Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Problems relating to immunoselection of neoplastic, in particular leukemic, cell lines are reviewed. Since there is ample evidence that specific immune reactions of the host against malignant neoplastic cells do occur, it becomes important to consider the effectiveness and the relevance of immunity in suppression or elimination of neoplastic growth. Emphasis is placed on experimental results obtained in syngeneic tumor-host combinations, because they more closely resemble the situation of spontaneous tumorigenesis or leukemogenesis than xenogeneic or allogeneic model systems. Studies of types of neoplasia observed in cases of human immunodeficiency syndromes offer an important insight into problems involved in immunoselection of leukemic cell lines: the marked predominance of leukemias and lymphoreticular neoplasias in immunodeficient patients invites speculation on both the mechanisms of leukemogenesis and the relative importance of the immune system in eliminating malignant neoplastic cells.
 ...
PMID:Problems relating to immunoselection of leukemias. 6 43

A case of tentorial meningioma occurring 12 years after radiation therapy for a verified craniopharyngioma is presented. The pertinent literature is reviewed and it is concluded that irradiation of the brain may be responsible for the late development of intracranial meningiomas, which are less common, however, than sarcomas. A long survival after irradiation, "misregeneration" in the chronic inflammatory processes induced by irradiation, and an immunodeficiency caused by irradiation and other factors, may play some role in developing oncogenesis.
 ...
PMID:Radiation-induced meningioma: with review of literature. 81 5

It is my great honor to dedicate this article to Professor Ludwig C. Yen at the occasion of the Annual Meeting of the Chinese Society of Microbiology, commemorating his 101st Birthday. I have had the privilege of being one of the earliest students of Professor Yen, and as a staff member working for 16 years under him, I have been benefited enormously from his teachings. I am most grateful to Dr. Czausiung Yang and the executive board members of the Chinese Society of Microbiology for giving me this opportunity to present some of my research activities which would be relevant to Professor Yen's teachings. Introduction to the evolutionary view of host-parasite relationship was one of the many contributions Professor Yen made to enlighten students and colleagues as early as in 1940. As promulgated by Professor Yen, natural history of infectious diseases has witnessed the reality of Theobald Smith's premise, "pathogenicity of microorganisms is an accident in the evolutionary processes of host-parasite relationship, and the outcome of evolutionary forces is a modus vivendi (a feasible compromise) according to which the parasite and the host reach some sort of equilibrium which permits the survival of both"(1). These evolutionary concept has since become a common knowledge for modern students of infectious diseases. The natural history of recently discovered human retroviruses such as HTLVs (human T-lymphotropic viruses) and HIVs (human immunodeficiency viruses) has amply demonstrated the truth of the premise. I shall review some results of our research which would be of relevance to the evolution of viral quasispecies and variants, viral oncogenes, and the cellular as well as viral regulatory genes. I shall focus on the roles played by these genes in the delicate and complex balance of host-virus relationships, and on their association with cellular differentiation and oncogenesis.
 ...
PMID:An evolutionary view of viral regulatory genes. 165 42

Tumour cell karyotypes from patients with Burkitt lymphoma (BL) or Burkitt's type leukemia (ALL3) were studied for correlation with survival, bone marrow and cerebral spinal fluid involvement (CSF), human immunodeficiency virus (HIV) serology, and for recurrent cytogenetic abnormalities. The records of 22 patients with BL from our institution and of 148 cases of BL and ALL3 reported in the literature with karyotypes were evaluated for clinical and cytological features. Overall survival was only 28 per cent and 88 per cent of deaths occurred within the first nine months after diagnosis. Those who survived at least 18 months were unlikely to relapse. Age and gender did not significantly affect survival. Patients presenting with advanced Ann Arbor stage, bone marrow or CSF involvement had lower survival rates. The association of translocations involving chromosome band 8q24 with this disease is confirmed. Sixty-two per cent of karyotypes had t(8;14)(q24;q32) translocations; the recognized variant translocations t(8;22)(q24;q11) and t(2;8)(p12;q24) affected 12 per cent and 9 per cent respectively. Seventeen per cent had abnormal karyotypes but no classic translocation. Patients with variant translocations had the poorest survival rates, and those with the classic t(8;14)(q24;q32) did the best. Despite a small sample size, the variant translocation t(8;22)(q24;q11) appeared to occur at an increased frequency in the patients with AIDS. In the entire group, recurrent involvement of chromosome regions 1q2, 6q11-14 and 17p1 suggests that alteration of genes at these loci, B Cell Growth Factor (BCGF) at 1q2 and p53 on 17p, may contribute to the development and progression of this tumour. Similarly, the frequent trisomies of chromosomes 7, 8, 12 and 18 may indicate an effect on tumour cell growth due to increased gene dosage. Trisomy 12 was found in eight tumours, five from patients with AIDS, suggesting that chromosome 12 has a site or gene whose allelic dosage is selected for in AIDS related lymphoma cells. Cytogenetic studies of adult Burkitt lymphoma and leukemia suggest several likely loci for gene alterations that in conjunction with myc translocations can lead to tumorigenesis.
 ...
PMID:Chromosomal abnormalities in adult non-endemic Burkitt's lymphoma and leukemia: 22 new reports and a review of 148 cases from the literature. 186 43

