Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 61-year-old white female with chronic hepatitis C virus (HCV) infection first diagnosed in 1994 was admitted with two newly discovered lesions in the liver suspected to represent hepatocellular carcinoma. The alpha-1-fetoprotein (AFP) level was within normal limits and there was neither clinical nor sonographic evidence of liver cirrhosis. Fine needle aspiration, however, showed an high-grade malignant centroblastic non-Hodgkin lymphoma (NHL). Staging failed to confirm extrahepatic involvement. Both a cryoglobulinemia and HIV infection were ruled out. Although the coincidence of HCV infection and NHL is not well recognized, recent studies have indicated an increased incidence of NHL and hepatitis C in up to 38% of patients with cryoglobulinemia. In these patients, the diagnosis is always one of a low-grade lymphoma. Based on its lymphoproliferative characteristics, an etiologic role for HCV in the development of NHL has been discussed, though the exact pathogenesis remains unclear.
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PMID:Intrahepatic high-grade malignant non-Hodgkin lymphoma in a patient with chronic hepatitis C infection. 868 60

Substantial evidence indicates that several common viruses are clearly or probable causal factors in the etiology of specific malignancies. These viruses either normally establish latency or can become persistent infections. Oncogenesis is probably linked to an enhanced level of viral activation in the infected host, reflecting heavy viral dose or compromised immune control. The major virus-malignancy systems include hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatocellular carcinoma; human lymphotropic virus-type 1 (HTLV-1) and adult T-cell leukemia/lymphoma (ATL); Epstein-Barr virus (EBV) and endemic Burkitt's lymphoma, nasopharyngeal carcinoma, and Hodgkin's disease; and human papilloma virus (HPV) and cervical cancer. Of these, a vaccine is available only for HBV. These malignancies tend to occur in early to mid-life and account for a substantial amount of morbidity and person-years lost. They are also likely to occur as "opportunistic malignancies" among individuals infected with human immunodeficiency virus type-1, particularly among those who experience prolonged survival.
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PMID:Overview: viral agents and cancer. 874 95

The hepatitis C virus (HCV) is a recently described and important cause of acute and chronic liver disease. A hallmark of HCV is its propensity to become chronic, some patients with chronic HCV progressing to cirrhosis and hepatocellular carcinoma (HCC). HCV is also lymphotrophic and we report 2 patients with HCV cirrhosis who developed non-Hodgkins lymphoma (NHL). These cases raise the possibility that chronic HCV infection of lymphocytes plays an aetiological role in this malignancy. However screening of a further 63 consecutive patients over the age of 50 years with NHL for HCV antibody by second generation enzyme linked immunoassay (ELISA) failed to identify any patients with evidence of HCV infection. This suggests that HCV is an uncommon contributory factor for the development of non-Hodgkins lymphoma in the United Kingdom.
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PMID:Non-Hodgkin's lymphoma and hepatitis C virus infection. 890 79

There are two ways of connecting Epstein-Barr virus (EBV) with the uncontrolled growth of EBV infected B lymphocytes: in case of evident immunosuppression when the control by cellular immunity is missing or in the case of pathological growth of malignant clone as a result of genetic translocations. Today, EBV is linked with the development of lymphomas in immunosuppressed patients, Hodgkin's and Burkitt's lymphoma and nasopharyngeal carcinoma. The presence of EBV genome in these patients can be confirmed in malignant cells, in lower or higher percent, as well as the high titers of antibodies against specific virus antigens. Hepatitis B viral infection (HBVI) of specific chronic course and associated with intensified inflammation and mitotic activity is of one of the most important factors in the appearance of hepatocellular carcinoma. Although the integration of viral DNA in DNA of hepatocytes has been one of the possible preconditions for carcinogenesis, recently a great attention has been paid to the inactivation of p53 suppressor gene, being a transcriptive transactivator. Other possible cofactors of carcinogenesis imply long-lasting viral replication, coinfection with HVB, HCV or HDV, interaction with other chemical carcinogens (hormones, aflatoxin, alcohol and similar). In distinction from other human DNA viruses, Hepatitis C virus (HCV) is a RNA virus which is not integrated in genome of hepatocyte and active replication of virus is maintained even when hepatocellular carcinoma is detected. It has been assumed that HCV inactivate or mutate the gene of tumor suppression p53 in an early stage of hepatocellular carcinoma development.
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PMID:[Epstein-Barr, hepatitis B and hepatitis C virus infections and their oncogenic potentials]. 947 11

