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

Seventy previously untreated patients with stage II, III, and IV intermediate- or high-grade lymphoma were treated with methotrexate, doxorubicin, cyclophosphamide, vincristine, prednisone, and bleomycin (MACOP-B) between September 1985 and November 1987. Forty-nine of these patients had diffuse large-cell lymphoma (DLCL), and eight of these patients were human immunodeficiency virus (HIV)-positive. Complete responses were achieved in 54% of all patients and 52% of those with DLCL. With follow-up extending to 36 months, 45% of all DLCL patients are alive, and 50% are still living, if the HIV-positive patients are excluded from the analysis. Chemotherapy was quite toxic. Seventy-five percent of patients had severe mucositis, 42% had peripheral neuropathy, 50% required hospitalization, and 54% experienced leukopenia with a WBC count below 1,000/microL. Seven percent (five patients) died of toxicity related to the chemotherapy. Our analysis of prognostic parameters indicated that B symptoms, a performance status below 80, and, to a lesser extent, elevation of serum lactic acid dehydrogenase (LDH) (in HIV-negative DLCL patients) were associated with an inferior survival. Advanced age, sex, and bulky disease were not found to have a statistically significant effect on survival. Our preliminary results indicate that MACOP-B chemotherapy is an effective regimen for high- and intermediate-grade lymphomas. However, the survival for patients with DLCL treated with MACOP-B is no different than that achieved with previous regimens at our institution.
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PMID:Treatment results with an aggressive chemotherapeutic regimen (MACOP-B) for intermediate- and some high-grade non-Hodgkin's lymphomas. 168 17

A man with previous addiction to parenteral drugs presented infection by human immunodeficiency virus (HIV) with persistent generalised lymph node enlargement. Sixteen months after diagnosis, he developed intermediate-grade lymphoma of the stomach. Partial response was achieved by chemotherapy, and the patient presented pulmonary and meningeal tuberculosis which led him to exitus.
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PMID:[Syndrome of persistent generalized lymphadenopathy with development into a gastric lymphoma]. 169 62

A culture of rhesus monkey peripheral blood lymphocytes was divided into two parts; one was kept as an uninfected control, and the other was infected with a strain of simian immunodeficiency virus (SIVmac251) originally isolated from a rhesus monkey that died of a malignant lymphoma associated with acquired immune deficiency syndrome. Both cultures were sampled at successive intervals from 1 to 40 days postinfection. Each sample was subjected to in situ hybridization for detection of viral mRNA, immunocytochemical detection of viral core protein (p27), reverse transcriptase assay, electron microscopy, and immunophenotypic characterization of infected cells. These techniques were used to define viral growth kinetics of this novel lentivirus in peripheral blood lymphocytes. The first evidence of SIVmac251 replication was obtained by an in situ hybridization signal for viral mRNA at 2 days postinoculation. This was followed by detection of viral p27 core protein by immunocytochemistry on day 4. Reverse transcriptase activity above control values was not detected until day 8. Budding particles were not found in the infected cultures until 14 days postinfection. Results of in situ hybridization, immunocytochemistry, and reverse transcriptase assay indicated that two bursts of viral replication occurred during the course of this study. The first, at 3 weeks postinfection, was due to infection and subsequent depletion of CD4+ lymphocytes, while the second, 3 weeks later, resulted from a cycle of replication in CD8+ lymphocytes and the remaining CD4+ cells, culminating in the death of all cells on day 39 postinoculation.
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PMID:Study of long-term cultures of simian immunodeficiency virus (SIVmac 251)-infected peripheral blood lymphocytes. 169 33

