid was probably the bronchus. Direct sequencing analysis revealed a novel missense mutation at codon 342 in exon 7 causing an amino acid change from alanine to proline (A342P) of the MEN1 gene. loss of heterozygosity (LOH) was also detected in the resected parathyroid tissue. This mutation appeared to play an important role in the tumorigenesis of the endocrine tissues in the present case.
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ranking = 0.9979838364387
keywords = tumorigenesis
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24/56. beckwith-wiedemann syndrome-associated hepatoblastoma: wnt signal activation occurs later in tumorigenesis in patients with 11p15.5 uniparental disomy.

    beckwith-wiedemann syndrome (BWS) patients with chromosome 11p15.5 uniparental isodisomy (UPD) have an increased risk for developing embryonal tumors. UPD in these patients involves maternal loss of heterozygosity (LOH) and paternal duplication, which leads to tissue overgrowth and tumor development. Although 11p15.5 UPD predisposes to tumorigenesis, the events leading to tumorigenesis in UPD patients remains unknown. We have examined two hepatoblastomas in the BWS patients with UPD to determine the sequence of genetic events. Constitutional 11p15.5 LOH was detected in the blood or nonneoplastic liver of the BWS patients with hepatoblastoma. mutation of beta-catenin gene (CTNNB1) was found in one hepatoblastoma. Although mutations in CTNNB1 were not found in the second hepatoblastoma, nuclear accumulation of beta-catenin was detected. However, mutation of CTNNB1 or nuclear accumulation of beta-catenin was not detected in the tissue with hepatomegaly which contains UPD cells. These data indicate that Wnt signal activation can be involved as a later event in BWS-associated hepatoblastoma involving 11p15.5 UPD.
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ranking = 5.9879030186322
keywords = tumorigenesis
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25/56. Operated hepatocellular carcinoma in two hiv- and HCV-positive hemophilic patients.

    Some hemophilic patients in japan suffer from infections with both human immunodeficiency virus (hiv) and hepatitis virus because they received contaminated nonheated blood products. coinfection with hiv appears to accelerate the course of chronic hepatitis. Although powerful antiviral therapy was introduced as hiv treatment and the prognosis of hiv patients was dramatically improved, the risk of rapid progression of hepatitis and carcinogenesis remains for the patients. Recently, we performed surgery for hepatocellular carcinoma (HCC) in two hemophilic patients with hiv and hepatitis c virus (HCV) coinfection. Case 1 was a 52-years-old man who suffered from liver cirrhosis, hypersplenism, and hyperammonemia due to portosystemic shunt. A recent abdominal computed tomography (CT) scan had revealed a low-density area in segment VI of the liver. splenectomy and partial resection of the liver were performed. Case 2 was a 66-year-old man who had been diagnosed with chronic hepatitis at age 50, and hiv infection at age 52 years. When his serum alpha-fetoprotein level was increased, CT scan of the liver revealed a mass in segment VIII. Subsegmentectmy of the liver was performed. Although the CD4 value in each patient was lower than 200 micro l, the operations were safely carried out and no major complication occurred. Because the chance of encountering HCC patients infected with hiv and HCV is increasing in japan, we should consider the perioperative care of these patients, as well as the protection of medical workers against hiv infection.
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ranking = 1
keywords = carcinogenesis
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26/56. Hepatocellular carcinoma associated with autoimmune hepatitis.

    Autoimmune hepatitis (AIH) is a disorder of unknown etiology, which often progresses to cirrhosis and carries a high mortality, even though its treatment with corticosteroids has become common. Hepatocellular carcinoma (HCC) has been reported as a rare complication of AIH. We describe herein a patient with HCC associated with AIH, in whom microwave coagulation therapy provided a means of definitive management, and we also review the literature. male sex and longstanding cirrhosis seem to be the risk factors for hepatocarcinogenesis in AIH. The prognosis of this disease is extremely poor because of the low resectability caused by poor hepatic reserve. It is important to pay attention to hepatic disorders and the possible development of HCC at the time of diagnosis of AIH. Surgeons should select suitable treatment, without undue surgical stress, whenever the diagnosis of HCC has been established. Microwave coagulation therapy is a preferred option for the treatment of high-risk patients with poor hepatic reserve or unresectable multiple HCCs.
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ranking = 1
keywords = carcinogenesis
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27/56. Ectopic liver and hepatocarcinogenesis: report of three cases with four years' follow-up.

