PubMed Health⌕ Search

Biomedical subjects

A Zander

Publications and source records attributed to A Zander.

At least 91 records · Page 5Linked to original sources
PubMed1981

Treatment of patients over 50 years of age with acute myelogenous leukemia with a combination of rubidazone and cytosine arabinoside, vincristine, and prednisone (ROAP).

We administered a combination of rubidazone, cytosine arabinoside, vincristine, and prednisone (ROAP) to 91 patients with acute myelogenous leukemia who were 50 yr of age or older. These patients had been identified in previous studies to be a group with a relatively poor prognosis. One-third of the patients had an antecedent hematologic disorder prior to treatment. Forty patients (48%) obtained a complete hematologic and clinical remission. A history of an antecedent hematologic disorder, male sex, and absence of Auer rods were adverse factors for achieving remission in this older population. More than half of the patients achieved remission in one course. The major cause of failure to obtain a remission was death due to infection, 40% of which were caused by fungi. Resistance to chemotherapy, although uncommon, was noted more frequently in patients with an antecedent hematologic disorder. Univariate and multivariate prognostic factor analysis was used to compare these patients with a historical control group treated with a program in which adriamycin was used instead of rubidazone (AdOAP). No significant difference in remission rate was detected. Cyclocytidine was used as a maintenance agent in this study, and while the median remission duration was only 37 wk, 30% of patients are expected to be in remission for 2 yr. Chemotherapy programs combining an anthracycline with cytosine arabinoside, given to older patients in similar fasion to younger patients will achieve remissions in one-half of a group of older patients. These remissions are of comparable quality to those of younger patients. Mathematical models derived from analysis of prognostic factors are of use in identifying patients likely to fail these programs who are in need of innovative approaches to treatment.

Aged↗
PubMed1980

High-dose combination chemotherapy with autologous bone marrow transplantation in adult solid tumors.

In order to determine whether high-dose combination chemotherapy was active in chemotherapy resistant patients, 19 patients, (9 with small cell bronchogenic carcinoma, 6 with embryonal cell carcinoma, 2 with diffuse histiocytic lymphoma, 1 with Hodgkin's disease and 1 with chondrosarcoma), 18 of whom had had extensive prior chemotherapy and failed, received 23 courses of high-dose chemotherapy with autologous bone marrow infusion (ABMT). Three patients received four courses of cytoxan (2-6 g/m2) and VP-16 (500-600 mg/m2) and 16 patients received 19 courses of cytoxan and VP-16 in these doses plus BCNU (300 mg/m2). Activity was observed in 6 of 8 evaluable small cell bronchogenic carcinoma patients (1 complete response (CR), 4 partial responses (PR), 1 less than PR), in 6 embryonal cell carcinoma patients (3 CR, 2 PR, 1 less than PR), in both patients with diffuse histiocytic lymphoma (1 CR, 1 less than PR), in the patient with Hodgkin's disease (1 PR); and in the patient with chondrosarcoma (stable). Only 2 patients who had received prior cytoxan and VP-16 extensively showed resistance to these programs. The median response duration was 11 weeks (range = 4-55 + weeks). Major toxicity consisted of bacterial infections. Two patients died from treatment related causes. Neutrophils recovered to levels of greater than or equal to 1.5 x 10(9)/liter by days 20-42 (median, day 27) and platelets to levels of greater than 100 x 10(9)/liter by days 21-56 (median, day 32) without any delayed BCNU toxicity. High-dose combination chemotherapy with ABMT causes acceptable toxicity and high response rates of relatively short duration in tumors refractory to conventional chemotherapy.

Adult↗
PubMed1980

Radiosensitive, thymic hormone-sensitive peripheral blood suppressor cell activity in cancer patients.

Suppressor cell activity which was radiosensitive in most subjects and thymic hormone sensitive in some was identified in patients with cancer, and compared to simultaneously studied normal controls. Suppressor cell activity was measured in cocultures of normal lymphocytes with patient lymphocytes added in microwells using the blastogenic response to phytohemagglutinin and concanavalin A as the measure of activity. Thirty-five patients (lung cancer, 21; leukemia in remission, seven; and various solid tumors, seven) and an equal number of controls were studied. Suppressor cell activity was identified in 71% of the patients. In approximately 75% of these, the suppressor cell activity was radiosensitive (4000 to 6000 rads). For the phytohemagglutinin response, suppressor cell activity was thymic hormone sensitive in approximately 40% (Thymosin Fraction 5 or thymic humoral factor), and for the concanavalin A response, it was thymic hormone sensitive in about 25% of the cases. There was a significant correlation between the presence of immunodeficiency (defined as a phytohemagglutinin response < 35,000 or a concanavalin A response < 12,000 cpm) and the presence of the suppressor cell activity. The suppressor cell activity was heterogenous relative to its radiosensitivity and thymic hormone sensitivity. Suppressor cell activity was observed in all the patient categories. These results indicate that certain available therapeutic manipulations may have significant effects on suppressor cell activity and should be an important subject for further investigation.

