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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review first considered some general problems in establishing causal links between a virus and a human cancer and offered some guidelines in the pursuit of this objective. Second, it reviewed the current causal associations for several candidate oncogenic viruses in relation to the tumors with which they are associated. These include Epstein-Barr virus in relation to Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, and non-Hodgkin's lymphoma; hepatitis B and C viruses in relation to hepatocellular carcinoma; human T-cell leukemia/lymphoma virus type 1 and atypical leukemia/lymphoma; and human papilloma viruses in relation to cervical carcinoma. For some, the causal relationship is strong: hepatitis B virus with hepatocellular carcinoma, and human T-cell leukemia/lymphoma virus with adult T-cell leukemia/lymphoma. For one, the causal relationship is moderate: Epstein-Barr virus with African Burkitt's lymphoma. For others it is incomplete or inconclusive: Epstein-Barr virus with Hodgkin's disease and non-Hodgkin's lymphoma, and hepatitis C virus with hepatocellular carcinoma. Current techniques do not permit an answer for some: human papilloma virus with cervical carcinoma.
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PMID:Viruses and cancer. Causal associations. 166 91

This paper aims to summarize current experience with alpha interferon and provide direction for future study. There are four areas in which alpha interferon has proven or potential activity: antiviral, premalignant, adjuvant and advanced disease settings. The three main viral diseases in which interferon alfa-2b has been shown to have activity are chronic viral hepatitis, acquired immunodeficiency syndrome, and human papilloma virus infections. In vitro studies suggest that alpha interferon may inhibit transformation of some premalignant conditions into malignant disease; e.g., vaginal intraepithelial neoplasia. In the adjuvant setting, it is possible that a biological response modifier, such as alpha interferon, may have a role in helping the immune system to destroy residual tumour cells following tumour bulk reduction with radiation or chemotherapy. A higher response rate has been seen in patients with small tumour bulk compared to those with large tumour bulk (e.g., malignant melanoma, ovarian carcinoma), and in patients with early, rather than late, disease (e.g., chronic myelogenous leukaemia, hairy cell leukaemia, multiple myeloma, non-Hodgkin's lymphoma). This may be due to efficacy in a small tumour bulk setting or due to an immunoadjuvant role. In advanced disease, the question is how best to exploit the possible synergistic effects between alpha interferon and other therapeutic modalities. The optimum dose, schedule and patient populations for combined treatment have yet to be determined. The major objective of this paper is to determine how best to capitalize upon the current state of knowledge to build for future trials of alpha interferon, and to determine whether the existing data suggest an adjuvant role for interferon after initial tumour regression.
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PMID:alpha Interferon: the potential drug of adjuvant therapy: past achievements and future challenges. 179 68

Last year, we reported that human papilloma virus type 16 genome (HPV 16 genome) was detected in a case (S.Y.) of bladder carcinoma in situ (bladder CIS) (Cancer Res., 1988). Since then, a number of bladder tumors other than CIS were searched for HPV genome. However, no HPV genome was detected in the bladder tumors. From the results, we consider that HPV may not have a relation with all types of bladder tumor but with only a part of it. In the current report, the case (S.Y.) is presented more precisely than before, in particular on the characteristic bladder lesion. The patient was a 40-year-old female with immunodeficiency and anemia who was referred from a hospital with a complaint of asymptomatic pyuria. Cystoscopic examination revealed a bladder tumor, well-demarcated, white and velvety lesion with slight elevation. On November 25, 1987, she underwent total cystectomy, resection of the anterior vaginal wall and of a part of vulval skin, and ileal conduit formation. Postoperative course was stormy because of bleeding from the wounds and thrombophlebitis in the right femoral vein. In spite of the episodes, she eventually recovered and was discharged 2 months later. However she was readmitted 9 months later due to severe anemia which was ascribed to acute myelogenous leukemia. She is now on cancer chemotherapy for leukemia.
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PMID:[Bladder carcinoma in situ which harbored human papilloma virus. A case report]. 255 17

To elucidate the cellular tropism of Moloney murine leukemia virus (MuLV), we have studied the transduction efficiency of a recombinant MuLV vector carrying the beta-galactosidase reporter gene on a variety of rodent cells. Under optimal conditions for in vitro cell transduction, primary cultures of adult rat fibroblasts derived from various organs were very poorly transduced by the ecotropic MuLV vector (0.02-0.12%) when compared to immortalized cells such as the F2408 (42%) and 3Y1 (defined as 100%) lines. Primary cultures of fibroblasts from neonatal (3.7%) or embryonic rat tissues (4.6%) and primary cultures of rat mammary epithelial cells (3-4%) were somewhat more susceptible. Immortalization of rodent fibroblasts with Polyomavirus Large T. SV40 Large T, and E6-E7 genes of human papilloma virus resulted in a modest or minimal increase in transduction efficiency, and introduction of the transforming genes v-Src, v-Ras, and v-Raf was in most instances associated with a decrease in MuLV vector entry. Variability of transduction efficiency was not related to differences in cellular growth rate and treatment of MuLV vectors in vitro with deoxyribonucleoside triphosphates and treatment of cells in culture with protease inhibitors failed to modify cellular entry of the MuLV vector. On the other hand, inhibition of cellular glycosylation with swansonine, 1-deoxymannojirimycin and, primarily, tunicamycin enhanced entry of the ecotropic vector by up to 220-fold, particularly into cells which were otherwise highly resistant. These findings demonstrate major differences in transduction efficiency of the ecotropic MuLV vector on rodent cells and indicate that cellular glycosylation plays a critical role in determining MuLV cellular tropism.
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PMID:Variable transduction efficiency of murine leukemia retroviral vector on mammalian cells: role of cellular glycosylation. 912 77

