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)

During a 2-year period 5 men positive for the human immunodeficiency virus (HIV) presented with 6 testis tumors among a total of 3,015 men seen at our hospital acquired immunodeficiency syndrome (AIDS) clinic. This testis tumor incidence of 0.2% is 57 times that of the United States average of 3.5 cases per 100,000 men. Two patients were only HIV positive and 3 others already had AIDS-related complex for 2 to 15 months at the time of tumor diagnosis. Tumor histology was mixed germ cell tumor in 4 patients, pure seminoma in 1 and Burkitt's lymphoma in 1. Patients underwent routine staging evaluations. Three patients had low stage mixed germ cell tumor (clinical stage 1 or 2A) and underwent retroperitoneal lymphadenectomy, which revealed pathological stage 1 or 2A disease in 1 and 2, respectively. These patients did not receive adjuvant chemotherapy. Two patients had advanced mixed germ cell tumor (clinical stage 2C) or Burkitt's lymphoma (clinical stage 4) and received combination chemotherapy from the onset. Outcome was evaluated with regard to progression of HIV disease and tumor status. The 2 patients who were only HIV positive remained so for 9 and 48 months. The 3 patients with AIDS-related complex had progression to AIDS within 1 to 9 months and 2 of these patients died 1 1/2 and 7 months after tumor diagnosis. All 3 patients with resected low stage disease had tumor recurrence within 1 to 9 months and were begun on platinum-based combination chemotherapy. The risk of false low clinical staging and early tumor progression may be higher in HIV positive men than in other testis tumor patients. Patient ability to tolerate chemotherapy and to obtain a satisfactory tumor response appeared to be primarily related to lack of progression of HIV disease to frank AIDS.
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PMID:Testicular tumors in men with human immunodeficiency virus. 155 81

The authors present seven autopsy cases of non-AIDS primary malignant lymphoma of the central nervous system to correlate the pathology with the findings of the most recent pre-mortem computed tomogram (CT). Of 10 primary contrast-enhancing (CE) lesions treated by chemotherapy alone, radiotherapy alone, radiochemotherapy, or surgery combined with radiochemotherapy, all but one completely disappeared after the initial course of therapy. However, in six of the seven patients, the final pre-mortem CT demonstrated CE lesions. In three cases CE lesions were at the same site as the primary lesion, in one case in a remote location, and in two cases in diffuse and multiple locations. In all but one case these CE lesions corresponded histologically to tumor nodules or to white matter densely infiltrated by tumor cells. The sole exception was diagnosed pathologically as delayed radiation necrosis. The final CT also showed five low-density areas (LDAs) which had evolved from CE lesions after the completion of therapy. These LDAs corresponded to rarefied or necrotic parenchyma in which tumor cells remained, mainly in the perivascular spaces. One case exhibited diffuse tumor infiltration of periventricular structures which appeared to have normal density and no CE on the final pre-mortem CT.
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PMID:Correlation of computed tomography with the histopathology of primary malignant lymphoma of the brain. 155 36

Kaposi's sarcoma (KS) is a pleomorphic spindle cell lesion whose incidence has markedly increased among patients infected with the human immunodeficiency virus (HIV), especially among those whose primary risk factor is homo/bisexual transmission. The question as to whether KS is even a true neoplasm still remains largely unsettled due to the body of epidemiologic and histologic evidence suggesting an infectious etiology of the lesion. Accordingly, very few studies have been published regarding systemic distribution or patterns of metastatic progression of the lesion. In the past, such studies have been primarily hampered by inadequate sampling of different tissue specimens and by the lack of a method whereby the data could be rationally interpreted. In the present study we have reviewed the clinical and pathologic features of 169 autopsied patients with either documented HIV infection or the acquired immunodeficiency syndrome, among whom 28 patients were found to have KS. Using cluster analysis, we constructed a novel data structure, called a "dendrogram," whereby patterns of metastasis could be examined. Our results show at least three patterns of metastasis of the lesions, predominantly involving the skin, upper gastrointestinal tract, or midgastrointestinal tract, within this cohort of autopsied patients. These three patterns suggest that there is no single pathogenetic mechanism in the acquisition and dissemination of HIV-associated KS.
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PMID:Cluster analysis of the metastatic patterns of human immunodeficiency virus-associated Kaposi's sarcoma. 155 40