Antineoplastic Agents↗
PubMed1980

Adherent cell-mediated inhibition of human leukemic myelopoiesis.

We investigated the possibility that the control of leukemic growth by autologous adherent marrow cells may explain the indolent behavior of oligoleukemia. Leukemic cluster growth was measured by in vitro agar culture. The following marrow fractions (Fr) were examined from 13 patients for leukemic growth: Fr I: ficollisopaque interface cells (density less than 1.077 g/ml); Fr II: adherent-cell depleted Fr I (4.8% +/- 2.1 (SE) monocytes); Fr III: adherent and phagocytic cell depleted Fr I (0.3% +/- 0.2 monocytes); and Fr IV: adherent cells removed from plastic surfaces by lidocaine plus EDTA (74% +/- 10.9 monocytes). Two patient groups were recognized: Group A showed cluster growth in Fr IV with no absolute increase in Fr III and no suppression of Fr III cluster growth with addition of Fr IV. In Group B, Fr III showed an absolute increase in cluster growth. Fr IV did not show cluster growth and addition of Fr IV to Fr III suppressed growth. This suggested that in Group B, monocytes may suppress leukemic growth, the failure to observe this in Group A indicated the possible leukemic nature of the adherent cell fraction and the absence of residual normal monocytes. Other possible explanations are discussed.

Bone Marrow↗
PubMed1980

One-step procedure for human T-lymphocyte colony growth and its regulation by T and B cells, and monocytes.

Previous systems for cloning human T-cells have been either one step procedures with small colony size (40 less than 40 cells) or two-step procedures with agglutination problems. These systems also require erythrocytes, thiols and human serum. We have regularly grown more than 10(3) colonies (more than 40 cells)/5 X 10(5) cells from purified T-cells or phagocytic and adherent cell depleted mononuclear cells in agar using phytohemagglutinin (PHA) as the mitogenic stimulus. The reason for the poor colony size in other single step procedures using agar may be related to cell-to-cell interaction. We found that both adherent (Ad) and phagocytic cells were suppressive of T-cell colony growth (TCCG) in donors with low or absent TCCG from whole mononuclear cells. This effect was reproduced by adding Ad cells to T-cell concentrated fractions. Both irradiated T and unirradiated enriched B-cells increased TCCG of T fractions. TCCG is possible in simple in vitro systems from both adherent and phagocytic cell depleted fractions and concentrated T-cell fractions. This allows for the examination of factor regulation of TCCG and has enabled the identification of a possible B-cell released T-cell growth factor. Previously described complex growth requirements may be related to cell interactions.

B-Lymphocytes↗
PubMed1980

Host defense deficiency in hairy cell leukemia and its correction by leukocyte transfusion.

A similar defect host defense mechanisms in hairy cell leukemia was defined in two patients. Surface-adherent monocytes were not detected in the peripheral blood nor were monocytes that mediate antibody-dependent cell-mediated cytotoxicity (ADCC) to isoantibody-coated human erythrocytes. In addition, lymphocytes of both patients failed to show blastogenic responses to concanavalin A (Con-A) and pokeweed mitogen (PWM) but showed a vigorous response to phytohemagglutinin (PHA). Other immunologic abnormalities were present but were either moderate in degree or were not present in both patients. In vitro lymphocyte blastogenic responses were fully restored by incubation of patients' leukocytes with a normal donor's adherent monocytes. One patient received daily allogeneic leukocyte transfusion for 4 days. This resulted in complete normalization of monocyte adherence and ADCC that persisted for several months after transfusion and was associated with hemotalogic improvement. Therapy in case 1 resulted in correction of the blastogenic responses to Con-A and PWM. Thus, a host defense defect in hairy cell leukemia has been defined in 2 patients and a preliminary result suggests that therapy with leukocyte transfusions may be useful in the postsplenectomy patient with an infectious complication and should be explored further.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1979

Autologous bone-marrow transplantation in relapsed adult acute leukaemia.

24 cases of adult acute leukaemia, of which 21 were evaluable, were treated in irreversible relapse with high-dose piperazinedione and supralethal total-body irradiation (T.B.I.) in conjunction with autologous marrow transplantation (A.B.M.T.). The grafted marrow cells had been collected and stored in liquid nitrogen at the time of remission. In 12 patients the marrow cells were fractionated on discontinuous albumin gradients in an attempt to separate normal cells from residual leukaemic cells. 11 patients achieved complete remission (C.R.); 7 other patients had signs of engraftment but died before C.R. The median remission duration was 4 months (2-14). 6 of 9 acute myeloblastic leukaemia patients, in whom bone-marrow transplantation was the first treatment of relapse, achieved C.R. 4 of 5 patients with acute lymphoblastic leukaemia, whose bone-marrow cells were collected during first remission, reached C.R. Autologous bone-marrow transplantation is a valuable first treatment for acute myeloblastic leukaemia in relapse and acute lymphoblastic leukaemia in second relapse.

