UMLS:C0019204 - FACTA Search

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

Chromosome 8p21-22 is a frequent site of loss of heterozygosity in many types of cancer, including hepatocellular carcinoma (HCC). Tumor necrosis factor-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2/DR5), a member of tumor necrosis factor receptor family, is mapped to chromosome 8p21-22. Mutations of TRAIL-R2 have been detected in lung cancer, breast cancer, head and neck cancer, and non-Hodgkin's lymphoma. In this study, we analyzed the entire coding regions and all splicing sites of TRAIL-R2 in 40 HCCs and the death domain region in additional 60 HCCs. We could detect one point mutation in the death domain in only one HCC (1%). Our data suggest that somatic mutations of TRAIL-R2 gene do not play an important role in the carcinogenesis of HCC.
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PMID:Mutation of the DR5/TRAIL receptor 2 gene is infrequent in hepatocellular carcinoma. 1217 36

Imaging techniques like ultrasonography (US) or computed tomography (CT) allow full liver scanning and the accurate detection of focal lesions of the liver parenchyma. The occurrence of such lesions in concomitance with non-Hodgkin's lymphoma (NHL), both at the onset of the disease and during follow-up, is of great significance, because it affects staging, prognosis and therapeutic choices. Moreover, the occurrence of focal liver lesions in the setting of a lymphoma is generally considered to be a marker of liver involvement. Nonetheless, data on the prevalence and clinical significance of focal liver lesions occurring in these clinical conditions are limited. Therefore, we retrospectively evaluated the prevalence, nature and clinical significance of focal liver lesions diagnosed by imaging techniques (US and CT) in 414 consecutive NHL patients. The nature of the lesions was established either by US-guided biopsy or by evaluation of the response to chemotherapy for the underlying disease and confirmed by clinical and US follow-up. Subtype of NHL (aggressive or indolent) and Hepatitis C virus (HCV) status were also considered. We detected 129 focal liver lesions (76 at onset and 53 during the follow-up). Hepatic involvement by NHL was found in 69 cases (53%). We observed 7 cases of Hepatocellular Carcinoma (HCC) and 3 cases of metastasis. At onset, only 39% of the detected lesions were due to lymphoma and 58% were benign. Conversely, 74% of the liver lesions detected during the follow-up were due to NHL while 15% to a malignancy other than NHL. All HCC cases occurred in HCV-positive patients with chronic liver disease. We concluded that the focal liver lesions detected at onset in NHL patients are frequently benign and unrelated to the underlying disease. Conversely, most focal liver lesions detected during the follow-up period are malignant and the possibility of HCC occurrence in HCV-positive patients should always be considered. Therefore, these lesions should undergo a full diagnostic work-up, including US-guided biopsy.
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PMID:Focal liver lesions in non-Hodgkin's lymphoma: investigation of their prevalence, clinical significance and the role of Hepatitis C virus infection. 1246 Jul 82

Hepatitis C virus (HCV) is a major causative agent for chronic liver diseases leading to hepatocellular carcinoma (HCC) and has also been suggested to be a possible etiologic factor for different lymphoproliferative diseases, including mixed cryoglobulinemia (MC) and B-cell non-Hodgkin's lymphoma (NHL). To understand the roles of HCV core protein in the pathogenesis of HCV related diseases, we produced two lines of the transgenic mice (HC82310 and HC9053) that express the HCV core transgene. One of the lines, HC9053, developed malignant lymphoma (ML, follicular center cell type) with a high frequency (80%) at the ages over 20 months. Hepatocellular adenoma was also observed in this line of transgenic mouse. We demonstrated expression of HCV core protein and mRNA in the liver of transgenic mice, and also detected the core mRNA in the enlarged lymph nodes of the transgenic mice which developed ML. These results suggest that the core protein may play an important role in the development of ML, and that the HC9053 transgenic mice provide suitable models for understanding the mechanism of HCV-related lymphoproliferative diseases.
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PMID:Expression of hepatitis C virus core protein associated with malignant lymphoma in transgenic mice. 1249 92

