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Biomedical subjects

P Stryckmans

Publications and source records attributed to P Stryckmans.

At least 73 records · Page 4Linked to original sources
PubMed1989

Tolerance and effectiveness of recombinant interleukin-2 (r-met Hu IL-2 [ala-125]) and lymphokine-activated killer cells in patients with metastatic solid tumors.

The tolerance of a recombinant human interleukin-2 (rIL-2, r-met Hu IL-2 [ala-125], Ortho Pharmaceutical) and its antitumor effectiveness in combination with lymphokineactivated killer (LAK) cells was examined in 26 patients with metastatic solid tumors, including 14 renal cell carcinomas, seven melanomas, three extragonadal germ cell tumors refractory to chemotherapy and two colon carcinomas. rIL-2 was administered as a bolus at 30,000 U/kg every 8 h on days 1-5 and days 12-19. Leukapheresis was done on days 8-12, lymphocytes were incubated with rIL-2 for 3 or 4 days in vitro and reinfused on days 12, 13 and 15. The mean number of reinfused cells was 5.1 x 10(10) per patient. IL-2 dose and schedule were adjusted according to toxicity. Patients received a median of 100% (range 87-100%) of planned rIL-2 on days 1-5 and a median of 71% (range 13-100%) on days 12-19. Capillary leak syndrome with hypotension and impaired renal function and CNS toxicity were the major reasons for dose modification. Patients with renal cell carcinoma, most of whom underwent a prior nephrectomy, had a reduced tolerance to rIL-2. Partial responses were documented in three renal cell carcinomas and one melanoma. The median response duration was 5.5 (range 1-6) months.

Adult↗
PubMed1989

Treatment of acute myelogenous leukemia. An EBMT-EORTC retrospective analysis of chemotherapy versus allogeneic or autologous bone marrow transplantation.

In a retrospective analysis, patients with acute myelogenous leukemia (AML), treated in first complete remission (CR) with chemotherapy or with allogeneic or autologous bone marrow transplantation were compared with respect to their leukemia-free survival from CR. Two hundred and thirty-six patients treated with chemotherapy according to the EORTC AML-5 and AML-6 trials were included. The data of the transplanted patients were taken from two EBMT registries; 453 with an allogeneic and 182 with an autologous BMT. The very different sources of the data (trials and registries) forced us to be cautious in our conclusions. However, for the patient cohorts analyzed in the present study, BMT patients tended to have a better leukemia-free survival than chemotherapy patients. This was especially the case for the allogeneic BMT after 6 months of transplant.

Adolescent↗
PubMed1989

Response to pentostatin in hairy-cell leukemia refractory to interferon-alpha. The European Organization for Research and Treatment of Cancer Leukemia Cooperative Group.

Interferon-alpha (IFN-a) or 2'-deoxycoformycin (pentostatin; DCF) have each been shown to be highly active in hairy-cell leukemia (HCL). In this phase II study of the Leukemia Cooperative Group of the European Organization for Research and Treatment of Cancer (EORTC), the efficacy and toxicity of DCF were investigated in patients who were resistant to IFN-a treatment. Resistance was defined as: (1) progressive disease (PD) under IFN-a therapy for more than 2 months; (2) stable disease (SD) after more than 6 months of IFN-a treatment; (3) relapse within 3 months of discontinuing IFN-a; and (4) intolerance to IFN-a because of World Health Organization (WHO) grade 3 or 4 toxicity. DCF was applied at a dosage of 4 mg/m2 weekly x 3, then 4 mg/m2 every other week x 3. Responders were given a maintenance therapy once per month for a maximum of 6 months. At the time of report, 33 patients with resistant disease were evaluable for response and toxicity. Median duration of IFN-a therapy before DCF administration was 14.7 months (range, 1 to 41 months). Complete remissions (CRs) were achieved in 11 patients and partial remissions (PRs) in 15, resulting in a total response rate of 78.8%. Median interval between beginning of DCF therapy to best response was 3.9 months with a range from 2.0 to 7.0 months. Two patients who achieved PR have relapsed 7 and 14 months after cessation of DCF therapy. The median duration of response was over 11.5 months (range, over 3.0 to over 24.0 months). Three patients died within the first 6 weeks of DCF treatment: one of drug-unrelated cardiomyopathy and two of fungal pneumonia. The patients with early death (n = 3) and nonresponsive disease (n = 4) received IFN-a treatment for a longer period (median, 18.0 months) than did the 26 responsive patients (median, 10.0 months). Major side effects included nausea, skin rash, and infections and were otherwise mild. Thus, DCF is highly active in patients with HCL resistant to IFN-a.

