Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1986 and 1988, 81 patients with high grade malignant non-Hodgkin lymphoma according to the Kiel classification were treated with the VIM-Bleo/CHOP-regimen: etoposide 100 mg/m2 intravenously on days 1-3, ifosfamide 1.5 g/m2 intravenously days 1-5 with mesna for prophylaxis of cystitis, methotrexate 30 mg/m2 intravenously on days 3, bleomycin 10 mg intravenously on days 8 and 15, cyclophosphamide 750 mg/m2 day 22, doxorubicin 50 mg/m2 day 22, vincristine 1.4 mg/m2 on day 22, and prednisolone 100 mg postoperatively on days 1-5 and 22-26. Cycles were repeated four times beginning on day 43. Regions with bulky disease were irradiated after chemotherapy. 36 patients (44%) had stage II, 12 (15%) stage III and 33 (41%) stage IV disease. B-symptoms were present in 49% of patients. Serum lactate dehydrogenase activity was elevated in 53%. Overall, 59 patients (73%) achieved a complete and 14 (17%) a partial remission. 8 (9%) had stable or progressive disease. After a median follow up of 30 months thus far, probability of long-term relapse free survival is 66% for patients in complete remission. Overall survival is 72% at 24 months. Toxicity from treatment was very low with leukopenia being the main side effect. Major infections were observed in only 2% of cycles with one treatment related death. VIM-Bleo/CHOP is a well tolerated regimen with remission rates in the range of other, more toxic regimens. However, cyclic alternating treatment did not improve results as compared with repeated treatment with a single standard protocol.
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PMID:Cyclic alternating chemotherapy of high-grade malignant non-Hodgkin lymphomas with VIM-Bleo and CHOP. 137 34

The prognosis of patients with refractory or relapsed malignant lymphoma is poor. To improve the outcome of such patients, a therapeutic regimen of VIM +/- B (etoposide/ifosfamide plus mesna/methotrexate/ with or without bleomycin) was administered. Of 47 patients treated, 15 had relapsed following complete remission (CR) after first-line chemotherapy, 28 had failed to achieve CR with first-line therapy, and four failed to respond to multiple salvage regimens. All patients had received extensive prior chemotherapy, and 36 had received combinations containing doxorubicin. Eight patients had low-grade non-Hodgkin's lymphoma (NHL), 28 had high-grade NHL, and 11 patients had Hodgkin's disease. Overall response rate was 87%, with 45% CR and 42% partial remission (PR). Median relapse-free interval was 8 months in patients with CR and 6 months in those with PR. Of patients with CR, 43% were predicted to be without relapse at 2 years and 31% at 5 years. Median survival time for all patients treated with 14 months-22 months for those with CR and 10 months for those with PR. Probability of survival at 2 years was 30% in all patients, 50% in patients with CR, and 15% in those with PR. VIM +/- B appears to be effective against refractory or recurrent lymphoma, resulting in response in a large number of patients and long-term survival and possible cure in a small but significant number. Results indicate that VIM +/- B is particularly effective in patients with high-grade NHL who have responded suboptimally to primary therapy.
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PMID:Etoposide, ifosfamide, and methotrexate with or without bleomycin in refractory or recurrent lymphomas. 171 Apr 86

A total of 15 patients with relapsed or resistant Hodgkin's disease were treated with a combination of etoposide (VP16), ifosfamide, mitozantrone and dexamethasone (VIM-D). The regime was well tolerated, the only major toxicity being myelosuppression. Complete remissions (CRs) were obtained in 4 patients and were maintained for 2, 4, 10 and 14 months. 10 subjects subsequently received an autologous bone marrow transplant with high-dose chemotherapy (ABMT). Previous exposure to VIM-D did not appear to predict for or prejudice the response to subsequent ABMT.
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PMID:VIM-D salvage chemotherapy in Hodgkin's disease. 224 34

