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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the immunologic surveillance theory of cancer, we reviewed the epidemiologic observations that have been made on cancer risk among population groups with immune deficiency. Lymphoproliferative neoplasms predominate in various groups, most notably renal transplant recipients treated with immunosuppressive agents and patients with primary immunodeficiency syndromes. In some immune disorders, specific forms of nonlymphoid neoplasia seem to occur excessively, although the patterns are not clear-cut or consistent. The available epidemiologic evidence fails to support the concept that immunosurveillance mechanisms are generally involved in carcinogenesis but does provide clues to immunologic processes that may predispose to particular neoplasms.
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PMID:Immunosurveillance and cancer: epidemiologic observations. 34

Cancer is a generic term for a variant manifestation of life caused by genetic mutations of somatic cells. It is not only carcinogenesis which is basically a genetic phenomenon, but also tumor progression which can be influenced by various genetic factors. A group of tumors is known to be inherited in a Mendelian fashion. In addition a great number of single gene disorders is associated with the development of maligne tumors. The further study of these diseases will allow new insights into the fundamental mechanisms leading to clinical cancer. In this respect a series of immunodeficiency diseases is of particular interest. Several organ tumors which seem to occur more frequently in relatives of tumor patients are of practical importance. A more sophisticated classification of these tumors may illuminate their genetic behavior. The geneticist cannot only define groups of individuals with a high cancer risk, but he can identify genetic, e.g. chromosomal, aberrations of cancerous cells which enables him the early detection of neoplasia.
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PMID:[Early diagnosis of neoplasms]. 72 76

The frequency of human immunodeficiency virus (HIV)-infected monocytes that spread on a model basement membrane was about twofold greater than that of an equal number of uninfected control cells through the initial 12 to 18 h of culture. By 24 h, virtually all HIV-infected and uninfected control cells spread on the basement membrane gel. The frequency of spread cells in the uninfected control population was less than 10% of total cells by 12 days. In contrast, 30 to 40% of HIV-infected monocytes remained spread through this time interval and formed a dense interdigitated network of cell processes on and into the gel matrix. Invasion of the basement membrane matrix by HIV-infected monocytes suggested increased secretion of proteases able to digest the gel. Indeed, levels of neutral protease activity in culture fluids from HIV-infected monocytes were significantly higher than those from equal numbers of uninfected control cells. High levels of protease activity in culture fluids of HIV-infected monocytes required productive virus infection and were not observed with cells exposed to T cell-tropic HIV isolates. The predominant protease activity in these cultures was a 92-kd neutral metallogelatinase. HIV-induced changes in monocyte metalloprotease activity may be important for extravasation of infected cells to tissue or for the development of AIDS-associated neuropathology, carcinogenesis, and opportunistic infection.
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PMID:Interactions between HIV-infected monocytes and the extracellular matrix: HIV-infected monocytes secrete neutral metalloproteases that degrade basement membrane protein matrices. 150 80

The analysis of cancers associated with immunodeficiencies (either congenital, iatrogenic or acquired) enabled us to define the possible role of these deficiencies in the sequence of events leading to cancer and in particular the emergence of hematopoietic proliferations. Immunodeficiency increases the risk of viral infection, and in severe deficiencies, uncontrolled infections (Epstein-Barr virus) are directly responsible for the appearance of polyclonal proliferations; in moderately severe deficiencies, the hyperstimulation of the immune system by repeated infections increases the number of mutagenic events, but the immortalization of a malignant clone is a late event, which may or may not be linked to a viral infection. On the other hand, some intrinsic congenital or acquired abnormalities of lymphoid cells may be responsible both for immunodeficiency and carcinogenesis (chromosomic fragility). Apart from any immunological reaction, the immune system plays a role in the proliferation and differentiation events in various tissues; and any dysregulation of the latter may indicate the emergence of a cancer.
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PMID:[Immunodeficiency and cancer]. 267 65