Adolescent↗
PubMed1979

High-dose BCNU therapy with autologous bone marrow infusion: preliminary observations.

Nine patients with solid malignancies and extensive prior treatment received high-dose BCNU therapy (600--750 mg/m2) with autologous bone marrow support; following this treatment hematopoietic recovery was studied. The only significant nonhematopoietic toxicity was a probable case of BCNU-induced pulmonary toxicity in a patient who had received massive amounts of prior chemotherapy and chest irradiation. The marrow aspirations prior to cryopreservations had revealed a hypoplastic marrow in four of nine patients. Despite using marrow exposed to prior chemotherapy, neutropenia beyond Day 40 after BCNU therapy was not observed in any patient. One patient did not develop neutropenia of less than 1.5 X 10(9) cells/liter and five patients did not develop neutropenia of less than 0.5 X 10(9) cells/liter. A partial response was observed in one patient and less than partial responses were observed in two other patients. Autologous bone marrow infusion may modify the neutropenia of high-dose BCNU therapy.

Adult↗
PubMed1979

High dose chemotherapy with autologous bone marrow transfusion.

Details are given of response and toxicity after high dose chemotherapy followed by autologous bone marrow infusion. High dose nitrosurea therapy (600-1000 mg/m2 BCNU) was predominantly associated with hematopoietic toxicity but recovery was within 4-5 weeks after BCNU therapy. High dose combination chemotherapy using cytoxan, VP-16-23 and +/- BCNU produced a response rate of approximately 80% (CR + PR + less than PR) of usually short duration in 18 evaluable patients, 17 of whom were previously treated. Hematopoietic recovery was usually complete in 4 weeks. Initial experience with the hematopoietic toxicity experienced after high dose mitomycin and ABMT is also detailed. Future proposals utilizing high dose chemotherapy with ABMT in selected tumors is presented with associated rationale.

Antineoplastic Agents↗
PubMed1978

Autologous bone marrow transplantation in patients with adult acute leukemia in relapse.

Nine patients with adult acute leukemia were treated in relapse with piperazinedione plus supralethal total body irradiation in conjunction with autologous marrow infusion. Bone marrow cells were collected and stored in first remission. Storage time varied from 3 to 23 months. Before storage, marrow cells were separated using density albumin gradients in order to reduce the number of leukemic cells in the graft. Three patients died before day 14 after transplantation because of complications already present at the time of transplantation. In six patients, hemopoietic recovery started to occur within 14 days after transplantation. In four patients leukemia-free periods were obtained, lasting 60+ days. The three patients with the longest leukemia-free period after transplantation (range 75 to 220+ days) are reported in more detail. One patient is still alive without evidence of leukemia, with full hematological recovery 220+ days after transplantation.

Acute Disease↗
PubMed1976

Mechanism of the increased splenic erythropoiesis in mice treated with estradiol benzoate.

Pharmacological doses of estrogens induce osteosclerosis of the bone marrow, and depress colony-forming units (CFU's) and platelet and leukocyte counts in mice. A compensatoryincreasts in mice. A compensatory increase in splenic erythropoiesis prevents a fall in the hematocrit. The mechanism of this compensation was investigated as follows, BDF1 female mice were injected subcutaneously thrice weekly for 6 weeks wiht 50 mugg of estradiol benzoate (EB) or sesame oil (SO). Subsequently the hematocrit, red cell mass (RCM), and 4 hour per cent of 59Fe uptake into the femurs and spleens were determined in groups of five mice for 4 consecutive days. The RCM and hematocrit were not significantly different in the two groups. The per cent of 59Fe uptake into the femurs of EB-treated mice was less than 30 per cent of that in SO-treated mice and the per cent of 59Fe uptake into the spleens of EB mice was more than two times that in SO mice. To ascertain whether the increase in plenic erythropoiesis resulted from an increase in the number of splenic erythropoietin-responsive cells (ERC), the 4 hours per cent 59Fe uptake into the spleen was determined in continuously hypertransfused EB and SO mice injected with erythropoietin (Ep). Whereas hypertransfuction depressed the splenic per cent of 59Fe uptake in EB and SO mice equally, injection of Ep increased the per cent of 59Fe uptake into the spleens of of EB mice to greater than two times that of SO mice. Next, the plasma Ep level of mice injected with EB or SO for 2, 4, or 6 weeks was determined after exposure of the animals to hypoxia. Ep titers were greater than three times higher in EB mice than in SO mice, We conclude that at least two mechanisms act to cause the compensatory increase in splenic erythropoiesis after marrow suppression by EB: (1) the Ep levels rise and (2) the splenic ERC population increases. The latter is probably not due to the increased plasma Ep level because it also occurs in mice whose Ep production is suppressed by plethora.

Animals↗