Iron transport in the plasma is carried out by transferrin, which donates iron to cells through its interaction with a specific membrane receptor, the transferrin receptor (TfR). A soluble form of the TfR (sTfR) has been identified in animal and human serum. Soluble TfR is a truncated monomer of tissue receptor, lacking its first 100 amino acids, which circulates in the form of a complex of transferrin and its receptor. The erythroblasts rather than reticulocytes are the main source of serum sTfR. Serum sTfR levels average 5.0+/-1.0 mg/l in normal subjects but the various commercial assays give disparate values because of the lack of an international standard. The most important determinant of sTfR levels appears to be marrow erythropoietic activity which can cause variations up to 8 times below and up to 20 times above average normal values. Soluble TfR levels are decreased in situations characterized by diminished erythropoietic activity, and are increased when erythropoiesis is stimulated by hemolysis or ineffective erythropoiesis. Measurements of sTfR are very helpful to investigate the pathophysiology of anemia, quantitatively evaluating the absolute rate of erythropoiesis and the adequacy of marrow proliferative capacity for any given degree of anemia, and to monitor the erythropoietic response to various forms of therapy, in particular allowing to predict response early when changes in hemoglobin are not yet apparent. Iron status also influences sTfR levels, which are considerably elevated in iron deficiency anemia but remain normal in the anemia of inflammation, and thus may be of considerable help in the differential diagnosis of microcytic anemia. This is particularly useful to identify concomitant iron deficiency in a patient with inflammation because ferritin values are then generally normal. Elevated sTfR levels are also the characteristic feature of functional iron deficiency, a situation defined by tissue iron deficiency despite adequate iron stores. The sTfR/ferritin ratio can thus describe iron availability over a wide range of iron stores. With the exception of chronic lymphocytic leukemia (CLL) and high-grade non-Hodgkin's lymphoma and possibly hepatocellular carcinoma, sTfR levels are not increased in patients with malignancies. We conclude that soluble TfR represents a valuable quantitative assay of marrow erythropoietic activity as well as a marker of tissue iron deficiency.
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PMID:Soluble transferrin receptor for the evaluation of erythropoiesis and iron status. 1258 62

Patients with HIV infection are at increased risk for developing Kaposi's sarcoma, non-Hodgkin's lymphoma, and several other cancers. The relative risks for the most common epithelial cancers in the general population--lung, breast, colon/rectum, stomach, liver, and prostate--are not increased substantially in people with AIDS, however. Accumulating data suggest that HIV-infected patients also are at increased risk for developing Hodgkin's lymphoma, cervical carcinoma in situ (CIS), other anogenital neoplasms (invasive cancer and CIS), leiomyosarcoma, and conjunctival squamous cell carcinoma. There is inconclusive evidence, however, with regard to HIV infection being associated with invasive cervical cancer, testicular seminoma, or hepatocellular carcinoma. Notably, other viral infections have been implicated in the etiology of many of these conditions. The introduction of highly active antiretroviral therapy (HAART) has decreased the incidence of AIDS-associated cancers in Western countries, but less than 1% of AIDS patients are receiving HAART in the HIV epicenter of sub-Saharan Africa. Further therapeutic advances that extend survival with HIV infection with varying reconstitution of immune competence may lead to additional alterations in cancer risk.
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PMID:Epidemiology of AIDS-related malignancies an international perspective. 1285 50

From January 1990 to December 2000, 202 patients with clinical evidence of liver disease underwent fine needle aspiration cytology of the liver. Of these, 102 patients were diagnosed as non-neoplastic lesions. These include diffuse parenchymal disease of liver, liver abscess, hepatitis, and granulomas. There were 100 patients with malignancies of the liver. Out of the above, 64 were due to metastatic carcinoma, 31 were primary hepatocellular carcinoma, 1 hepatoblastoma and in 4 patients the diagnosis of non-Hodgkin's lymphoma was made. By comparing with clinical and biochemical parameters, the diagnostic accuracy of the fine needle aspiration cytology, in this study, was found to be more accurate in malignant nodules of the liver as compared to other pathological lesion. The findings of fine needle aspiration cytology of the liver reported by other authors are discussed and it is concluded that this diagnostic method is a safe, useful and economic procedure with minimum complication and can be routinely done for assisting diagnosis of liver diseases in our clinical set up.
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PMID:Fine needle aspiration cytology of liver: a study of 202 cases. 1451 82

