Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pleural effusion (PE) has been increasingly diagnosed over the last eight years in the Department of Internal Medicine of the Centre Hospitalier of Kigali, Rwanda. To determine the etiology of PE and to examine its possible association with HIV-1 infection and tuberculosis (TB), the authors performed an etiological work-up, including thoracocentesis and pleural punch biopsy, of all new patients with PE of undetermined etiology referred to the Division of Pulmonary Diseases at the hospital between September 14, 1988, and October 16, 1989. 81 men and 46 women of mean age 34 years were enrolled in the study. Pleural TB was diagnosed in 86% and confirmed histologically and/or bacteriologically in 82%. 82 of the 98 pleural TB patients tested for antibody to HIV-1 were HIV-1-seropositive. Metastatic cancer was responsible for PE in six patients, Kaposi's sarcoma in three, lymphoma in one, anaplastic carcinoma in one, and adenocarcinoma in one. Non-TB pneumonia was documented in five patients and was associated with HIV-1 infection in four. Other causes of PE were congestive heart failure, decompensated cirrhosis, constrictive pericarditis, or undetermined; only one of these latter patients was HIV-seropositive. The authors therefore found TB to be the predominant cause of PE and it is strongly associated with HIV-1 infection. In an African area highly endemic for HIV-1 and Mycobacterium tuberculosis co-infection, PE should therefore be considered a good marker of TB as well as HIV-1 infection.
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PMID:Pleural effusion, tuberculosis and HIV-1 infection in Kigali, Rwanda. 844 20

Kaposi's sarcoma (KS) is an unusual neoplasm that has proved to be an enigma in many ways since its original description by Kaposi in 1872. Its epidemiology has stimulated tremendous interest, amplified markedly in 1981 when it became known as an original defining part of the complex of immune disorders now known as AIDS. The cell of origin, etiology, and therapy for both AIDS-associated and AIDS-unassociated KS continue as matters of intense investigation. In fact, whether it is a reactive hyperplasia or a true malignancy is still a matter of debate, as is the concept of multicentricity versus metastases. Epidemiologic studies suggest that a separate agent apart from HIV-1 may cause KS. A newly postulated KS-associated herpes virus may be linked. The role of the HIV-1 tat gene product, basic fibroblast growth factor, scatter factor, oncostatin M, and other factors that regulate the growth of KS cells are discussed, as well as therapeutic options.
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PMID:Kaposi's sarcoma: advances and perspectives. 863 78

A 48 yr old HIV seropositive female presented with a right breast mass and bilateral axillary lymphadenopathy. Fine needle biopsy (FNB) revealed an adenocarcinoma with abundant mucin production and features suggestive of a cribriform and micropapillary ductal carcinoma in situ (DCIS). Histopathological examination of the tumor confirmed an invasive mixed colloid carcinoma with extensive DCIS. There have been 4 previous reports in the literature of breast carcinoma associated with HIV seropositivity. This case initially diagnosed by FNB is the first case reported in Australia. In spite of the somewhat more favourable histological type of breast carcinoma, this tumor shows numerous unfavourable prognostic factors and has had an aggressive clinical course with relapse of disease in the contralateral breast and distant metastases within 4 wks of surgery, probably related to the patient's immunodeficiency.
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PMID:FNB diagnosis of breast carcinoma associated with HIV infection: a case report and review of HIV associated malignancy. 871 81

The FACS-analysis of diseases as different as cancer, autoimmune disorders and chronic (retro)viral infections, including HIV-infection, shows -at least temporarily- a common feature of lymphocyte hyperactivation, characterized by cellular activation markers (HLA-DR, CD26, CD38, CD69, CD2R and/or CD30), as well as by solubilized membrane structures, such as beta-2m, sICAM-I, sIL-2R/sCD25, sCD8, and by some oversecreted immunocyte products (e.g. neopterin, lysozyme and/or cathepsin D). We tested two potential approaches to down-regulate the pathologically elevated CD8+ and HLA-DR+ T cells: (a) In animal model, we tested the sensibility of these, disease inducing and maintaining T cell subsets to in vitro pretreated (cell death preprogrammed) semi-syngeneic and allogeneic donor T cells in tumor-bearing mice. (b) In the first clinical study, we used a novel combination of FDA-approved drugs which inhibits Ca(2+)-influx and concomitantly down-regulates cytosolic cAMP in patient's overstimulated immunocompetent cells. We could achieve a 94.6-100% long-term survival in tumor-bearing mice. In patients, large primary tumors and large metastases shrinked by 80-85% and small metastases disappeared completely. Since in HIV-infected persons, the increased number of HLA-DR+ CD38+T (T8) cells is associated with a fall in CD4-level and with development of AIDS, we are looking for the elimination of these HLA-DR+ targets by our novel technique in two AIDS-simulating (FIV/FeLV and SIV) animal models.
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PMID:Treatment of solid tumors should obligatorily be combined with the in vivo codepletion of tumor-protecting, CD8+/HLA-DR(+)-suppressor T cells by alloreactive donor T cells whose preprogrammed cell death allows a high GvL-effect before GvHD can be established. Results of animal experiments, including more than 6000 mice. 873 48

Persistent human immunodeficiency virus (HIV) infection induces an immuno-suppressive state and therefore malignant tumors are a very common complication. Hepatocellular carcinoma is very rare, however, because it is associated with chronic liver disease by the persistent infection of hepatitis B or C virus (HBV or HCV). We reported a case of HCC with HIV infection who had no evidence of HBV or HCV infection, and that had a rapid growth and active pulmonary metastases. Pathological findings of the resected liver showed moderately differentiated HCC and no chronic liver disease. Despite efforts to find potential HBV integration in tumor and non-tumor tissue, none was observed. To our knowledge, this is the first report of HCC in HIV-infected patient with no evidence of hepatitis virus infection.
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PMID:A case of hepatocellular carcinoma in HIV-infected patient. 888 41