Treatment of cultured Hodgkin disease (HD) cells with neuraminidase results in decreased reactivity of monoclonal antibody VIM-D5 with its antigen, the X hapten, a fucosyl-N-acetyllactosamine. The other feature characteristic of HD cells is the expression of high levels of ectosialyltransferase activity. We present evidence for a cause-effect relationship between these two findings in that VIM-D5 antigenicity can be restored on neuraminidase-treated HD cells by modulating transferase activity. This can be interpreted in terms of a lectin activity of the ectosialyltransferase that binds the X hapten's desialylated galactosyl residues, thereby preventing antigen recognition by VIM-D5 antibody. This proposed mechanism is indistinguishable from the autoinhibition phenomenon described for another galactophilic binding protein, the hepatic binding protein (HBP), which binds its own terminal galactosyl residues following neuraminidase treatment. We establish a close relationship between the HD galactophilic binding site and HBP in that antiserum to HBP (i) inhibits the neuraminidase-induced loss of VIM-D5 antigenicity, (ii) blocks the binding of asialoglycoprotein to hepatocytes after being absorbed by and eluted from HD cells, and (iii) recognizes a single HD protein, which in its high level of expression is unique to HD cells. The presence of lectin activity in its classic sense on the surface of HD cells is confirmed by the erythrocyte-agglutinating ability of these cells. This lectin activity, which appears to be related to an ectosialyltransferase on the surface of HD cells, may serve as a marker for the abnormal cells characteristic of HD.
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PMID:Lectin activity as a marker for Hodgkin disease cells. 242 50

A total of 20 patients with intermediate or high-grade non-Hodgkin's lymphomas who failed to LNH 84 regimen were treated with a combination of VP 16, ifosfamide and methotrexate (VIM regimen). Nineteen patients are evaluable for response. Eight patients (42%) achieved complete responses and four (21%) attained partial responses. Most of the complete responders are still in remission with a follow-up of more than 30 months for 5 patients.
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PMID:VP-16, ifosfamide, and methotrexate combination chemotherapy for aggressive non-Hodgkin's lymphomas after failure of the LNH 84 regimen. 247 82

In 42 patients with high-grade malignant non-Hodgkin lymphomas, a new treatment program was used in an attempt to improve results without increasing toxicity. Two effective but relatively well tolerated and non-cross resistant drug combinations were given sequentially according to the response of disease. Therapy was started with a combination consisting of cyclophosphamide, doxorubicin, bleomycin, vincristine, procarbazine and prednisone (CABOPP). In patients with complete remission after a maximum of 4 cycles of CABOPP, this regimen was continued for a total of 6 cycles. In patients with progressive disease or with only a partial remission after 4 cycles of CABOPP, therapy was switched to a combination consisting of etoposide, ifosfamide and methotrexate (VIM). Complete remission (CR) was achieved in 86% of patients. Sixty-nine percent achieved CR with CA-BOPP alone and 17% after changing to VIM. The CR rate was 100% in patients with stage I or II and 78% in those with stage III or IV of disease. The projected survival at 2 years is 66%. Fifty-six percent of patients with CR are predicted to have continued CR at 2 years. Thus, CABOPP/VIM appears to be an effective and well tolerated program for the treatment of aggressive lymphomas. The value of this program, however, can only be established comparing it with other newly developed protocols in randomized studies.
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PMID:Sequential combination chemotherapy (CABOPP/VIM) for the treatment of high-grade malignant non-Hodgkin lymphoma. 247 48

Hodgkin's disease-derived giant cell lines (HD-cells) express high levels of ectosialyltransferase activity presumed to be a galactose-specific lectin recognizing the desialylated 3-fucosyl-N-acetyllactosamine structure (X-hapten). Both the anti-X-hapten monoclonal antibody VIM-D5 and a polyclonal antiserum to another galactose-lectin, the hepatic asialoglycoprotein receptor (HBP), recognize a 55,000-mol wt HD-cell protein (Paietta, E., R. J. Stockert, A. G. Morell, V. Diehl, and P. H. Weirnik. 1986. Proc. Natl. Acad. Sci. USA. 83:3451-3455.) That the expression of the 55,000-mol wt protein is restricted to HD-cells among X-hapten positive cells lines is confirmed in this study. The 55,000-mol wt protein is shown to be present on the cell surface and intracellularly, where an additional immunocrossreactive 150,000-mol wt protein is recognized. Extraction of the 55,000 mol wt protein from HD-cell lysates by affinity chromatography results in the loss of sialyltransferase activity. While evidence for a single protein possessing both the antigenic and the enzymatic activity is not direct, these results suggest that the ectosialyltransferase unique to HD-cells is a 55,000-mol wt membrane glycoprotein possessing the X-hapten oligosaccharide.
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PMID:Unique antigen of cultured Hodgkin's cells. A putative sialyltransferase. 373 96