Cytotoxic feline immunodeficiency virus (FIV) infection was established in feline T4 thymic lymphoma 3201 cells with the Petaluma isolate of the feline immunodeficiency virus (FIV-Petaluma). Mg2(+)-dependent, reverse transcriptase (Mg2+ RT) activity and FIV p24/28-positive cells were evident beginning at 18 days postinoculation (dpi). Cell death was observed beginning at 22 dpi, with a maximum of 40% dead (trypan blue dye exclusion at 26 dpi). This cytocidal change was not observed in cultured Crandell feline kidney fibroblasts similarly infected with FIV-Petaluma. The surviving cells grew out and a chronic FIV-producer cell line was established. The 3201 cell-derived FIV (FIV-3201) was far more virulent for FIV-naive feline 3201 cells, with FIV p24/28-positive cells and Mg2+ RT activity first detectable by 4-8 dpi and subsequent loss of cell viability detectable by 8-12 dpi. Maximum kill (40% dead) was observed at 16 dpi. Comparison between viral infectivity of FIV-Petaluma and FIV-3201 for FIV-naive 3201 cells showed an increase of 1 log10 tissue culture infectious doses (TCID50) by amplification/passage in 3201 cells. Cytologic and electron microscopic examination of 3201 cells in FIV-infected cultures showed frequent budding lentiviral particles. This lytic infection system opens the way to the routine detection, isolation, and quantitation of FIV from FIV-infected cats, to the large-scale propagation of the virus, and to a system for evaluation of the mechanisms of FIV lymphocytotoxicity and the development of therapies to counteract lentiviral cytopathicity.
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PMID:In vitro replication and cytopathogenicity of the feline immunodeficiency virus for feline T4 thymic lymphoma 3201 cells. 169 55

The CD4 molecule is expressed on T-helper cells and serves as the cellular receptor for the human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2) and for the simian immunodeficiency viruses SIVmac and SIVagm. HIV-1, HIV-2, and SIVmac infectivity can be blocked by monoclonal antibodies (MAbs) directed against the CD4 molecule and by soluble CD4 proteins (sCD4). In the present study, we demonstrated not only lack of inhibition, but 10- to 100-fold sCD4-dependent enhancement of SIVagm infectivity of human T-cell lymphoma lines, although SIVagm infection was blocked by MAbs OKT4a and Leu3a. SIVagm enhancement with sCD4 was suppressed by MAbs OKT4a and Leu3a to levels observed without addition of sCD4. The infectivity of all four tested SIVagm variants was enhanced by sCD4 on all tested lymphoma cell lines. These results suggest a second step (second or secondary receptor) required for enhancing virus entry into the cell and may have serious implications for approaches to the treatment of acquired immunodeficiency syndrome on the basis of modified sCD4 molecules.
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PMID:Soluble CD4 enhances simian immunodeficiency virus SIVagm infection. 170 Aug 34

The principal neutralizing determinant (PND) of human immunodeficiency virus (HIV)-1 resides within the V3 loop of the envelope protein. Antibodies elicited by peptides of this region were able to neutralize diverse isolates. Serum from one of three animals immunized with the human T cell lymphoma virus (HTLV)-IIIMN PND peptide, RP142, neutralized MN and the sequence-divergent HTLV-IIIB isolate. Serum from one of three animals immunized with a 13-amino acid IIIB PND peptide (RP337) also neutralized both of these isolates. Characterization of these sera revealed that the cross-neutralizing antibodies bound the amino acid sequence GlyProGlyArgAlaPhe (GPGRAF) that is present in both isolates. This sequence is frequently found in the PNDs analyzed in randomly selected HIV-1 isolates. Sera from two rabbits immunized with a peptide containing only the GPGRAF residues neutralized divergent isolates, including IIIB and MN.
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PMID:Broadly neutralizing antibodies elicited by the hypervariable neutralizing determinant of HIV-1. 170 22

