Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diffuse abnormal uptake of 201Tl-chloride in the bone marrow is described in an AIDS patient with Kaposi's sarcoma who received chemotherapy. The patient developed severe leukopenia that was treated by granulocyte stimulating factor (GCSF). The white blood cells increased from 1500 to 6200 over a period of 4 days. After chemotherapy, the tumor was negative for thallium uptake.
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PMID:Diffuse thallium-201-chloride uptake in hypermetabolic bone marrow following treatment with granulocyte stimulating factor. 127 40

Monocyte/macrophage-mediated tumor cytotoxicity was studied in patients infected with human immunodeficiency virus-1 (HIV-1) at various stages [Center for disease control (CDC) classification] of the disease. using the P-815 tumor cell line as target cells, the results demonstrated reduced monocyte/macrophage cytotoxicity early in HIV-1-related disease (CDCIII, P < 0.01). This cellular dysfunction sustained during the progression of the disease. Evidence could be presented that neither exogenous application of macrophage-stimulating cytokines (e.g. interferons) nor their endogenous induction in vitro restored monocyte/macrophage cytotoxicity. However, enhanced tumor necrosis factor (TNF)-alpha production, which parallels the observed reduced capacity to lyse P-815 tumor cells, might be the major source for monocyte/macrophage-mediated cell lysis. TNF-alpha-induced cytotoxicity can be inhibited by addition of anti-TNF-alpha. Other experimental models using TNF-sensitive tumor target cells may, therefore, mimic monocyte/macrophage-mediated lysis. Suppression of monocyte/macrophage cytotoxicity in later stages of HIV-1 infection (AIDS-related complex, AIDS) could partly be reverted by treatment with the cyclooxygenase blocker, indomethacin. The responsible arachidonic acid product mediating suppression was found to be prostaglandin E2, suggesting that in addition to the direct viral interference cellular dysfunction is at least in part a result of altered cytokine regulation.
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PMID:Cytokine-mediated regulation of monocyte/macrophage cytotoxicity in human immunodeficiency virus-1 infection. 128 2

This report describes a clinical case of a large cell, immunoblastic plasmacytoid malignant B-cell lymphoma of the rectum in an AIDS patient coinfected with HTLV-I. The malignant cells showed clonal genetic rearrangement of the HC (JH) and LCK genes. Infection by EBV was demonstrated serologically and with slot blots using genomic DNA of the cancer cells. Southern blot analysis with DNA extracted from the lymphoma cells were negative for HTLV-I. The patient received seven cycles of VACO-B which induced complete but transient clinical remission of the tumor. The final outcome of the patient is unknown.
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PMID:Primary B cell lymphoma of the rectum in a patient coinfected with HIV-1 and HTLV-I. 128 27

In a series of 33 cynomolgus monkeys (Macaca fascicularis) experimentally infected with Simian Immunodeficiency virus (SIV), strain smm3, 13 animals developed malignant Non-Hodgkin lymphomas. These lymphomas presented with unusual primary manifestations like in the orbita, testes, and brain. The morphological features and immunophenotyping identified the tumors as high malignant B-cell lymphomas. In all tumors as well as in tumor-derived cell lines a cynomolgus B-lymphotropic herpes virus (CBLV) with structural homogeneity to the Epstein-Barr virus (EBV) could be demonstrated by Southern blotting with EBV-specific probes. The lymphoma cells also expressed CBLV-associated nuclear antigens involved in B-cell transformation crossreacting with EBNA-specific human sera and monoclonal antibodies. Ig-gene rearrangement studies revealed clonal populations, however, no translocations of the c-myc oncogene could be detected. The lymphomas developing with high frequency in SIV-induced immunodeficiency resemble a major subtype of human EBV-associated AIDS lymphomas. This animal model can therefore be used to further elucidate interactions of HIV and EBV in AIDS-related lymphomagenesis.
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PMID:[Opportunistic malignant lymphomas in SIV infected primates--a model for Epstein-Barr virus associated lymphomas in AIDS]. 128 56

Fourty-three primary cerebral lymphomas (PCL) were histologically classified and examined for genome expression of Epstein Barr Virus (EBV) and human herpes virus 6 (HHV6) using dot blotting, polymerase chain reaction, and Southern blotting. Only 20 tumors (16 high grade and 4 low grade lymphomas) could be suitably placed into a category of the Updated Kiel Classification, whereas the non-classified 23 tumors were highly malignant B-lymphomas and referred to as small-cell (SC) or large-cell (LC) blastic PCL. Most of the LC PCL showed a tumor-like infiltration pattern with high cellular density and little remaining parenchyma, whereas the SC PCL more often showed an inflammation-like pattern characterized by loose arrangement of tumor cells and marked astrocytic, microglial and T-lymphocytic reaction. EBV genome was found in 3/3 AIDS cases, but in none of 40 immunocompetent cases, while HHV6 was detected in 2 tumors of immunocompetent patients. We conclude that (1) the Updated Kiel Classification is not applicable to a majority of PCL, and (2) EBV and HHV6 do not appear to play a major role in the pathogenesis of PCL in immunocompetent subjects.
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PMID:[Classification and virus expression of primary cerebral lymphomas]. 128 60