Adult↗
PubMed1989

Pentostatin (2'deoxycoformycin) for the treatment of lymphoid neoplasms.

Knowledge of the vital role of adenosine deaminase in lymphatic tissues has led to the development of enzyme inhibitors for treatment of lymphoid neoplasms. Deoxycoformycin is a potent ADA inhibitor and has been shown to be active in acute lymphoblastic leukemia at high doses but associated with unpredictable toxicity. In indolent lymphocytic leukemia or lymphoma with low ADA concentrations, this drug is effective at low doses with mild toxicity. The on-going EORTC trial shows that pentostatin is highly effective in hairy cell leukemia and can achieve durable complete remissions even if interferon alpha has failed. It will probably play an important role in the treatment of prolymphocytic leukemia, T- and B-cell chronic lymphocytic leukemia and Sézary syndrome.

Adenosine↗
PubMed1989

Controversies in the management of gastrointestinal non-Hodgkin's lymphomas.

Although more than a thousand GI non-Hodgkin's lymphomas have been reported, the literature does not indicate a clear optimal therapeutic approach. This is primarily due to histological confusion and to the absence of uniform staging procedures and therapeutic modalities. This overview attempts to summarize controversies in the multidisciplinary approach to GI non-Hodgkin's lymphomas and to introduce a European multicentric prospective randomized study for the treatment of this rare disease.

Combined Modality Therapy↗
PubMed1989

Comparison of in vitro inhibition of etoposide (VP16) on leukemic and normal myeloid, erythroid clonogenic cells.

We have compared in various clonogenic assays the in vitro sensitivity to etoposide (VP16) of 1) human leukemic precursors (leukemia colony-forming units; L-CFU), 2) normal erythroid progenitors (erythroid burst-forming units; BFU-E, and 3) normal committed myeloid progenitors (granulocyte-macrophage colony-forming units; CFU-GM and more primitive hemopoietic precursors (PPC) that adhere to cultured marrow stromal cells. Bone marrow samples were obtained from 15 normal subjects and 16 leukemic patients: 9 in the acute phase of acute nonlymphoblastic leukemia (ANLL) and 7 in complete remission. VP16 was tested at concentrations ranging from 10(-8) to 10(-3) M. The median recoveries at 10(-3) M VP16 were respectively 0%, 0.5%, 0%, and 0% for leukemic progenitors, CFU-GM from leukemic patients in complete remission, normal CFU-GM, and BFU-E, and 23% for PPC. This indicates that CFU-GM, BFU-E, and L-CFU are highly sensitive to VP16, whereas PPC, more primitive myeloid precursors, are spared. These results suggest that VP16 may be used as an "ex vivo" purging agent for autologous bone marrow.

Cell Survival↗
PubMed1988

Daunorubicin in patients with relapsed and refractory acute nonlymphoblastic leukemia previously treated with anthracycline.

While the efficacy of daunorubicin (DNR) in first induction of patients with acute nonlymphoblastic leukemia (ANLL) has been well documented, little data are available concerning the activity of DNR in patients with relapsed and refractory ANLL previously treated with anthracycline. We administered DNR (60 mg/m2/day for 3-5 days) in 21 patients with relapsed (n = 12) or refractory (n = 9) ANLL previously treated with anthracycline. The general response rate was 48%, with a complete response (CR) rate of 38%. Five of 12 patients with relapsed ANLL and 3 of 9 patients with refractory ANLL achieved CR. Among these cases with CR in refractory ANLL, the evolution of one patient is particularly illustrative since he had received previously a large cumulative dose of anthracycline (540 mg/m2) and has been shown to be refractory to high-dose cytosine arabinoside. This study suggests that previous administration of DNR or adriamycin does not induce significant resistance to anthracycline: DNR appears to be almost as efficient in patients with relapsed and refractory ANLL previously treated with anthracycline as in first induction.

