Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The French-Italian Cooperative Study Group included patients with poor-prognosis AIDS-related non-Hodgkin's lymphoma (NHL), defined as those with performance status (PS) > or = 3 and/or opportunistic infections (OI), in a prospective study with a 50% reduced-dose combination chemotherapy regimen: CHVmP-Vincristine-bleo (cyclophosphamide 300 mg/m2 i.v. day 1, doxorubicin 25 mg/m2 i.v. day 1, teniposide 30 mg/m2 i.v. day 1, prednisone 20 mg/m2 per os days 1-5, vincristine 2 mg i.v. day 15, and bleomycin 10 mg i.v. day 15), given every 21 days for eight cycles, and concomitant zidovudine 500 mg per os per day. The aims of this combined treatment were to reduce bone marrow toxicity and infectious complications related to chemotherapy (with a low-dose chemotherapy regimen), and to control the HIV and related infectious complications (with zidovudine therapy). Thirty-seven patients entered this prospective study. At the time of the NHL diagnosis, 41% of the patients had asymptomatic HIV infection, 27% had ARC and 32% had already had CDC-defined diagnoses of AIDS. The median CD4+ cell count was 35 mm3. Only 29 patients are evaluable for response, since 8 received only one cycle of chemotherapy. Fifteen of 29 (52%) patients obtained objective responses, with only 4 (14%) achieving complete remissions (CR) of 1, 4, 14 and 29+ months. Three (16%) CRs were achieved in 19 evaluable patients included in the study because of poor PS, and only one CR was observed in 10 evaluable patients with histories of OI, either alone or with poor PS. The most common side effect was bone marrow toxicity with 2 related toxic deaths.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Prospective study with combined low-dose chemotherapy and zidovudine in 37 patients with poor-prognosis AIDS-related non-Hodgkin's lymphoma. French-Italian Cooperative Study Group. 128 47

HIV-1-related neurological diseases, excluding opportunistic infections and HIV encephalitis, are considered here. Most occur in severely immunosuppressed patients, with CD4 counts of under 200 x 10(6) l-1. Primary brain lymphoma and metastases from systemic non-Hodgkin's lymphoma, the second commonest cause of cerebral mass lesions in AIDS, are usually aggressive B cell tumours. Their poor median survival after treatment, compared with that of lymphomas in non-AIDS patients, seems related to systemic complications, particularly opportunistic infections. Kaposi's sarcoma produces neurological symptoms exceptionally. Cerebral infarction is often unrecognized clinically but large vessel arteritic occlusions may occur. Intracranial haemorrhages occur mostly in thrombocytopenic patients. Seizures are frequently referred to the neurologist; investigation may lead to a diagnosis of AIDS. Nearly 50% of patients with seizures have cerebral toxoplasmosis or cryptococcal meningitis; HIV-1 encephalitis is presumed to be the cause in 30%. A subacute or chronic vacuolar myelopathy with pyramidal and posterior column signs is the commonest form of spinal cord involvement in AIDS; its cause remains unknown. Peripheral nerve syndromes occur at all stages of HIV-1 infection. Distal symmetrical peripheral neuropathies are the most frequent, particularly a painful form with axonal atrophy, associated with CMV infection, and seen during ARC or AIDS. Mononeuritis multiplex due to vasculitis, CMV, or lymphoma and a serious lumbosacral polyradiculopathy due to CMV are infrequent. The commonest myopathy is due to zidovudine (AZT); it usually responds to drug withdrawal. The nature, prognosis and optimal management of most other myopathies is yet to be determined.
 ...
PMID:Other neurological diseases in HIV-1 infection: clinical aspects. 134 49

Cutaneous manifestations are common in patients with HIV infection and mainly due to the immunodeficiency. In the initial stage of HIV infection, we frequently observe a rash of macular lesions. During the asymptomatic phase, the patients may typically show the following skin diseases: seborrhoic dermatitis, acneiform folliculitis, persistent herpes simplex, and infections with the human papilloma virus. In ARC and AIDS patients, 3 groups of skin disorders are found: cutaneous infections, skin tumors, and other mixed skin diseases. Herpes simplex and herpes zoster may develop into ulcerating and necrotising forms especially in patients with advanced immunodeficiency. The most frequent skin tumors in AIDS patients are the disseminated Kaposi's sarcoma and non-Hodgkin's lymphoma. More than 50% of the AIDS patients treated with trimethoprim/sulfamethoxazole developed a severe drug eruption. African and Caribbean patients with AIDS frequently suffer from pruritic skin lesions, the pathogenesis of which is not known. Aside from these cutaneous manifestations, a variety of other skin disorders have been reported in patients with HIV infection, ARC, or AIDS; future research will furnish definite proof whether they are correlated with HIV infection.
 ...
PMID:[Skin manifestations in patients with HIV infection]. 220 61