HIV caregivers face many challenges following initiation of ART. The development of jaundice is uncommon but worrisome. In this case, two distinct and contrasting episodes of jaundice were observed. In the first instance, isolated elevation of the indirect bilirubin without elevation of the alkaline phosphatase was noted. The normal PT and serum aminotransferase levels indicate the absence of intrinsic liver dysfunction. Elevations in the indirect bilirubin may result from either impaired uptake/conjugation or excess production. The latter, usually from acquired hemolysis, may be a complication of an occult NHL. A work-up for this AIDS-related malignancy was not initiated since the caregivers recognized jaundice as a complication of IDV, which inhibits UDP-glucuronyl transferase and produces a Gilbert's-like syndrome. Physicians can expect to encounter this syndrome even more frequently with ATV. Experienced patients given RTV-boosted ATV have experienced elevations of unconjugated hyper-bilirubinemia in up to 45 percent of cases in clinical trials. However, such elevations do not reflect liver dysfunction and symptomatic jaundice requiring dosage reduction that occurred infrequently (7 to 8 percent of study patients). Counseling patients about this syndrome may promote adherence and prevent self-directed interruptions of ATV that compromise efficacy. The second case of jaundice provides a more formidable diagnostic challenge. The triad of LFT abnormalities (mild elevation of aminotransferases, normal PT, and marked cholestatic jaundice) implies an acute process that is mildly toxic to hepatocytes without affecting their synthetic function. The subacute nature of the patient's cholestatic jaundice suggests either intrahepatic infiltrative disease of the liver or extrahepatic obstruction of the biliary tree, most likely due to the patient's relatively modest level of pain and lack of fever. Despite LFT abnormalities occurring 17 months after a switch in his ART, cumulative drug-related toxicities must still be considered. Ritonavir can produce significant elevations in the AST/ALT, especially with pre-existing chronic liver disease as with hepatitis C virus coinfection. The NRTIs can produce hepatic steatosis, a result of mitochondrial toxicity and impaired fatty acid oxidation. However, jaundice and cholestasis are not typical of the latter syndrome. With a negative contrast CT that excludes parenchymal liver disease, investigation of the biliary tree to assess the presence of AIDS-related cholangitis was the next step. Performing a sphincterotomy or stent placement, and obtaining brushings or biopsy specimens to determine the extent of extrahepatic obstruction may help define a pathogen and be life-saving. The negative results of the ERCP justify the final diagnostic step, a liver biopsy to evaluate microscopic infiltrative disease that might not have been detected on contrast abdominal CT. Examples might include granulomatous disease (MAC), fungal etiologies (histoplasmosis), carcinomatosis (lymphoma, hepatoma, cholangiocarcinoma), and microvascular disease (bacillary angiomatosis). The failure to observe granulomatous inflammation in the liver does not exclude MAC infection, as MAC may involve other peri-aortic or mesenteric lymph nodes. This form of IRIS is unlikely given the abdominal CT findings, lack of systemic complaints, and extended persistence of liver aminotransferases. The nonspecific results of the liver biopsy are a common outcome in advanced AIDS patients with elevated alkaline phosphatase levels. Despite not having identified a pathogen, the biopsy establishes chronic liver disease and prompts re-evaluation and change of treatment to NFV. The subsequent normalization of the patient's aminotransferase levels suggests a prior adverse effect of LPV/r in the setting of unexplained, chronic liver disease. Most importantly, this case highlights the importance of HIV caregivers to review ART for safety when noting chronic liver dysfunction. Patients need to be counseled to minimize acetaminophen use, to consume alcohol in moderation, and to avoid behavior with risk for hepatitis C. Finally, all HIV patients should receive appropriate vaccination against hepatitis A and B if serology shows lack of protective immunity.
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PMID:Clinical vignette in antiretroviral therapy: jaundice. 1498 14

We report a case of primary hepatic non-Hodgkin's lymphoma in a 77-year-old man with chronic hepatitis C. Laboratory data revealed slightly elevated liver function parameters and positive antibody for hepatitis C virus (HCV). Abdominal ultrasonography showed a low-echogenic tumor, about 5 cm in diameter, in the left lateral segment. Abdominal computed tomography showed that the tumor was marginally enhanced in the early phase, but no enhancement was seen in the late phase. Magnetic resonance imaging showed that the tumor was hypointense in relation to the liver on T1-weighted images, but hyperintense on T2-weighted images. Hepatic angiography showed a homogeneously stained hypervascular tumor. Under the diagnosis of a liver tumor, thought to be a hepatocellular carcinoma, left lateral segmentectomy was performed. Histological examination confirmed a diagnosis of non-Hodgkin's diffuse large B-cell lymphoma that was positive for L-26 and CD79Alpha, but negative for CD3 and UCHL-1. The surrounding liver tissue showed signs of chronic active hepatitis. Multiple recurrent lesions were found in the liver, spleen, and iliac bones 4 months postoperatively. However, complete remission was achieved after five courses of systemic chemotherapy using pirarubicin, cyclophosphamide, vincristine sulfate, and prednisolone. The patient has been carefully followed up for about 1 year since his operation, and has been doing well. We review the literature on primary non-Hodgkin's lymphoma arising in the liver infected by HCV.
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PMID:Primary hepatic non-Hodgkin's lymphoma in a patient with chronic hepatitis C: report of a case. 1505 56