Small-noncleaved-cell (SNC) lymphoma is a high-grade, biologically aggressive neoplasm notable for poor response to therapy, high relapse rate, and less than a 20% long-term survival. We treated 20 patients with SNC lymphoma with a novel chemotherapeutic regimen using intensive doses of chemotherapy at frequent intervals in the inpatient setting. All patients were previously untreated. Sixteen patients (80%) had stage IV disease. Most patients (95%) had at least one other characteristic associated with poor prognosis (bulky [greater than 10 cm] disease, multiple extranodal sites, poor performance status), and 85% had two or more characteristics associated with poor prognosis. Seventeen patients (85%) achieved a complete response (CR) to therapy, including all three patients with human immunodeficiency virus (HIV)-associated disease. There have been three relapses, all occurring less than 18 months after treatment, and two of three relapses occurred in patients who were unable to complete therapy. At a median follow-up of 29 months, 13 patients (65%) remain disease-free; the calculated 5-year actuarial disease-free survival is 60%. Toxicity, chiefly myelosuppression, was severe but manageable. There were two treatment-related deaths, both in elderly patients with poor performance status and advanced-stage disease. These data suggest that such a dose-intensive approach improves the response and survival of patients with SNC lymphoma.
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PMID:Effective treatment of small-noncleaved-cell lymphoma with high-intensity, brief-duration chemotherapy. 170 85

Multimodality and differentiated treatment of small-intestinal diseases is to combine methods of etiological action with pathogenetic treatment of the main clinical syndromes: chronic diarrhea, malabsorption syndrome, hypercatabolic exudative enteropathy. Each nosological form should be treated specifically. Pathogenetic treatment involves diet therapy, chemotherapeutic correction of metabolic processes (vitamin administration, recovery of normal protein and lipid metabolism, water and electrolyte balance, anemia), management of chronic diarrhea. Treatment regimens are specified for gluten enteropathies, total variable immunodeficiency, Whipple disease, small-intestinal diverticulosis, Crohn's disease, amyloidoses, intestinal lymphoma and retroperitoneal lymph nodes. Clinical experience justifies the above methods as highly effective.
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PMID:[Treatment of chronic diseases of the small intestine]. 172 19

Transgenic mice carrying the exogenous c-myc gene under regulation of the Ig enhancer (Ig-c-myc) were mated with mice carrying exogenous c-fos gene under control of the H-2Kb promoter (H2-c-fos) to examine their functional collaboration in in vivo lymphomagenesis. Two of the 33 (c-fos x c-myc) mice developed pre-B cell lymphomas within 22 weeks of age. None of the other F1 progeny expressing c-fos or c-myc alone showed malignant change within 14 months of age, suggesting that the exogenous c-fos and c-myc collaborate in in vivo lymphomagenesis. The exogenous c-myc RNA was overexpressed in the lymphomas, but the amount of exogenous c-fos RNA was not affected, suggesting that the large abundance of c-myc protein is a prerequisite for lymphoma onset or progression and c-fos protein plays a complementary role. C-fos protein induced immunodeficiency in the (c-fos x c-myc) mice like H2-c-fos mice. Natural killer cell activity of (c-fos x c-myc) mice was partially impaired. Therefore, these lymphomas may be a consequence of the synergism of two independent actions caused by the exogenous c-myc (lymphomagenesis) and the exogenous c-fos (low NK activity) in (c-fos x c-myc) mice.
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PMID:Possible collaboration between c-fos and c-myc proto-oncogene products in in vivo lymphomagenesis. 172 94

Lymphoma has been well described in various states of congenital, acquired, and iatrogenic immune dysfunction, and the clinical and pathologic characteristics in these settings are similar to those seen in patients with HIV-induced immunodeficiency. High grade B cell lymphomas are expected, with widespread extranodal disease at the time of initial presentation. Unusual sites of disease may be seen, such as the CNS. Factors predictive of short survival include low performance status, history of AIDS prior to the diagnosis of lymphoma, stage IV or bone marrow involvement, and low CD4 cells. Use of intensive multiagent chemotherapy may be associated with demise from opportunistic infections. Less intensive regimens may be indicated in patients with poor prognostic indicators, whereas patients lacking these factors may be able to tolerate greater dose intensity.
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PMID:AIDS-associated malignant lymphoma. 172 39


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