AIDS (acquired immune deficiency syndrome) and ARC (AIDS-related complex) are associated with a spectrum of lymphoproliferative disorders ranging from lymphadenopathy syndrome (LAS), an apparently benign polyclonal lymphoid hyperplasia, to B cell non-Hodgkin's lymphoma (B-NHL), i.e., malignant, presumably monoclonal B cell proliferations. To gain insight into the process of lymphomagenesis in AIDS and to investigate a possible pathogenetic relationship between LAS and NHL, we investigated the clonality of the B or T lymphoid populations by Ig or T beta gene rearrangement analysis, the presence of rearrangements involving the c-myc oncogene locus, and the presence of human immunodeficiency virus (HIV) sequences in both LAS and B-NHL biopsies. Our data indicate that multiple clonal B cell expansions are present in a significant percentage of LAS (approximately 20%) and B-NHL (60%) biopsies. c-myc rearrangements/translocations are detectable in 9 of our 10 NHLs, but not in any of the LAS cases. However, only one of the B cell clones, identified by Ig gene rearrangements carries a c-myc gene rearrangement, suggesting that only one clone carries the genetic abnormality associated with malignant B cell lymphoma. Furthermore, the frequency of detection of c-myc rearrangements in AIDS-associated NHLs of both Burkitt and non-Burkitt type suggest that the biological alterations present in AIDS favor the development of lymphomas carrying activated c-myc oncogenes. Finally, our data show that HIV DNA sequences are not detectable in LAS nor in NHL B cell clones, suggesting that HIV does not play a direct role in NHL development. Taken together, these observations suggest a model of multistep lymphomagenesis in AIDS in which LAS would represent a predisposing condition to NHL. Immunosuppression and EBV infection present in LAS can favor the expansion of B cell clones, which in turn may increase the probability of occurrence of c-myc rearrangements leading to malignant transformation.
 ...
PMID:Multiple monoclonal B cell expansions and c-myc oncogene rearrangements in acquired immune deficiency syndrome-related lymphoproliferative disorders. Implications for lymphomagenesis. 349 Nov 76

Infection with the human immunodeficiency virus (HIV) leads to selective depletion of the helper/inducer lymphocyte subset and a subsequent state of acquired cellular immunodeficiency. Simultaneously, evidence of B-cell hyper-activity may exist. A subset of patients infected with HIV demonstrates a syndrome of persistent generalized lymphadenopathy (PGL). Lymph node biopsies reveal benign reactive changes with a pattern of florid follicular hyperplasia. A polyclonal hypergammaglobulinemia reflects humoral immune dysfunction. Patients with PGL are similar to those with full-blown AIDS with regards to demographics, immune and virologic studies. Our prospective natural history study of PGL patients initiated in November 1981 reveals a 15% rate of evolution to AIDS in the 200 patient cohort. Factors associated with increased risk of transformation to AIDS include severity of constitutional symptoms, shrinking adenopathy, oral candidiasis or viral hairy leukoplakia, peripheral cytopenias, elevated erythrocyte sedimentation rate or an antecedent episode of herpes zoster. Therapeutic interventions to prevent evolution to AIDS in high risk subsets of lymphadenopathy patients have been investigated. In addition to benign B-cell proliferation associated with HIV infection, malignant lymphomas have also been diagnosed in 29 patients in AIDS risk groups in our clinic population. All patients were male; 26 homosexuals, 2 IV drug abusers and 1 multiply transfused sickle cell anemia patient. Seven patients had antecedent PGL. Non-Hodgkin's lymphoma was diagnosed in 19 patients. Histologies were predominantly diffuse undifferentiated or large cell. Eleven patients were Stage IV at diagnosis. Of 10 patients with mixed cellularity Hodgkin's disease, 7 were Stage IV-B at presentation. Extranodal disease was frequent in patients with lymphomas. Fourteen patients lacked peripheral lymphadenopathy. Response to chemotherapy was good, but complicated by prolonged marrow suppression and development of AIDS-related opportunistic infections. Median survival was 7 months. Laboratory studies investigating the possible role of lymphotropic retroviruses in the development of AIDS-related lymphomas revealed that serum from all patients with high grade non-Hodgkin's lymphoma contained antibodies to HIV and that the majority also expressed antibodies to HTLV-I. This degree of seroreactivity to HTLV-I and HIV was characteristic only of lymphoma patients as sera from only 10 - 15% of AIDS and ARC patients in San Francisco had similar findings.
 ...
PMID:AIDS-related benign lymphadenopathy and malignant lymphoma: clinical aspects and virologic interactions. 382 9