Interferon gamma (IFN-gamma) production has been attributed exclusively to activated T cells and NK cells. We sought to determine whether human B cells express IFN-gamma. We studied 28 B cell lines including Epstein-Barr virus (EBV)+ normal lymphoblastoid B cell lines (N = 7), EBV+ B cell lines derived from patients with Burkitt's lymphoma with (N = 6) or without AIDS (N = 8), as well as seven EBV- B cell lines. All cell lines were studied by reverse transcription-polymerase chain reaction (RT-PCR). We detected constitutive expression of IFN-gamma in every B cell line. The tumor promoters PMA and teleocidin appeared to enhance this IFN-gamma expression in nearly every B cell line. The 517 bp amplicons spanning the entire protein coding region of the IFN-gamma mRNA from three representative lines were sequenced, definitively establishing that B cell IFN-gamma is identical to IFN-gamma from activated T cells and is not altered by derivation of the B cell lines from AIDS patients or by EBV status. Detection of IFN-gamma in the entire panel of EBV+ and EBV- cell lines suggests that the IFN-gamma gene is broadly expressed by human B cells. Our data imply that human B cells can be activated to produce IFN-gamma, further enmeshing B cells in the dynamics of immunoregulation.
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PMID:Human B cell lines express the interferon gamma gene. 129 29

Clinical and paraclinical experience in HIV infection, though the time elapsed since the first observations is relatively short, begins to get typical outlines. In the case of AIDS, the lung is the main place of opportunistic infections, other inflammatory processes and neoplasia. The present work deals with six clinical cases with positive serum tests for HIV and secondary respiratory phenomena such as: Kaposi sarcoma, pneumonia with Pneumocystis carinii, tuberculosis, candidosis, pneumonia with common germs. Particular aspects of treatment and disease evolution are commented.
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PMID:[The pulmonary manifestations in AIDS]. 129 94

Certain human genital papillomaviruses (HPV) are strongly associated with cervical dysplasia and cancer. Evidence is accumulating that HPV infection and ano-genital cancers are more common in patients with the acquired immunodeficiency syndrome. The objective of our study was to evaluate the extent to which HPV infection and associated cervical disease constitute opportunistic complications of human immunodeficiency virus (HIV) infection in a population of sexually promiscuous, HIV-infected women in Kinshasa, Zaire. In 1989 we obtained Pap smears and cervicovaginal lavage specimens for HPV DNA testing from 47 HIV-seropositive and 48 HIV-seronegative prostitutes who were part of a cohort under observation since 1988. Thirty-eight percent of the HIV-seropositive and 8% of the seronegative women (odds ratio = 6.8; p = 0.001) had HPV DNA detected by either ViraType, a dot-blot assay which detects specific genital HPV types, or low-stringency Southern blot, which detects all HPV types. Eighty-two women (86%) had an interpretable Pap smear; 11 of 41 (27%) HIV-seropositive women and one of 41 (3%) seronegative women had cervical intra-epithelial neoplasia (CIN) (odds ratio = 14.7; p = 0.002). HIV seropositivity, HPV infection and CIN were highly associated. Eight (73%) of 11 seropositive women with CIN had HPV detected. Both HPV infection and cervical cancer may emerge as opportunistic complications of HIV infection in populations in which HIV, HPV and cervical cancer are common.
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PMID:Genital papillomavirus infection and cervical dysplasia--opportunistic complications of HIV infection. 130 59

The prevalence of lower genital neoplasia and Human Papilloma-virus-related genital lesions were evaluated in a cohort of 75 women with Human Immunodeficiency Virus type 1 (HIV-1) infection at different stages of HIV disease. The overall rate of cervical intraepithelial neoplasia (CIN) in the group studied was 29.3% (22/75). Eight out of 10 high-grade CIN lesions contained 'high-risk' HPV-DNA 16/18 and/or 31/35/51 as demonstrated by 'in situ' hybridization with biotinylated probes. Vulvar and/or perianal condylomata were histologically diagnosed in 14 patients (18.7%); nine of these biopsies contained detectable HPV-DNA which was always related to HPV 6/11. The rate of high-grade CIN in symptomatic HIV-infected patients was 28% (7/25) as compared to 6% (3/50) of the other cases (P = 0.022). CD4 lymphocyte counts, white blood cell counts, CD4+/CD8+ cell ratio and percentage of CD4+ lymphocytes were lower in patients with high-grade CIN in comparison to the patients with negative colposcopical and/or cytological examination. After adequate standard treatment (cryotherapy, electrocauterization, cold-knife conization) only one case of CIN 2 recurred during the 2 years of follow-up period. The prevalence of lower genital neoplasia and HPV-related lesions among HIV-infected women is high and seems to correlate with the severity of HIV disease.
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PMID:Prevalence, diagnosis and treatment of lower genital neoplasia in women with human immunodeficiency virus infection. 131 1

Mice infected with various tumor retroviruses have been used as models for evaluating therapeutic substances for the treatment of some cancers, and more recently, for human immunodeficiency virus (HIV) infection, the causative agent of acquired immune deficiency syndrome (AIDS). Consequently, there is a need to determine the ability of biological response modifiers (BRMs) to specifically reduce virus-infected cells, as compared to their non-specific anti-proliferative effects. To address this need, a BRM, imexon, was evaluated in this study using three strains of mice having different Friend virus (FV)-specific immunological capabilities. The first strain, (B10.A x A/WySn)F1, was genetically capable of producing FV-specific neutralization and cytotoxic antibodies, the second, Balb/c, was not, and the third, SCID mice, lacked functional T and B cell immunity. Imexon treatment reduced virally-induced splenomegaly in all 3 strains; however, the concentration of splenic viral infectious centers (IC) were not affected. Since imexon was efficacious in reducing splenomegaly in SCID mice, the mode of action was concluded to not require functional T or B cell immunity. The observation that imexon did not affect splenic IC titers also suggested that imexon did not specifically eliminate virally infected cells, but may have functioned by other mechanisms. This study also demonstrated the use of various mouse strains as a strategy for delineating the modes of action of BRMs against murine retroviral infections.
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PMID:Elucidation of mode of retroviral-inhibitory effects of imexon through use of immune competent and severe combined immune deficiency (SCID) mice. 131 37


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