Acute Disease↗
PubMed1988

Intermediate and high dose Ara-C and m-AMSA for remission induction and consolidation treatment of patients with acute myeloid leukemia: an EORTC Leukemia Cooperative Group phase II study.

Seventy-nine patients (aged 17-76 years) with acute myelogenous leukemia in first (56) or second (3) relapse, primary refractory leukemia (15) or leukemia occurring as secondary malignancy that developed after a preleukemic phase (3) or after another tumor (2) were given remission induction therapy consisting of cytosine arabinoside (Ara-C, 1 g/m2 as a 2-h infusion every 12 h for 6 days) and m-AMSA (120 mg/m2, i.v. on days 5, 6, 7). In total 45 patients (57%) achieved complete remission. Younger patients and those with a relatively low initial white blood cell count, a good performance status or in first relapse had a higher response rate. Thirty-five patients were given one or two courses of consolidation chemotherapy consisting of Ara-C (3 g/m2 as a 2-h infusion every 12 h for 4 days) and m-AMSA (120 mg/m2 i.v. on day 5). Three patients received an allogeneic bone marrow graft after the induction courses and four patients received an autologous bone marrow transplantation after consolidation therapy. The median of the disease-free survival curve was 21 weeks. The median duration of survival was 25 weeks. The response rate for this intermediate dose Ara-C regimen is satisfactory and does not differ from that reported for high dose Ara-C. The impact of consolidation chemotherapy in bad risk acute myelogenous leukemia is questionable.

Adult↗
PubMed1988

Deoxycoformycin in therapy of refractory lymphoid neoplasms.

Knowledge of the vital role of the purine degradative enzyme adenosine deaminase (ADA) in the differentiation of T and B lymphocytes has stimulated interest in the pharmacologic inhibition of ADA as specific cytotoxic therapy for lymphoproliferative diseases. 2'-Deoxycoformycin (DCF) is a tight-binding ADA-inhibitor and has shown activity in T and B cell neoplasms. In this phase-II study, the efficacy and toxicity of DCF in chronic T and B cell neoplasms is investigated. We report the preliminary results of treatment in 27 patients (8 with Sézary syndrome, 11 with B-chronic lymphocytic leukemia (CLL), and 8 with hairy cell leukemia (HCL)), who were refractory to conventional therapy. DCF was applied at a dosage of 4 mg/m2 weekly x 3, then 4 mg/m2 every other week x 3. Three of the 8 patients with Sézary syndrome and 3 of the 11 patients with B-CLL attained a partial remission. One complete and 7 partial remissions have been achieved thus far in the 8 patients with HCL refractory to interferon alpha treatment. Other than nausea in 10 patients (mainly grade 1 and 2), transient skin rash in 4 patients and Herpes infections in 4 patients (mainly grade 2), no other major toxicities were observed. Thus DCF is highly active in hairy cell leukemia that did not respond to interferon alpha, and shows moderate activity in refractory Sézary syndrome and B-CLL.

Antineoplastic Agents↗
PubMed1988

Decreased production of IL-6 by peripheral blood mononuclear cells of patients with chronic lymphocytic leukemia and related disorders.

The present study has shown a decreased production of IL-6 by LPS-stimulated mononuclear cells of B-CLL blood. This decrease with attributed to an abnormality of either monocytes or T lymphocytes. A similar decrease was seen in HCL and NHL. Experiments with mixtures of normal and CLL cells suggest that the decreased IL-6 production in CLL is due neither to an inhibition of normal blood mononuclear cells IL-6 production by B-CLL lymphocytes nor to the absence in CLL blood of cell(s) or cytokine(s) needed for IL-6 production.

Humans↗