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)

AIDS-associated Kaposi's sarcoma (KS), which in 80% of cases occurs in the oral cavity, usually presents with characteristic clinical features such as brown-bluish pigmented macules or tumorous lesions. In later stages the tumor, most probably originating from the vascular endothelium, may secondarily induce erosion of the underlying bone. The primary, intraosseous occurrence of KS has prompted the present 2 case reports. The tumor presented as extensive, diffuse osteolysis within the mandible without causing clinical symptoms. Although rare, intraosseous KS must be included in the differential diagnosis of isolated bone defects in HIV-infected patients.
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PMID:Primary intraosseous AIDS-associated Kaposi's sarcoma. Report of two cases with initial jaw involvement. 177 Feb 44

A new tumor marker, tumor-associated trypsin inhibitor (TATI), was studied in 5 patients who received successful kidney or pancreas grafts and in 30 subjects with antibodies against human immunodeficiency virus. Serum TATI concentrations were very high during the four first days after transplantation. Thereafter the serum levels decreased when the peptide was eliminated through the kidney. Consequently, the urine values were very high. The TATI concentrations of HIV positive subjects were compared with serum levels of HIV antigen and antibody, by Western blotting and determination of peripheral T-lymphocyte subpopulations. The occurrence of high concentrations of TATI in some HIV positive subjects and especially in AIDS patients, suggests that TATI could be useful in exploring physiopathological aspects of severe immunodeficiencies even if TATI levels were not correlated with the commonly used markers of the immune system status. The increased levels of TATI in immunological disorders suggests its possible use in assessing the immune response against cancer.
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PMID:Tumor-associated trypsin inhibitor in induced and acquired immunodeficiency. Studies on transplanted and HIV-infected patients. 178 Jun 93

Kaposi's Sarcoma (KS) is a tumor of mesenchymal origin of unclear etiology and pathogenesis. The epidemic form of KS (AIDS-associated) occurs in up to 30% of HIV-1 infected individuals with lesions characterized by mixed cellularity, spindle cells proliferation and neoangiogenesis. The establishment of in vitro and in vivo model systems (AIDS-KS cell cultures and nude mouse) have allowed studies toward the understanding of the pathogenesis of KS. The data presented here support the hypothesis that KS is a cytokine mediated disease and that interactions between mesenchymal cell types and HIV-1 gene products might lead to a composite lesion such as KS. In fact, in vitro and in vivo studies indicate that the HIV-1 Tat protein acts as a growth factor for cells derived from AIDS-KS lesions, thus establishing an experimental link between HIV-1 infection and the development of KS in humans. Human immunodeficiency virus (HIV-1) is implicated in various clinical manifestations associated with AIDS, including KS. KS represents the most frequent tumor arising in infected individuals, particularly homosexual and bisexual men. This form of KS (epidemic or AIDS-KS) is aggressive and often results in dissemination and invasion of lymph nodes and viscera. Histologically, KS is characterized by the proliferation of spindle-shaped cells ("KS cells"), considered to be the tumor element of the lesions, associated with endothelial cells, fibroblasts, inflammatory cells and new blood vessel formation (early stage lesions). In a later stage, the spindle cells tend to coalesce in larger tumor masses, although the slit-like spaces, which are characteristic of the lesion, usually remain evident. The histogenesis of the KS spindle cells, however, is still controversial and both types of mesenchymal cells, endothelial and smooth muscle cells, have been proposed as potential cell progenitors. Although KS is clearly associated with HIV-1 infection, little is known about the molecular events underlying its pathogenesis. Recently, however, two experimental advances (the establishment of long-term cell cultures derived from KS lesions of AIDS patients and the development of animal models) have made the study of the pathogenesis of AIDS-KS possible. Here we discuss results obtained from these new systems suggesting that the induction of the AIDS-KS lesions involves a pathway of events mediated by specific cytokines and that the HIV-1 tat gene product may play a crucial role in the development and/or progression of KS in HIV-1 infected individuals.
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PMID:Molecular mechanisms in the pathogenesis of AIDS-associated Kaposi's sarcoma. 180 71