Clinical and biological features of three HIV-infected adults with soft tissue sarcoma are reported. Epstein-Barr Virus (EBV) detection was negative using in situ hybridisation, PCR analysis and Southern blot analysis in the two cases for which tumour samples were available, contrary to all previously reported paediatric cases. All three patients developed metastases. Chemotherapy was feasible but only afforded tumour stabilisation. The cause of death in all three cases was distant spread and not AIDS. Soft tissue sarcoma associated with HIV infection are not exclusively found in children, do not appear to be EBV-related in adult patients, and fare dismally despite vigorous therapy.
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PMID:Soft tissue sarcomas in HIV-infected adult patients. 898 95

Direct gene transfer to solid tissues or metastatic cancer cells requires vectors capable of in vivo transduction to specific cells. The predominant retroviral vectors of murine origin are inactivated by human complement, which precludes their use in vivo. Such inactivation does not take place with vectors based on human retroviruses. Murine retroviral vectors are also limited to proliferating cells, which human retroviruses are not. In this study we examined whether or not a vector using components from the human retroviruses HIV-1 and HTLV-1 could infect small-cell lung cancer cells and resting CD34+ hematopoietic stem cells. While HIV-1 itself was unable to infect cells lacking the CD4-membrane molecule, chimeric viral particles (pseudotype virus) with HIV-1 genome and HTLV-1 envelope components were able to infect both CD4-containing lymphocytic cells, CD4-negative tumour cells and hematopoietic stem cells. After infection with the pseudotype vector, the RNA genome was reverse transcribed and integrated. Transduction efficiency and gene expression under the HIV-1 LTR promoter in both tumour and stem cells were found to be of a similar or greater magnitude than in lymphocytic cells. These results suggest that gene transfer targeting proliferating as well as resting cells in vivo may be realized using components from human retroviruses.
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PMID:Transduction potential of human retroviruses in highly proliferating small-cell lung cancer cells as well as non-proliferating hematopoietic stem cells. 935 Feb 17

Although it is not proven by causative association, several studies indicate that patients with acquired immune deficiency syndrome (AIDS) have a high risk for developing cutaneous malignancies, especially lymphoma and Kaposi's sarcoma. Other malignant cutaneous lesions seen in this patient population include basal-cell carcinoma, squamous-cell cancer, Bowen's disease, and rarely, malignant melanoma. We review the clinical course of a human immunodeficiency virus (HIV)-infected man with a superficial spreading melanoma of the scapula treated with wide local excision. Ten years later, he was diagnosed as having metastatic and widespread disease. By placing our patient's experience in context with other case reports, we sought to determine whether malignant melanoma in the HIV-infected population presents atypically or has a more aggressive natural history. The appearance of malignant melanoma in homosexual men may be coincidental or reflective of the expanding spectrum of HIV-associated diseases. Of the 22 patients reported to have malignant melanoma and HIV, approximately one-third had metastatic disease at the time of initial examination, and those with a decreased CD4+ cell count were most likely to have systemic symptoms. Melanomas among patients with HIV infection were often atypical in appearance, being multiple or metastatic, as is the case in other well-defined immunosuppressed groups. Further epidemiological and clinical studies are required to determine whether melanoma occurs more frequently or is more likely to metastasize in persons with HIV disease. Laboratory investigators must also concentrate on those factors in the setting of HIV disease that may contribute to melanocyte activation. Our patient's fulminant clinical course should alert clinicians to carefully evaluate patients with HIV infection and unusual pigmented cutaneous lesions, or who have a prior history of malignant melanoma.
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PMID:Malignant melanoma in an HIV-infected man: a case report and literature review. 958 30

The advent of highly active antiretroviral therapy (HAART) and quantitative viral load assays has revolutionized the care of HIV-infected patients. However, this paradigm shift has also had unexpected, sometimes adverse consequences that are not always obvious. Before antiretroviral therapy, physicians learned how to accompany patients through their illness; to bear witness to sickness and dying; and to help patients and their families with suffering, closure, and legacy. Since we have become better at treating the virus, a new temptation has emerged to dwell on quantitative aspects of HIV management and monitoring, although the skills that we learned earlier in the epidemic are no less necessary for providing good care. Our new-found therapeutic capabilities should not distract us from the sometimes more difficult and necessary task of simply "being there" for patients for whom HAART is no longer effective. The definition and practice of end-of-life care for patients with AIDS will continue to evolve as AIDS comes to resemble other chronic, treatable, but ultimately fatal illnesses, such as end-stage pulmonary disease and metastatic cancer, in which clinicians must continually readdress with their patients the balance of curative and palliative interventions as the disease process unfolds over time. The coming challenge in HIV care will be to encourage the maintenance of a "primary care" mentality-with attention to the larger psychosocial issues, end-of-life care, bereavement, and a focus on the patient as opposed to the illness-alongside our new antiretroviral paradigm. Otherwise, we run the risk of forgetting what we learned about healing, from a disease that we could not cure.
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PMID:From fate to tragedy: the changing meanings of life, death, and AIDS. 1041 43

One of the most important concerns of patients with cancer, particularly those with metastatic disease, is "Will I be in constant pain?" This is a similar concern voiced by patients with late-stage human immunodeficiency virus infection. The management of chronic pain has enormous implications on a patient's ability to function and on his or her quality of life. In June 1996, Medical Interface convened a panel of experts in Chicago to discuss pain management therapies, guidelines, and how these issues will affect, and be affected by, the managed care environment.
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PMID:Pain management guidelines: implications for managed care--a roundtable discussion. 1016 85


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