Dimethylhydrazine (DMH) induces colonic cancer and angiosarcomas in mice. In order to determine pertinence of mouse angiosarcoma as a model to AIDS associated Kaposi's sarcoma (KS), we investigated if immune dysfunction occurred during tumor development by DMH. Outbred CD1 male mice received once weekly DMH a 20 mg/kg body weight dose s.c. for 33 weeks. Every two weeks initially and then every week groups of DMH-treated and control animals were sacrificed to determine a) peripheral blood and splenic T cell subset ratio b) 4-day plaque forming cell (PFC) response to i.p. sheep red blood cells (SRBC) and c) mitogenic response of spleen cells to Concanavalin A (Con A) and lipopolysaccharide (LPS). No change in T helper/T suppressor + cytotoxic T cell (Th/Tsupp. + CTL) and mitogenic response to spleen cells to Con A was noted whereas PFC response of animals to SRBC and mitogenic response of spleen cells to LPS decreased. These data suggest that either infection with T cell depleting virus such as LP:BM5 or immunosuppressive drugs affecting T cell function, such as steroids may be required to bring the immune status of DMH treated animals closer to that of AIDS associated KS bearing human subjects.
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PMID:An animal model of Kaposi's sarcoma. I. Immune status of CD1 mice undergoing dimethyl hydrazine treatment to induce angiosarcomas and other malignancies. 156 54

PCR cloning and cDNA sequencing have been used to identify mRNAs of two splice products of the vascular endothelial growth factor (VEGF) gene, VEGF121 and VEGF165, in cells isolated from Kaposi's sarcomas (KS) of AIDS patients (AIDS-KS). As demonstrated by Northern blot analysis, AIDS-KS cells as well as tumor cells show a high expression level of the VEGF gene as compared to primary human vascular cells like smooth muscle cells or endothelial cells. In addition to the lower expression of the gene, vascular cells express a 3.9 kb band together with a 3.2 kb band instead of a 3.9 kb and a 4.3 kb band in AIDS-KS cells. Our data suggest that the angiogenic properties of AIDS-KS cells might be mediated by the secretion of this growth factor and that this factor alone or in combination with other endothelial mitogens may be involved in endothelial proliferation associated with Kaposi's sarcoma.
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PMID:AIDS-associated Kaposi's sarcoma cells in culture express vascular endothelial growth factor. 156 95

A retrospective analysis of 41 patients with cryptococcal meningitis and AIDS or neoplastic disease was done. Patients with AIDS were younger and predominantly male; they had a shorter duration of prior illness, higher initial serum cryptococcal antigen titers, and lower initial cerebrospinal fluid white blood cell counts than those with neoplastic disease. The median overall survival for patients with AIDS was 9 months compared with 2 months for those with neoplastic disease (P = .004). Seventy-eight percent of patients with AIDS and 43% of those with neoplastic disease were cured or improved 6 months after diagnosis (P = .039). Toxicity from amphotericin B and flucytosine was similar for both groups. One patient with AIDS relapsed. Multivariate predictors of survival included headache (P = .007) and an AIDS diagnosis (P = .009). Examination of outcomes for other opportunistic infections associated with AIDS and other immunosuppressive illness may distinguish prognostic features for different patient populations.
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PMID:Cryptococcal meningitis: outcome in patients with AIDS and patients with neoplastic disease. 156 50

In at least 65% of patients with acquired immunodeficiency syndrome (AIDS), the lung is the site for life-threatening illness. To establish a basis for understanding the pulmonary pathology of such illness, we first review briefly the effects of the human immunodeficiency virus on the immune system and then review the pathological pulmonary processes occurring in AIDS in terms of their various etiologies: infections, idiopathic processes, and neoplasia. In the section on each etiology, we discuss clinical manifestations, pulmonary pathology, diagnostic findings, and therapeutic options. In the last section, we outline our overall initial diagnostic approach to the patient with AIDS who presents with respiratory symptoms, and we discuss the integration of clinical, laboratory, and radiographic findings.
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PMID:Pulmonary manifestations of acquired immunodeficiency syndrome. 157 69