In this paper we describe the use of polymerase chain reaction (PCR) to amplify DNA sequences suitable for studies on the activity of DNA-binding drugs of possible interest in anti-tumor as well as anti-viral therapy. To this aim (a) we amplified by PCR two regions of the HIV-1 genome (one localized within the LTR, the other within the env gene), known to bind nuclear factors and (b) we determined whether different aromatic polyamidines are able to differentially affect the electrophoretic mobility of these HIV-1 PCR fragments. We found that aromatic polyamidines differentially affect the electrophoretic migration of PCR-amplified HIV-1 genomic regions. This differential effect, related to a differential DNA-binding activity, could lead to a differential inhibition of protein-DNA interactions.
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PMID:Effects of aromatic polyamidines on the electrophoretic mobility of HIV-1 genomic regions amplified by polymerase-chain reaction. 181 18

The ability to clone and express proteins at high levels of abundance and purity has led to their increasing consideration as therapeutic agents. The use of various protein engineering and recombinant DNA techniques has enabled progression to where proteins can be tailored so that they have not only the ability to interact with a unique (extra)cellular component in order to produce a pharmacological effect, but their structure can be altered so as to achieve a selective biological disposition. This ability to control the biological dispersion of proteins is becoming a key element in the design of therapeutic polypeptides and proteins, finding application in modalities intended for treating HIV infections, accessible tumor masses, and diseases of the hematopoietic system, etc. For recombinant site-specific systems to be successfully introduced into the clinic, radically different approaches are required during their development and clinical testing. These relate not only to the pharmacokinetics and receptor availability of the drug, but also its pharmacodynamics, its analytics and its safety pharmacology. This contribution examines how the control of the biological disposition of proteins may be achieved using both site-directed mutagenesis, sequence re-ordering, hybrid protein formation, protein resurfacing, as well as synthetic adduction to polymers.
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PMID:Design of site-specific protein drugs. 181 86

16 HIV seropositive patients among the 180 treated at the Hospital Muniz and the Hospital Posadas in Buenos Aires between December 1988 and December 1989 were referred to the Hospital Posadas Endoscopy Service for esophageal studies. The 16 patients were prospectively studies by means of fiberoscopy, radiology, biopsies, virology, mycology, and brush cytology. Early treatment is of utmost importance because opportunistic infections may aggravate the general condition, increase immune system effects, and probably permit greater replication of HIV, in addition to producing symptoms. 14 patients were male and 2 female. Ages ranged from 18 to 41 and averaged 32 years. 10 were male homo- or bisexuals and the other 6 were intravenous drug users. 14 of the patients consulted because of specifically esophageal symptoms. 12 reported dysphagia, 8 odynophagia, and 6 retrosternal pain. 9 patients presented various symptoms. 15 of the 16 symptomatic patients had some pathology related to HIV. The remaining case presented a small submucus tumor and gastroesophageal reflux. The symptoms had appeared between 10 days and 1 year prior to study. Symptoms did not provide accurate diagnostic clues. 11 cases of esophageal candidiasis were diagnosed endoscopically by isolated or confluent white plaques. 3 patients classified as grade 1 or 2 on the basis of the intensity and density of plaques had mild symptoms, and 8 classified as grade 3 or 4 had more severe symptoms. 7 of the 11 patients also had oral candidiasis. 4 of 6 patients presenting ulcerative pathology were diagnosed virologically with herpes simplex virus type 2. Herpetic ulcers were single or multiple and were deep with slightly raised edges. No ulcers attributable to cytomegalovirus were diagnosed. 4 of the 11 patients with candidiasis also had ulcers, in 2 cases herpetic. The studies indicated a change in the stage of HIV infection following Centers for Disease Control criteria in 10 cases. AIDS was diagnosed in 7 cases based on esophageal findings. Endoscopic study and the samples obtained guided treatment in the 16 patients. In 1 case a repeat endoscopy led to a change in treatment. It is recommended that endoscopy be performed in all patients with esophageal symptoms. Radiology was relatively ineffective, with 50% of diagnoses in error. Histopathology required multiple biopsies and was less sensitive than endoscopy and cytology. Cytology was highly specific and sensitive.
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PMID:[Esophageal pathology in patients with the AIDS virus. Etiology and diagnosis]. 182 Jun 92