We analysed problems on the front line of the AIDS medicine through our experience of a with hemophilia A, who had HIV infection developed to ARC and the AIDS and in addition, had non-Hodgkin's lymphoma in his rectum and died of pneumonitis caused by pneumocystis carinii. We have learned from the poll on medical worker's recognition of the disease through the experience of this case that the nurses who were concerned with the care of this patient did not have opinions against acceptance of patients with AIDS, although they have a fear, from the professional point of view, to a possibility of infection of the virus from patients with AIDS. What should be done in the practical part of the AIDS medicine are (1) a repetitive education of accurate knowledge of the disease, (2) completion of practical guide lines for medical care of patients with AIDS and (3) legal establishment of an insurance system for accidental infections of HIV to medical or paramedical staffs.
 ...
PMID:[Issues in the AIDS medicine based on the analysis of medical worker's recognition of the disease]. 822 68

To assess whether monitoring of antibodies (Ab) directed against the HIV-1 p25 core protein may be used as a predictive marker in the biological monitoring of HIV-infected patients, a study was performed on a transversal cohort of 68 CDC stage II-III, and 36 ARC and 26 AIDS stage IV patients, 37 of whom were being treated with anti-retroviral therapy. A second cohort included 56 patients followed for 3-7 years: 15 stage II-III, 11 ARC and 30 AIDS patients (opportunistic infections: 14; Kaposi's sarcoma: 11; non-Hodgkin's lymphoma: 5). p25 antigenemia and CD4+ blood lymphocyte counts were determined in parallel. Stage II-III patients usually had high and stable anti-p25 Ab levels, ARC patients exhibited more heterogeneous Ab values, while those with AIDS had very low values. No significant difference was observed in the serum anti-p25 levels of patients treated or not with anti-retroviral therapy. In patients whose CD4(+)-cell counts were going to fall below 200/mm3 and/or who were going to progress towards AIDS, the Ab levels started to decrease at a rate of > 1 log U/ml (expressed in arbitrary units/ml) per 5 years at least 2 to 4 years, respectively, before the appearance of the index symptom, despite the fact that the CD4(+)-cell count only differed significantly between progressors and non-progressors one year before the appearance of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Predictive value of the assay of serum anti-p25 antibodies in patients with human immunodeficiency virus (HIV-1) infection]. 829 42

Arsenic trioxide (As2O3) has recently been shown to induce complete remission in acute promyelocytic leukemia (APL). As2O3 reportedly has dose-dependent dual effects on APL cells, triggering apoptosis at relatively high concentrations and inducing differentiation at lower concentrations. However, its effect is still controversial for other AML cells and hematological neoplasms. We studied the in vitro effect of As2O3 on lymphoid lineage cells: lymphoma cell lines, NOL-3, Raji and Daudi, a myeloma cell line, NOP-1, normal peripheral blood lymphocytes (PBL), non-Hodgkin's lymphoma (NHL) cells and chronic lymphocytic leukemia (CLL) cells, and compared it with the effect on APL cell line, NB4, as well as other myeloid cell lines, HL-60 and NKM-1. As2O3 at a concentration of 1 micromol/l markedly inhibited both proliferation and viability of NB4, NOP-1, NOL-3 and NKM-1 cells, but it reduced only viability in normal PBL, CLL cells and NHL cells. As2O3 induced apoptosis and down-regulated bcl-2 expression in NB4, NOP-1 and NKM-1 cells. On the other hand, in HL-60, Raji and Daudi cells, 1 micromol/l As2O3 inhibited only the proliferation weakly, and neither induced apoptosis nor down-regulated bcl-2 expression, but arrested only cell cycle at G1 phase. As2O3 at a low concentration of 0.1 micromol/l had no effect on proliferation and viability of these cells except for NB4. These results showed that As2O3 exerted variable and definite effects on lymphoid cells and indicated that As2O3 might be clinically useful in lymphoid neoplasms such as malignant lymphoma and CLL.
 ...
PMID:The induction of apoptosis and cell cycle arrest by arsenic trioxide in lymphoid neoplasms. 973 86