Comparison of human leukocyte antigen (HLA) frequencies in patients with hepatitis C virus (HCV)-associated hepatocellular carcinoma (HCC) and in patients with HCV-associated non-Hodgkin's lymphoma (NHL) has not been addressed previously. To this aim, we investigated the distribution of HLA class II alleles in two selected groups of HCV-infected patients. Group 1 included 50 patients with HCV-associated NHL; group 2 included 29 patients with HCV-associated HCC. A control group included 144 hospitalized patients without NHL or HCC and who were negative for HCV, hepatitis B virus, and human immunodeficiency virus antibodies. Polymerase chain reaction sequence DRB1 and DQB1 specific-primer methods were used. DRB1*1101/DQB1*0301 haplotype, which mainly favors the spontaneous clearance of HCV infection, was lower in HCC subjects than in controls, whereas HLA-DRB1*1104/DQB1*0301, was higher in NHL patients. These findings suggest different pathogenic pathways in HCC and in NHL development. In patients with HCV-associated HCC, a major protective role of DQB1*0301 allele, rather than DRB1*11, was found, probably because of a better HLA class II-associated virus clearance. By contrast, the same allele as HLA-DRB1*04 showed an increase in HCV-associated NHL. These data suggest that NHL and HCC development may be associated to a different response with respect to chronic HLA class II-restricted antigen presentation (perhaps a switch toward CD4+Th2 response in NHL?) or, alternatively, that these alleles could be in linkage disequilibrium to unrelated gene(s), or are in synergy with other immunomodulatory genes that may confer increased risk for NHL.
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PMID:Hepatitis C virus-related hepatocellular carcinoma and B-cell lymphoma patients show a different profile of major histocompatibility complex class II alleles. 1555 90

The fragility of the evidence for SV40 association with human cancer is seen in studies of NHL. A publication in 1999 stated that SV40 is rarely present in NHL. In 2002, two laboratories reported SV40 sequences in 42% to 43% of cases of NHL . One of these laboratories also detected SV40 sequences in small proportions of pediatric tumors (e.g., Wilm's tumor, hepatoblastoma, rhabdomyosarcoma, medulloblastoma, osteosarcoma, and retinoblastoma) and adult carcinomas (e.g., lung, colon, breast, and prostate) These positive results were not confirmed in subsequent studies published in 2003. Capello et al and Mackenzie et al failed to detect SV40 sequences in NHL tissues. Sanjose et al examined sera from patients with NHL and from controls for antibodies reactive to SV40 VLPs, and they detected no significant differences between the two groups. The association of SV40 with NHL is in doubt. An etiologic link between a virus and a cancer becomes plausible when evidence from different lines of enquiry (e.g., epidemiology, pathogenesis, and molecular mechanisms) is mutually reinforcing and together provides a coherent picture that can connect the biology the virus to the characteristics of the disease. The associations of human papillomaviruses with cervical cancer and hepatitis B and C viruses with hepatocellular carcinoma are examples in which the etiologic link is clear. With SV40 and mesothelioma, the data on viral sequences in tumors is inconsistent and disputed, and serologic evidence does not support any association. The epidemiologic data do not show that documented exposures tt SV40 increase the risk of mesothelioma. It seems improbable that a single virus (which cannot be conclusively demonstrated to be present in the community) contributes to the development of such a wide variety of tumors, spanning all age groups and histologic types. The weaknesses in the evidence linking SV40 with mesothelioma are summarized in Box 11 It seems unlikely that infection with SV40 contributes to the development of human mesothelioma or any other human cancer.
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PMID:Causality of mesothelioma: SV40 question. 1555 56

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