In populations with non-HIV immunodeficiency, non-Hodgkin lymphoma and soft tissue sarcoma, especially Kaposi's sarcoma, are the most prominent tumours, but Hodgkin's disease, gastric carcinoma, squamous cell skin cancer, malignant melanoma, hepatoma, myeloid leukaemia and/or colorectal carcinoma have been linked in various studies. Population based cancer registries and cohort studies of HIV infected persons have generally failed to detect HIV related increases in total cancer incidence or in specific tumours other than non-Hodgkin lymphoma and Kaposi's sarcoma; however, associations with anal carcinoma, hepatoma and Hodgkin's disease have been suggested by some studies. Although not indicating increased risk, HIV induced immunosuppression has been linked to an acceleration of cervical and anal neoplasia and to increased aggressiveness of Hodgkin's disease with a relative excess of the mixed cellularity type. Advances in treatment for HIV infection will delay progression to AIDS and may allow an altered natural history to emerge, including the occurrence of excesses of additional cancer types.
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PMID:HIV infection and cancers other than non-Hodgkin lymphoma and Kaposi's sarcoma. 182 20

Whereas previously KS represented a very rare and obscure neoplasm, it has become over the past decade a significant disease. Its appearance in various well defined risk populations and in immunosuppressed individuals and the mounting epidemiological evidence that KS may well represent a sexually transmitted disease in certain groups make KS an important tumour to study as a model for carcinogenesis. Among the various forms of KS described, it is the epidemic form of KS, most frequently associated with HIV infection, that is now the most prevalent form seen around the world. Clinically, the mucocutaneous and lymph node involvement are its most frequently recognized manifestations. Skin lesions in epidemic KS, unlike those in classical KS, appear anywhere on the skin or oral mucosa and at any age in patients with AIDS. Visceral lesions are often present, sometimes in the absence of cutaneous KS. Epidemic KS is rarely the cause of death in AIDS patients, even in those with visceral involvement, unlike the HIV-1 unrelated African endemic form of KS, which is an aggressive and malignant tumour. HIV testing is necessary to establish the diagnosis of AIDS in patients with epidemic KS, even in those patients with risk factors for HIV infection, since epidemic KS may represent an epidemic disease caused by a yet unidentified transmissible agent distinct from HIV. Concurrent transmission of HIV and the putative "KS agent" may have occurred in the homosexual patients with AIDS in whom KS has been so prevalent, and the recently identified form of epidemic KS in individuals not infected with HIV may well become yet a new form of this curious disease.
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PMID:Clinical aspects of epidemic Kaposi's sarcoma. 182 22

Kaposi's sarcoma is the neoplasm most commonly associated with HIV infection. Since its presence in the proper clinical context is an AIDS defining event, histopathological confirmation is often required for diagnosis. It is essential that clinicians know the criteria for histopathological diagnosis. When the criteria outlined are followed, the diagnosis can be made with certainty in most cases. A number of conditions may simulate KS both clinically and histologically, and it is important that those who care for patients with HIV infection are aware of these.
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PMID:Histopathological features of Kaposi's sarcoma in HIV infected individuals. 182 25

CD3,4 (anti-CD3:anti-CD4) bispecific monoclonal antibodies (BSMAB) cause a profound decrease in CD4+ T cells and a marked proliferation of CD8+ T cells in peripheral blood mononuclear cells in vitro. CD3,8 (anti-CD3:anti-CD8) BSMAB causes a reciprocal decrease in CD8+ T cells and a proliferation of CD4+ T cells. The major effector of CD4+ T cell cytolysis in the presence of CD3,4 resides in the CD8+ T cell population. In contrast, both the CD4+ and CD8+ T cells are effective mediators of cytolysis of the CD8+ T cells in the presence of the CD3,8. The likely underlying mechanism in each case is bridging of the CD4 and CD8 of the target cells to the CD3 complexes of the effector cells by antibodies, mimicking the natural encounter between a cytolytic T cell and its target. Proliferation studies indicated that CD3,4 and CD3,8 each can induce proliferation of both CD4+ and CD8+ T cells in the presence of accessory cells. These results suggest that the major selection of the BSMABs occurs via selective destruction of one T cell subset with concurrent stimulation of the remaining CD3+ population. Potential applications of the selective destruction and proliferation include study and manipulation of the T cell subsets in HIV infections, tumor infiltrating lymphocytes, autoimmune diseases, and graft rejection.
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PMID:Selective reduction and proliferation of the CD4+ and CD8+ T cell subsets with bispecific monoclonal antibodies: evidence for inter-T cell-mediated cytolysis. 182 87


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