Pluripotent stem cells (CFU-GEMM) give rise to multilineage hemopoietic colonies in culture. The cellular composition revealed that mixed colonies contain cells of different myeloid lineages and mononuclear cells with T-cell surface antigens. T-lymphocytes of primary colonies, replated secondary and tertiary colonies from a patient with Hodgkin's Lymphoma were identified by their reaction with the monoclonal antibody OKT 8. Evidence for a common progenitor of myeloid and lymphoid cells is provided by analysis of individual secondary and tertiary colonies using OKT 3, OKT 4, OKT 8, VIM-D 5, and Ig M + D antibodies for each individual colony. Primary mixed, replated secondary and tertiary colonies revealed OKT 8 positive cells. No reaction with OKT 3, OKT 4, VIM-D 5, or Ig M + D was observed.
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PMID:Suppressor T-cell clones derived from pluripotent stem cells (CFU-GEMM) of a patient with Hodgkin's lymphoma. 621 80

Pluripotent stem cells (CFU-GEMM) give rise to multilineage hemopoietic colonies in culture. The cellular composition revealed that mixed colonies contain cells of different myeloid lineages and mononuclear cells with T-cell surface antigens. T lymphocytes of primary colonies and replated secondary clones from 5 patients with Hodgkin's lymphoma (stage I--II) were identified by their reaction with the monoclonal antibody OKT-8. Replated secondary clones do act functionally as cytotoxic cells using K562 as target cells. Evidence for a common progenitor of myeloid and lymphoid cells is provided by analysis of individual secondary colonies with the use of OKT-3, OKT-4, OKT-8, VIM-D5, and IgM + D antibodies for each individual clone. Primary mixed and replated secondary colonies revealed OKT-8-positive cells. No reaction with OKT-3, OKT-4, VIM-D 5, or IgM + D was observed. In mixed colonies grown from putative bone marrow transplant donors, only OKT-3-positive cells could be observed. Secondary replated colonies did not stain for OKT-8 and failed to lyse 51Cr-labeled K562 cells.
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PMID:Cytotoxic T-cell clones derived from pluripotent stem cells (CFU-GEMM) of patients with Hodgkin's lymphoma. 698 34

We treated 40 patients with poor prognosis lymphomas. Patients with non-Hodgkin's lymphoma (NHL, n = 14) received MINE chemotherapy (mesna, ifosfamide 1330 mg/m2 and etoposide 65 mg/m2 by i.v. infusions on days 1-3, mitoxantrone 8 mg/m2 i.v. on day 1), and those with Hodgkin's disease (HD, n = 26) received VIM chemotherapy (mesna, ifosfamide 1200 mg/m2 by i.v. infusion on days 1-5, etoposide 90 mg/m2 by i.v. infusion on days 1, 3 and 5, and methotrexate 30 mg/m2 i.v. on days 1 and 5). Chemotherapy was followed by G-CSF (10 or 16 microg/kg in two divided doses daily) to mobilize PBSC. We performed 134 aphereses (median three leukaphereses per patient) starting on either day 13 (median; VIM) or day 12 (median; MINE). The median yield was 9.9x10(6) CD34+ cells/kg and 53.2x10(4) CFU-GM/kg for VIM, and 13.5x10(6) CD34+ cells/kg and 53.4x10(4) CFU-GM/kg for MINE. Except for predictable myelosuppression, no serious toxicity was seen. Response rate using MINE was 63% (18% CR, 45% PR) and using VIM 50% (17% CR, 33% PR). We conclude that VIM and MINE are effective and well-tolerated salvage regimens in patients with lymphomas and, followed by G-CSF, they also exhibit good capacity to mobilize stem cells in a predictable time interval.
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PMID:Ifosfamide and etoposide-based chemotherapy as salvage and mobilizing regimens for poor prognosis lymphoma. 1010 May 53


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