Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression profiling of cellular genes was performed using a 10,000 cDNA human gene array in order to identify expression changes following chronic infection of human hematopoietic cells with Kaposi's Sarcoma-associated Virus (KSHV) also known as Human Herpesvirus 8 (HHV8) and Human T cell leukemia virus-1 (HTLV-1). We performed cell-free in vitro infection of primary bone marrow derived CD34+ cells using semi-purified HHV8 and a mature IL-2 dependent T cell line, KIT 225, using highly concentrated viral stocks prepared from an infectious molecular clone of HTLV-1. Thirty days post infection, mRNA was isolated from infected cultures and uninfected controls and submitted for microarray analysis. More than 400 genes were differentially expressed more than two-fold following HHV8 infection of primary bone marrow derived CD34+ cells. Of these 400, interferon regulatory factor 4 (IRF4), cyclin B2, TBP-associated factor, eukaryotic elongation factor and pim 2 were up-regulated more than 3.5 fold. In contrast, less than 100 genes were differentially expressed more than two-fold following chronic infection of a mature T cell line with HTLV-1. Of these, only cdc7 was up-regulated more than 3.5 fold. These data may provide insight into cellular signatures of infection useful for diagnosis of infection as well as potential targets for therapeutic intervention.
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PMID:Potential cellular signatures of viral infections in human hematopoietic cells. 1179 Aug 84

HHV8 has been consistently linked to both classical and endemic Kaposi's Sarcoma (KS), primary effusion lymphoma and multicentric Castleman's disease. HHV8 has also been associated to other oncologic diseases although such reports have not been confirmed. Little is known about the transmission routes of HHV8. The main transmission route may differ between developed and developing countries. We carried out a serologic study by Immunofluorescence of antiHHV8 antibodies on 40 children with Acute Lymphoblastic Leukaemia (ALL) and their relatives. 5 children with ALL were positive (12.5%). Seroprevalence was not significantly higher than the western Sicily pediatric population. The variation in seroprevalence between the relatives of HHV8 seropositive and seronegative patients was not significant. Therefore HHV8 does not appear to be correlated with ALL and the main transmission route in our cases could occurr outside the family.
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PMID:[HHV8 infection and acute lymphoblastic leukaemia in children]. 1271 68

Infectious agents, mainly viruses, are among the few known causes of cancer and contribute to a variety of malignancies worldwide. The agents and cancers considered here are human papillomaviruses (cervical carcinoma); human polyomaviruses (mesotheliomas, brain tumors); Epstein-Barr virus (B-cell lymphoproliferative diseases and nasopharyngeal carcinoma); Kaposi's Sarcoma Herpesvirus (Kaposi's Sarcoma and primary effusion lymphomas); hepatitis B and hepatitis C viruses (hepatocellular carcinoma); Human T-cell Leukemia Virus-1 (T-cell leukemias); and helicobacter pylori (gastric carcinoma), which account for up to 20% of malignancies around the globe. The criteria most often used in determining causality are consistency of the association, either epidemiologic or on the molecular level, and oncogenicity of the agent in animal models or cell cultures. However use of these generally applied criteria in deciding on causality is selective, and the criteria may be weighted differently. Whereas for most of the tumor viruses the viral genome persists in an integrated or episomal form with a subset of viral genes expressed in the tumor cells, some agents (HBV, HCV, helicobacter) are not inherently oncogenic, but infection leads to transformation of cells by indirect means. For some malignancies the viral agent appears to serve as a cofactor (Burkitt's lymphoma-EBV; mesothelioma - SV(40)). For others the association is inconsistent (Hodgkin's Disease, gastric carcinomas, breast cancer-EBV) and may either define subsets of these malignancies, or the virus may act to modify phenotype of an established tumor, contributing to tumor progression rather than causing the tumor. In these cases and for the human polyomaviruses the association with malignancy is less consistent or still emerging. In contrast despite the potent oncogenic properties of some strains of human adenovirus in tissue culture and animals the virus has not been linked with any human cancers. Finally it is likely that more agents, most likely viruses, both known and unidentified, have yet to be implicated in human cancer. In the meantime study of tumorigenic infectious agents will continue to illuminate molecular oncogenic processes.
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PMID:Infectious agents and cancer: criteria for a causal relation. 1548 39

Around the world, infection is one of the most important causes of cancer. Almost one in every five malignancies can be attributed to infectious agents. Among infection-related neoplasms, cancers of the stomach, liver and cervix uteri detain the highest incidence figures, and are known to be largely attributable to Helicobacter pylori, hepatitis B and C viruses, and human papilloma virus, respectively. Other infectious organisms can also cause cancer; these include the Epstein-Barr virus (nasopharyngeal carcinoma, and different types of lymphoma), Human herpes virus-8 (Kaposi's Sarcoma), human T-cell leukemia virus type I (leukaemia, lymphoma), liver flukes (cholangiocarcinoma) and schistosomiasis (bladder cancer). Infection with human immunodeficiency virus, although strongly associated with an excess of cancer incidence at many cancer sites, is probably not carcinogenic per se, but acts mainly via immunodeficiency. The burden of infection-related cancers is still underestimated worldwide, due to the use of conservative population prevalence and risk ratio estimates. Furthermore, associations with new infectious agents remain yet to be explored.
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PMID:Infections and cancer: established associations and new hypotheses. 1880 2

Transforming viruses can change a normal cell into a cancer cell during their normal life cycle. Persistent infections with these viruses have been recognized to cause some types of cancer. These viruses have been implicated in the modulation of various biological processes, such as proliferation, differentiation and apoptosis. The study of infections caused by oncogenic viruses had helped in our understanding of several mechanisms that regulate cell growth, as well as the molecular alterations leading to cancer. Therefore, transforming viruses provide models of study that have enabled the advances in cancer research. Viruses with transforming abilities, include different members of the Human Papillomavirus (HPV) family, Hepatitis C virus (HCV), Human T-cell Leukemia virus (HTLV-1), Epstein Barr virus (EBV) and Kaposi's Sarcoma Herpesvirus (KSHV).Apoptosis, or programmed cell death, is a tightly regulated process that plays an important role in development and homeostasis. Additionally, it functions as an antiviral defense mechanism. The deregulation of apoptosis has been implicated in the etiology of diverse diseases, including cancer. Oncogenic viruses employ different mechanisms to inhibit the apoptotic process, allowing the propagation of infected and damaged cells. During this process, some viral proteins are able to evade the immune system, while others can directly interact with the caspases involved in apoptotic signaling. In some instances, viral proteins can also promote apoptosis, which may be necessary for an accurate regulation of the initial stages of infection.
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PMID:The modulation of apoptosis by oncogenic viruses. 2374 82

A genetically engineered human interferon is now available for treating genital warts. Trials are also underway for its effectiveness against certain types of leukemia and AIDS-related Kaposi's Sarcoma.
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PMID:Genital warts treatment available. 2741 70