Physicians who think epidemiologically are rare. A method is suggested for detecting their aptitude early in their career when help may be offered to make the most of their special talent. Clusters geographically or in families may provide clues to cancer etiology. Clusters have been systematically thought by mapping cancer mortality in the US and independently in China. Case-control studies have revealed environmental exposure responsible for some of the clusters. Clusters noted by alert clinicians or other astute observers have revealed most of the known environmental causes of human cancers. Genetic influence in carcinogenesis has been identified by studies of peculiar cancer occurrence, such as familial aggregation, multiple primary cancer or the occurrence of cancer with other diseases as, for example, congenital malformations and immunodeficiency disorders. Ethnic differences in cancer occurrence may be revealing. Thus, in Japan there is low frequency of B-cell lymphoma but high frequency of certain autoimmune diseases, as if inherent protection against one predisposes the other. As a rule of thumb, the occurrence of three rare observations is not likely to be due to chance. Examples include ideal carcinoma in three persons with cystic fibrosis of the pancreas who survived to about 30 years of age, and the occurrence in Klinefelter's syndrome of germ cell tumor of the pineal--a neoplasm that has an unusually high frequency in Japan. Finally, the history of discoveries concerning cancer etiology, an aspect of what Comroe has called "research on research", can point the way to new discoveries in the future.
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PMID:Nakahara memorial lecture. Rare events and cancer epidemiology. 333 98

The immune system has evolved under Darwinian pressures as a defence against ubiquitous viruses. Immune surveillance against viral antigens protects the normal host. Individuals with inherited or acquired immune-deficiency disorders can become vulnerable to ubiquitous viruses and neoplasms can ensue, such as B-cell lymphoma, hepatocellular carcinoma, squamous-cell carcinoma, Kaposi's sarcoma, and carcinoma of the penis and uterine cervix. Immunodeficiency permits Epstein-Barr virus, hepatitis B virus, papillomavirus, herpes simplex virus, and cytomegalovirus to induce sustained target-cell proliferation. Each virus selects specific cellular targets bearing viral receptors and the infection leads to proliferation of the target cells rather than lysis. Various co-factors, including nutrition, exposure to tumour-promoting agents, parasitic infection, and ultraviolet light, may promote carcinogenesis. Depending on the type and severity of the immune deficiency, gradual proliferation may lead to evolution of a malignant clone. Conversion of polyclonal virally infected proliferating cells to give monoclonal malignancy is probably due to specific cytogenetic rearrangements which allow oncogene activation and endow an altered tumour cell with selective growth advantages over normal diploid cells. Prevention of viral oncogenesis may be possible by treatment of immune-deficient individuals with premalignant disorders. Immunotherapy and antiviral therapy may prevent progression of viral-induced proliferation to malignancy. The purpose of this paper is to discuss and evaluate the role of immune deficiency and viruses in the induction of malignancies commonly occurring in Africans residing in sub-Saharan Africa (Purtilo, 1976). The types of malignancies commonly occurring in this region are believed to be due to ubiquitous viruses. A failure of immune surveillance mechanisms to recognize viral antigens and abrogate proliferation of infected target cells predisposes to malignancy by increasing the chance of a proliferating cell undergoing a cytogenetic or molecular alteration which endows it with malignant characteristics. The immunological surveillance hypothesis has been elaborated during this century by Ehrlich, Thomas, Burnet, and Schwartz (reviewed by Purtilo & Linder, 1983). This hypothesis rests on several assumptions: that neoplastic cells possess unique tumour antigens: tumour antigens provoke an immune response in the host; and the immune response is protective and eliminates the tumour.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Squamous-cell carcinoma, Kaposi's sarcoma and Burkitt's lymphoma are consequences of impaired immune surveillance of ubiquitous viruses in acquired immune deficiency syndrome, allograft recipients and tropical African patients. 610 Feb 88

A case of Kaposi sarcoma (KS) with cutaneous and splenic involvement is reported. Carcinoma of the left colon and basal cell epithelioma arose eleven years after KS. Genetic, viral, and immunologic factors which may promote initiation and development of Kaposi sarcoma are reviewed. The responsibility of immunodeficiency, whether resulting from therapy or from other causes, in carcinogenesis is discussed. Prolonged survival may be seen after KS. Another primary malignant disease (lymphoma or solid tumor) may arise. The authors suggest that the risk of immunologic disorders, occurring spontaneously or induced by therapy, should be considered specifically for each patient with KS.
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PMID:[Colic carcinoma and basal cell epithelioma eleven years after Kaposi sarcoma with splenic and cutaneous involvement (author's transl)]. 628 76