We have prepared EMBL3 libraries of DNA extracted from the cervix of a patient with cervical intraepithelial neoplasia (CIN) and isolated seven recombinant clones containing sequences that hybridize to human cytomegalovirus (HCMV) DNA. Restriction analysis of one clone with BamHI and SalI endonucleases revealed that the insert DNA showed a high degree of homology to the HCMV Ad169 genome over the region between the HindIII K/E site and the SalI site located within the BamHI P fragment. The HCMV insert in the CIN clone is integrated and flanked by cellular sequences. The major immediate early gene that encodes a polypeptide of approximately 69 kD was found to be conserved in the CIN clone. Transfection of clones encoding the immediate early region of HCMV resulted in cells that were positive in immunofluorescence studies with two monoclonal antibodies directed against the HCMV 69 kD immediate early polypeptide. Infection of human ectocervical cells with HCMV Ad169 revealed that they could express the 69 kD polypeptide encoded by the immediate early gene but could not replicate the virus, whereas HCMV was able to replicate productively in cultured endocervical cells. HCMV has been shown to activate endogenous retroviruses and also to transcriptionally activate the long terminal repeat of human immunodeficiency virus. Activation of virus and cellular genes by HCMV may be a means by which this virus is involved in the multistage process of oncogenesis and/or the activation of latent infections.
 ...
PMID:Molecular cloning of DNA sequences from cervical intraepithelial neoplasia that hybridize to human cytomegalovirus DNA. 255 81

This paper reviews current theories on the etiology of acquired immunodeficiency syndrome (AIDS), recent advances in the mechanisms of oncogenesis, and the relationship of immunodeficiency to the development of cancer. It then attempts to synthesize these concepts into a hypothesis to explain the AIDS-cancer connection. 2 major theories have been advanced to explain the etiology of AIDS. The 1st postulates a viral infection of T helper lymphocytes leading to cell destruction and secondary immunodysregulation, while the 2nd postulates that AIDS is mainly a B cell disease with T cell destruction as a secondary consequence. In either case, progressive, irreversible immunodeficiency results in greatly increased susceptibility to lymphoreticular neoplasia and severe opportunistic infections. Of considerable relevance to the AIDS epidemic is an association between cytomegalovirus and Kaposi's sarcoma. DNA virus infection is probably 1 of many possible cellular insults that perturb the resting state, induce proliferation, and increase the chance of genetic accidents that lead to cancer. Available knowledge suggests the outlines of possible mechanisms for the development of Kaposi's sarcoma and non-Hodgkin's lymphoma in AIDS patients. An obvious susceptibility factor appears to be the high prevalence of virus infections in the AIDS risk groups, and virtually all of these viruses are associated with human cancer. Thus, activation of these endogenous viruses by an immunodysregulated state could lead to perturbation of the resting state of the host cells. A central question is why Kaposi's sarcoma and non-Hodgkin's lymphoma shadow homosexual AIDS patients. It is suggested that AIDS should be viewed as a primary lymphoproliferative disorder.
 ...
PMID:AIDS and oncogenesis. 388 53

Although supported by a number of experimental models, the assumption assigning a crucial role to the immune system in the antineoplastic defense mechanisms has not been convincingly demonstrated so far for human tumors. Should the theory be correct, severe functional impairment of the immune system would obviously result in the occurrence of tumors with abnormally high frequency. Registry holdings systematically collecting pertinent information on the malignancies developed in patients with primary immunodeficiency diseases or in organ transplant recipients maintained on therapeutically-induced immune depression, as well as the observation of tumors occurring in patients treated with immunosuppressive agents and of second malignancies arising after radio- and/or chemotherapy of the primary tumor consistently indicate that depressed immunity is usually associated with an increased incidence of cancer as compared with that expected in the general control populations. However, not all types of tumors are increased to the same extent, in that lymphoreticular neoplasias (especially non-Hodgkin's lymphomas), acute leukemias as second tumors and, among solid neoplasms, squamous cell carcinomas are those most frequently reported. These observations suggest that even deeply impaired tumoricidal immune mechanisms may facilitate the growth of certain tumors only, especially of those arising from the cells of the immune system itself, in remarkable contrast with their frequency in the general population. Oncogenesis may be favoured in various states of depressed immunity by a number of ways. Their elucidation might have bearing on the comprehension of the more general phenomenon of the neoplastic transformation.
 ...
PMID:[Immunological deficiency syndromes, immunosuppression by drugs and occurrence of neoplasms: a casual association?]. 409 54

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)
 ...
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

The immune system is constantly challenged by ubiquitous viruses. Multiple immune defenses have evolved to meet these challenges, and thus immunocompetent individuals successfully respond to infection without sequela. X-linked lymphoproliferative syndrome patients, renal allograft recipients, and acquired immunodeficiency syndrome patients share impaired immune surveillance as a common feature. Such individuals are variously susceptible to numerous untoward complications following infection with Epstein-Barr virus, cytomegalovirus, herpes simplex virus, human papillomavirus, and hepatitis B virus. We hypothesize that failure of the immune system to control these viruses is instrumental in the occurrence of some B-cell lymphomas. Kaposi's sarcoma, and squamous-cell and hepatocellular carcinomas. Herein we review some mechanisms responsible for the breakdown of immune surveillance and the permissive role immunodeficiency plays in viral oncogenesis.
 ...
PMID:Oncological consequences of impaired immune surveillance against ubiquitous viruses. 630 92

The authors underline a synergism of HPV + HSV and HPV + CIN that, together with general immunodeficiency and local factors are responsible for the oncogenesis of cervico carcinoma. This thesis takes on importance after literature reports of an increase of 10% in viral infections from HSV and HPV with a middle incidence of the 1-2% in all the colpocytologic examination cases not in women between 18 and 65 years. To obtain a successful preventive treatment the authors recommend a colpocytologic examination each year, possibly in association with colposcopic, histologic and molecular studies in all HPV positive cases.
 ...
PMID:[The Pap-test in the study of viral infections of the female genital tract]. 763 May 8


1 2 3 4 5 6 7 8 9 10 Next >>