The production of TNF-alpha and TNF-beta by human B-cell lines was studied at both the molecular and biological levels. The 24 B-cell lines studied included EBV+ cell lines (n = 13), EBV- cell lines (n = 8), and AIDS-associated B-cell lines (AABCL) (n = 3) which are EBV+/HIV-. Whereas radioimmunoprecipitation using TNF-alpha antisera detected 17-kDa TNF-alpha as expected, similar studies with anti-TNF-beta antisera revealed TNF-beta microheterogeneity. In the AABCL three bands with approximate MW of 26, 24, and 22 kDa were detected under reducing conditions, and in the non-AABCL, two bands only with 26 and 22 kDa were observed. To determine whether the size heterogeneity of TNF-beta is due to glycosylation, TNF-beta deglycosylation studies were done in two AABCL (PA682BM-2, PA682PE-1) and one non-AABCL (IM-1178). As control, the normal lymphoblastoid B-cell line RPMI-1788, which is known to secrete TNF-beta with MW 25 and 20 kDa, has been used. Deglycosylation studies using N-glycanase + neuraminidase + O-glycanase reduced the various bands in all cell lines to one band with 18.6 kDa, which is compatible with the TNF-beta backbone. In attempt to determine whether the differential glycosylation of TNF has any functional significance, all 24 cell lines were studied for TNF secretion and for TNF neutralization by monoclonal antibodies and polyclonal antibodies to TNF-alpha and TNF-beta. Constitutive secretion of TNF-alpha and TNF-beta has been detected only in the three AABCL. Following activation with the tumor promoter teleocidin, the secretion of both TNFs has been triggered in 2/8 EBV- cell lines and in 8/13 EBV+ non-AABCL. Using rabbit polyclonal antibodies to human TNF-alpha and to human TNF-beta, only little if any neutralization of these TNFs has been shown. Our data suggest that the differences in glycosylation of B-cell-derived TNFs may account for the incomplete neutralization, and may influence the cytotoxic biological activity of this lymphokine.
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PMID:Human B-cell TNF-beta microheterogeneity. 157 46

A marked increase has recently been noted in the incidence of lymphoma in patients with AIDS. These lymphomas are generally high-grade, of B-cell origin, and often involve extranodal sites. Reported here are twenty patients with AIDS in whom symptoms and physical findings developed related to the head and neck region as a result of lymphoma. The tumor was observed in a variety of sites, including the nasopharynx, orbit, submandibular triangle, anterior and posterior cervical triangles, supraclavicular fossa, and the hypopharynx. Sixteen tumors were large cell nonHodgkin's B-cell lymphomas, three were small cell nonHodgkin's B-cell lymphomas, and one was Hodgkin's disease, mixed cellularity. All were treated with combination chemotherapy. A high degree of suspicion for lymphoma is required in treating any patient with AIDS who has a rapidly enlarging mass in the head and neck. If needle aspiration is nondiagnostic, excisional biopsy should be performed after a complete head and neck evaluation. Although the development of lymphoma associated with AIDS portends a grave prognosis, prompt diagnosis will allow an improved chance of remission of the lymphoma.
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PMID:Head and neck lymphoma in patients with the acquired immune deficiency syndrome. 158 18

Intramedullary spinal cord tuberculoma in a young, homosexual man with AIDS was detected with the use of MR and confirmed pathologically. MR findings were similar to those seen in other intramedullary lesions, eg, astrocytoma, ependymoma, hemangioblastoma, metastasis, lymphoma, and opportunistic infections. Delineation of the lesion improved with administration of Gd-DTPA; enhancement of the lesion, however, does not always correlate with true tumor margins at pathologic examination.
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PMID:Intramedullary spinal cord tuberculoma in a patient with AIDS. 159 Feb 2


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