Glutathione depletion may play a pivotal role in the pathogenesis of human immunodeficiency virus type-1 (HIV-1) infection. Since certain compounds prevent experimental carcinogenesis by elevating the levels of glutathione and phase II detoxication enzymes, we compared the potencies of several inducers with their ability to inhibit basal levels of HIV-1 replication in H9 cutaneous T-cell lymphoma cells. All monofunctional inducers tested elevated the levels of glutathione and quinone reductase, a marker for phase II enzyme induction. However, only oltipraz [4-methyl-5-(2-pyrazinyl)-1,2-dithiole-3-thione] was effective at inhibiting HIV-1 replication (IC50 = 14.8 +/- 3.1 microM). The antiviral effect of oltipraz was potentiated by 3'-azido-3'-deoxythymidine. Thus, 1,2-dithiole-3-thiones represent a hitherto unrecognized class of anti-HIV-1 agents. Oltipraz behaves kinetically as an irreversible inhibitor of HIV-1 reverse transcriptase in the template-primer binding domain. Oltipraz has been used to treat schistosomiasis in humans and is undergoing clinical evaluation as an anticarcinogen. Thus, oltipraz (and other 1,2-dithiole-3-thiones) may have therapeutic utility in HIV-1-infected individuals, not only because of their antiretroviral activity, but also by preventing the development of HIV-1-associated neoplasms.
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PMID:Oltipraz, an inhibitor of human immunodeficiency virus type 1 replication. 768 14

Data from a young adult man with epidermodysplasia verruciformis (EV) and multiple metachronous spinaliomas in the head and neck region are presented. Diagnosis of this rare, human papilloma virus (HPV)-associated disease was based on: (1) Typical skin lesions, including viral warts, verruca plana-type lesions and pityriasis versicilor; (2) typical histological features, including "foamy giant keratinocytes"; (3) evidence of HPV 5, 8 and 20 in pityriasis versicilor-like lesions; (4) a cellular immunodeficiency due to a relative T-helper-cell deficit. No specific treatment of EV is known, so that therapy concentrates on early removal of spinaliomas and treatment of intercurrent infections. Since EV patients have numerous benign skin lesions and frequently develop metastatic and non-metastatic carcinomas, molecular changes of HPV during carcinogenesis can be studied.
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PMID:Multiple metachronous skin squamous cell carcinomas and epidermodysplasia verruciformis in the head region: a human papilloma virus-associated disease. 784 44

Viruses implicated in the development of human cancers include hepatitis B (and C) viruses in hepatocellular carcinoma; human papillomaviruses in anogenital cancers; Epstein-Barr virus in nasopharyngeal carcinoma and Burkitt's lymphoma; human T-cell leukaemia/lymphoma viruses in adult T-cell leukaemia/lymphoma; and indirectly, human immunodeficiency viruses in Kaposi's sarcoma and B-cell lymphoma. Together, they contribute significantly to the cancer statistics in the Southeast Asian region. Neoplastic proliferation may be instigated by the presence and expression of viral oncogenes which may be integrated into the host genome and/or exist in episomal molecules. Critical viral genes may also interfere with host genes, resulting in the activation of cellular proto-oncogenes and/or the inactivation of anti-oncogenes and their products. The molecular pathogenesis of virally-induced cancers has led to major breakthroughs in the understanding of carcinogenesis at a molecular level. The occurrence of some of these viruses in a significant proportion of normal individuals suggests long latency periods necessitating multi-step co-operating events arising from multi-factorial agents such as host genetic susceptibility, immunological and hormonal status, as well as chemical and physical cocarcinogens in the environment. Successful intervention achieved with effective vaccines such as the hepatitis B vaccine and measures to severe the chain of viral transmission culminating in reduced incidence of the corresponding cancer will provide conclusive evidence for the virus-cancer relationship.
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PMID:Cancer and viruses. 810 16


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