We are giving an overview over the clinical features and different therapeutic options of HIV associated malignancies. There are three AIDS-defining malignancies: - Kaposi's sarcoma - Non-Hodgkin's lymphoma (NHL) - cervical cancer. In Kaposi sarcoma there is a broad therapeutic spectrum from cryotherapy to systemic chemotherapy depending on the site and stage of the Kaposi sarcoma. In NHL early therapeutic intervention is necessary because of the fast progress of the tumor. The cervical cancer in HIV-infected women seems to be more aggressive than in non-infected and also needs early therapeutic intervention. Many other tumors seem to occur more frequently in patients with HIV infection: anorectal cancer, malignant testicular tumors, lung cancer, Hodgkin's lymphoma, basal cell carcinoma, squamous cell carcinoma, and even malignant melanoma. The cancer incidence in HIV-patients seems to be higher among nonblacks. Most of the immunodeficiency associated tumors are virus induced and they are accompanied by a persistent viral infection, including HHV-8 in Kaposi's sarcoma; Epstein Barr virus (EBV) in NHL; and human papillomavirus (HPV) in cervical cancer. But there are also types of virus induced tumors which are not frequently associated with HIV-infection like the primary hepatocellular carcinoma in patients with hepatitis B virus infection.
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PMID:Clinical manifestations and therapies of AIDS associated tumors. 950 54

In a retrospective study of a 12-year period (1981-1992) liver histology was analyzed in 227 autopsied patients infected with the human immunodeficiency virus. Normal histology could only be documented in 29 patients (13%). In the majority of cases (56%) uncharacteristic changes were seen such as steatosis (34%), hemosiderosis (10%) or non-specific reactive hepatitis (7%). The finding of hepatic peliosis obtained in 4 patients was not associated with inflammatory liver changes, especially infections from Rochalimaea. Within a wide range of opportunistic infections recorded in 50 patients (22%), hepatitis caused by Cytomegalovirus (8%), Toxoplasma gondii (5%), Leishmania donovani (1%), Cryptococcus neoformans and Pneumocystis carinii (each 0.5%) was diagnosed. Among 16 cases (7%) of mycobacterial liver infections typical mycobacteria were found in two patients and atypical mycobacteria in 14 patients, respectively. In 23 patients (10%) chronic viral hepatitis, caused by HBV (7%) or HCV infections (3%), respectively, was observed. Hepatitis was typed as mild only in each 5 patients with HBV or HCV infection, whereas the remaining cases showed a transition towards cirrhosis. Two patients with HBV-associated cirrhosis developed hepatocellular carcinoma. The remaining 32 malignant liver tumors represented secondary neoplasms, including 13 cases of non-Hodgkin's lymphomas.
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PMID:[Liver changes in AIDS. Retrospective analysis of 227 autopsies of HIV-positive patients]. 964 44

Immunodeficiency, be it congenital, therapeutic, or infectious in origin, increases the risk of certain, but not all, types of cancer. A common feature of these cancers is that specific infectious agents appear to be important in their etiology, not only in immunodeficient subjects but also in the general population. People with acquired immunodeficiency syndrome (AIDS) are at an increased risk of Kaposi's sarcoma, non-Hodgkin's lymphoma, Hodgkin's disease, squamous cell carcinoma of the conjunctiva, and childhood leiomyosarcoma. It is striking that most of these cancers have been associated with specific human herpesvirus (HHV) infections: HHV-8 with Kaposi's sarcoma and the closely related Epstein-Barr virus with non-Hodgkin's lymphoma, Hodgkin's disease, and possibly also with childhood leiomyosarcoma. Moreover, similar associations between these viruses and cancer have been found, albeit inconsistently, in people who are not immunosuppressed. Further research is needed to establish whether the risk of other cancers is also increased in people with AIDS, although, if so, the cancers are likely to be rare or to have comparatively small associated relative risks. Existing evidence suggests that there may be no marked increase in the risk of two common cancers that are known to be caused by infectious agents--hepatocellular carcinoma and invasive carcinoma of the uterine cervix. The apparent lack of an increase in invasive cervical cancer is unexpected and needs further investigation, especially since the prevalence of cervical infection with human papillomaviruses and of low-grade preneoplastic changes in the cervical epithelium is increased in women with AIDS. With the prospect of improved survival in people with AIDS, the effect of immunosuppression on cancer is likely to become an increasingly important issue.
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PMID:Overview of the epidemiology of immunodeficiency-associated cancers. 970 94