The c-abl tyrosine kinase is the proto-oncogene of the v-abl oncogene of the Abelson murine leukemia virus. Although mutational variants of c-Abl can exhibit gain of function and can produce a transformed phenotype, the function of c-Abl in transformation remained unclear. Here, we report that the loss of c-abl facilitates transformation. c-abl-knockout mouse embryonic fibroblasts (MEFs) immortalized by SV40 T antigen acquired anchorage-independent growth, and by constructing mutational variants of T antigen we showed that binding of large T antigen to p53 and RB was necessary to induce anchorage-independent growth. Although c-abl/p53 double-knockout MEFs did not undergo anchorage-independent growth, those expressing human papilloma virus 16 E7, which mainly inactivates RB, did. Our results show that the loss of c-abl facilitates anchorage-independent growth in the context of p53 and RB deficiency, and suggest that loss of function of c-abl facilitates some types of transformation.
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PMID:Loss of c-abl facilitates anchorage-independent growth of p53- and RB- deficient primary mouse embryonic fibroblasts. 1537 21

It is estimated that 15% of all cancers are etiologically linked to viral infection. Specific cancers including adult T-cell leukemia, hepatocellular carcinoma, and uterine cervical cancer are associated with infection by human T-cell leukemia virus type I, hepatitis B virus, and high-risk human papilloma virus, respectively. In these cancers, genomic instability, a hallmark of multistep cancers, has been explicitly linked to the expression of oncoproteins encoded by these viruses. This review discusses mechanisms utilized by these viral oncoproteins, Tax, HBx, and E6/E7, to mediate genomic instability and cellular transformation.
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PMID:Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation. 1564 40

Spontaneously arising tumor cells are not usually angiogenic at first. The phenotypic switch to angiogenesis is usually accomplished by a substet that induces new capillaries that then converge toward the tumor. The switch clearly involves more than simple upregulation of angiogenic activity and is thought to be the result of a net balance of positive and negative regulators. Tumor growth is although to require disruption of this balance and hence this switch must turned on for cancer progression. Progenitor endothelial cells, the crosstalk between angiogenic factors and their receptors and the interaction between vasculogenesis and lymphangiogenesis are all factors that may contribute to the switch. Its promotion is also the outcome of genetic instability resulting in the emergence of tumor cell lines. This review describes the history of the angiogenic switch illustrated in the literature and with particular reference to the three transgenic mouse models, namely RIP1-TAG2, keratin-14 (K14) (human papilloma virus) HPV16 and papilloma virus, used for stage-specific assessment of the effects of antiangiogenic and antitumorigenic agents.
Leukemia 2007 Jan
PMID:The history of the angiogenic switch concept. 1699 Jul 61

In order to promote carcinogenesis multiple factors must be orchestrated. The alteration of the cellular genome after a carcinogenic exposure may result in malignancy if apoptosis is prevented and the immune surveillance fails to eliminate the transformed cell. Infectious agents may exert these properties and transform a host cell. Viruses associated with human cancer are known as 'tumor viruses'. Most of them are capable of integrating into the host genome and have the ability to immortalize the target cell in order to allow their own replication. The infected cell expresses the viral genes, which are able to induce cell growth, proliferation and prevent apoptosis. This review focuses on Epstein-Barr virus, human papilloma virus, hepatitis C virus, hepatitis B virus, human herpes virus 8 and human T-cell leukemia virus, since they have been already established as causative agents of human cancer. An understanding of the viral replication mechanism may provide new targets for the development of specified viral therapy that may have an impact not only on viral infections but in human cancer as well.
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PMID:Viral infections as a cause of cancer (review). 1748 74

The skin is an organ in which direct contact with viruses, solar UV irradiation and increased susceptibility to immune suppression gather to support viral tumorigenesis. Viruses transform keratinocytes by activation of cancer-promoting genes. Viral proteins may directly act as oncogenes that drive cells to proliferate or generate inflammatory responses and cause regeneration of injured cells that eventually lead to malignant transformation. Accelerated viral carcinogenesis is observed in the immune-deficient host. Decreased T-cell reactivity and lower number of antigen-presenting cells in the skin assist in viral escape and emergence of skin tumors. Three pathogenic human viruses associated with skin neoplasms are described: human papilloma virus (HPV), Kaposi's sarcoma (KS)-associated herpesvirus and human T-cell leukemia virus type 1. HPV was linked to squamous cell carcinoma (SCC) of the skin after its role in SCC of the cervix has been discovered. In the rare autosomal recessive epidermodysplasia verruciformis, an increased susceptibility to specific HPV strains initially results in widespread wart infection and later in life in the development of SCC over the sun-exposed skin. The role of HPV in nonmelanoma skin cancer of immune competent hosts is more difficult to prove. The discovery of human herpesvirus 8 as the causative pathogen of KS was made following the AIDS epidemic, and its role in all clinical variants of this tumor was confirmed. KS-associated herpesvirus exerts its tumorigenic effect through a wide repertoire of genes that regulate angiogenesis, inflammation, and cell cycle. Human T-cell leukemia virus type 1 causes adult T-cell leukemia and is often associated with skin eruptions that share common features with cutaneous T-cell lymphoma. In summary, studies of oncogenic viruses shed light on molecular mechanisms leading to tumor formation and aid in recognition of new pathways of carcinogenesis.
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PMID:Viral carcinogenesis in skin cancer. 1764 89

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


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