    Hepatocellular carcinoma (HCC) may arise in ectopic livers, which are autonomous islands of normal liver parenchyma located in the abdomen or thorax. The majority of HCCs in ectopic livers are reported in oriental patients. We describe here three new cases of HCC in Caucasian patients. The clinical presentation varied from dull epigastric pain in one patient, to abrupt onset with signs and symptoms of acute abdomen caused by intra-abdominal bleeding in another patient, to an unexplained progressive increase of alpha-fetoprotein serum levels in a third patient. None had risk factors for HCC or liver disease. One of the patients developed HCC at age 34 years; she is the youngest patient ever described to develop HCC in ectopic liver. Our data further strengthen the hypothesis that ectopic livers are particularly predisposed to developing HCC. The patients were followed up for 4 years after surgery: two remain free of disease, suggesting that the unique localisation and growth pattern may render these tumours particularly susceptible to curative resection.
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ranking = 4
keywords = carcinogenesis
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28/56. tissue distribution of Thorotrast and role of internal irradiation in carcinogenesis.

    carcinogenesis in Thorotrastosis has been assumed due to direct bombardment by alpha-particle with high linear energy transfer during decay of 232Th. To revisit the mechanism of carcinogenesis by Thorotrast (THR), we examined the tissue distribution of THR granules and two-dimensional distribution of radioactivity in the organs of Thorotrastosis patients and studied their spatial relationship to histopathological changes. The high radioactivity in the patients' organ was predominantly derived from decay of thorium series and showed unique distribution, while the far lower natural radioactivity was mainly from uranium series decay and fairly evenly distributed. It was found that a large majority of THR granules were phagocytized by macrophages and were embedded in extensive fibrosis. Cancer was rarely in the center of THR deposition but rather at a distance from the deposits. These observations may indicate that the predominant feature of THR deposition is the tissue damage by direct hit of alpha-particles and subsequent fibrosis. The effect of THR resembles action of toxic chemical agents, as several authors have pointed out. We therefore assume that carcinogenesis in Thorotrastosis is a combination of events, such as regeneration of liver tissue after radiation damage, emission of secondary electrons, ionization of the surrounding tissue, and beta- or gamma-ray from daughter nuclei of thorium (Th). In this context, the role of alpha-particle is important but more intriguing.
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ranking = 6
keywords = carcinogenesis
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29/56. mutation of TP53 gene is involved in carcinogenesis of hepatic undifferentiated (embryonal) sarcoma of the adult, in contrast with Wnt or telomerase pathways: an immunohistochemical study of three cases with genomic relation in two cases.

    BACKGROUND/AIMS: Hepatic undifferentiated (embryonal) sarcoma (HUS) is an exceptional hepatic malignant tumor in adults. Genetic studies were never reported in adult cases. methods: In this study concerning three cases of HUS occurring in adult, we studied the three classical ways of carcinogenesis i.e. the TP53 (p53), Wnt (CTNNB1/beta-catenin and AXIN1) and telomerase (hTERT) pathways. We studied the expression of p53, beta-catenin and telomerase catalytic subunit hTERT by immunohistochemistry in the three cases; we determined TP53 gene mutation in two cases and the genome-wide allelotype, AXIN1, and CTNNB1/beta-catenin gene mutation in one case. RESULTS: immunohistochemistry showed an overexpression of p53 in more than 80% of tumoral cells; furthermore, mutations of TP53 were observed in two cases, involving the sequence-specific dna binding domain. In contrast, no mutation was found in CTNNB1/beta-catenin and AXIN1 genes. Tumoral cells did not show hTERT staining nor nuclear expression of beta-catenin. In addition, allelotype analysis in one case showed loss of heterozygosity of chromosome 7p, 11p, 17p, 22q, and allelic imbalance of 1p, 8p, 20q. CONCLUSIONS: In this report of HUS in three adult patients, we emphasize the role of TP53 pathway in carcinogenesis of this rare tumor. This point could be of interest for therapeutic strategies.
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ranking = 6
keywords = carcinogenesis
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30/56. Hepatic tumorigenesis in acute hepatic failure.

    We report on a 59-year-old woman and a 31-year-old man with no previous medical history of liver disease presenting with acute liver failure probably caused by drug toxicity. High urgency liver transplantation was performed 30 and 51 days after the onset of symptoms, respectively. Histomorphological evaluation of the explanted livers revealed incidental dysplastic nodules and hepatocellular carcinoma of up to 8 mm in diameter. Up to now only a few cases of metastatic liver disease and even fewer cases of primary liver cancer presenting as acute liver failure have been described. Our cases indicate hepatic tumorigenesis not as a cause of hepatic failure but either as an event taking place in parallel or as a process being induced by progressive liver failure.
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ranking = 4.9899191821935
keywords = tumorigenesis
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