Cytogenetic and molecular studies have frequently shown chromosome 6q deletions in non-Hodgkin lymphoma and several human cancers. There have been few studies concerning chromosome 6q deletion in hepatocellular carcinoma (HCC), and most of these studies have focused on region 6q26-27. We previously described frequent allelic loss at 6q14 in HCC. As a step toward narrowing the scope of search for tumor suppressor genes, we used a series of yeast artificial chromosome clones that map to the long arm of chromosome 6 (6q14-6q22) by fluorescence in situ hybridization (FISH) to define the minimal common region of allelic loss in 25 cases of HCC. Altogether, 12 tumors had allelic loss on 6q (48%). Eleven of the 12 tumors had polysomy of chromosome 6 with evident intratumor cytogenetic heterogeneity. The minimal common region of allelic loss lies within a 2-cM region at 6q14, flanked by D6S458 (849_d_8) and D6S275 (911_a_3). Clinicopathologic correlation between the 12 patients with allelic loss at 6q and the 13 patients without allelic loss showed no significant differences in any basic characteristics except survival. Patients with allelic loss at 6q had a much longer median survival time than those without allelic loss (50 months vs. 11 months, P = 0.0019). Only 5 of the 25 HCC patients were still alive at the time of this study, and all of them had allelic loss at 6q, which is also statistically significant (P = 0.037, alive vs. dead). The association of allelic loss at 6q with polysomy implies that this may be a progression-associated event in HCC. The correlation of allelic loss at 6q with long survival suggests a complex mechanism of tumorigenesis in HCC and is worthy of further investigation.
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PMID:Allelic loss at chromosome band 6q14 correlates with favorable prognosis in hepatocellular carcinoma. 1061 27

Neoplasms of the liver may arise from any cell type within the liver parenchyma. Hepatocellular carcinoma is by far the most common primary malignant tumour of the liver in adults. Indeed, it is one of the most common tumours in the world with striking geographic differences. These incidence rates can be explained by differences in Hepatitis-Virus carrier rates which they closely reflect. Nearly 10% of malignant liver tumors are represented by cholangiocarcinoma which originates from small intrahepatic bile ducts. Hepatoblastoma accounts for approximately 5% of malignancies in childhood. Most hepatoblastomas fall into epithelial or mixed epithelial and mesenchymal categories. Fetal-type cells and embryonal-type cells represent the epithelial components. Rare primary malignant non-epithelial tumours are angiosarcomas, leiomyosarcomas or fibrosarcomas, arising from vascular or mesenchymal components of the liver respectively. All types of Hodgkin and Non-Hodgkin Lymphomas may secondarily involve the liver. Most primary hepatic lymphomas are of diffuse large B-cell type and are extremely rare.
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PMID:[Pathology of liver tumors]. 1096 Sep 66

Hepatitis C virus (HCV) is a hepatotropic virus, but its genome and replicative intermediates also have been detected in peripheral blood mononuclear cells in patients with chronic hepatitis C. Chronic HCV infection may lead to hepatocellular carcinoma and, in a small percentage of cases, to B-cell non-Hodgkin lymphoma. To our knowledge, coexistence of these 2 tumors has not been reported previously. We describe a case of chronic hepatitis C and cirrhosis with 2 small hepatocellular carcinomas and incidental non-Hodgkin lymphoma of a hilar lymph node found during liver transplantation. Although the mechanisms of HCV oncogenesis in hepatocellular carcinoma and in lymphoma are unclear, the presence of these 2 tumors in a single patient are in agreement with the tropism of HCV and its role in oncogenesis.
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PMID:Hepatocellular carcinoma and non-Hodgkin lymphoma in a patient with chronic hepatitis C and cirrhosis. 1103 91


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