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At least 433 records · Page 24Linked to original sources
PubMed1985

Marrow transplantation: the Seattle experience.

Marrow transplantation is effective treatment for a number of hematological diseases in patients under the age of 50 who have an HLA-identical sibling donor. It is successful in the treatment of aplastic anemia with 70-85% long-term survival. It offers 10-30% apparent cures for patients with acute leukemia who have relapsed at least once, and for those with chronic myelocytic leukemia in blast crisis. Although still somewhat controversial, it appears to be the treatment of choice for patients with acute nonlymphoblastic leukemia in first chemotherapy induced remission, and for those with chronic myelogenous leukemia in the chronic phase since approximately 50-60% of these patients experience long-term, disease-free survival. Patients with acute lymphoblastic leukemia grafted in second or subsequent remission may expect a 30% "cure" of their disease. Marrow grafting is the only effective treatment for many patients with inherited immunologic deficiencies and certain genetic storage diseases. Cures of congenital Fanconi's anemia, Blackfan-Diamond anemia, osteopetrosis, paroxysmal nocturnal hemoglobinuria and thalassemia major have been achieved. Marrow transplantation is being explored for the therapy of patients with lymphoma, Hodgkin's disease, preleukemia, multiple myeloma, hairy cell leukemia, small cell lung cancer, testicular cancer, ovarian cancer and neuroblastoma. Marrow transplantation has been limited by the fact that many patients do not have HLA-identical siblings and very few have monozygotic twins. More recently, marrow transplants from HLA-nonidentical family members and even from unrelated donors have been successfully explored.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia, Aplastic↗
PubMed1979

Chromosome analysis in two unusual malignant blood disorders presumably induced by benzene.

Two patients with presumably benzene-induced malignant blood disorders with preleukemic phases were cytogenetically monitored through the courses of their diseases. Patient 1, in addition to a familial chromosome translocation [t(3;16)], developed karyotypic abnormalities in 100% of the marrow cells, including two translocation: t(9;16)] and t(4;15). Monosomy of chromosome 7 characterized the cells of patient 2. Cytogenetic monitoring of the patients at various phases of their diseases served as an important indicator of the transformation or progression of the preleukemia into frank leukemia and of the unusual behavior of such leukemic cells.

Adult↗
PubMed1980

Induction of leukemia-associated inhibitory activity and bone marrow granulocyte-macrophage progenitor cell alterations during infection with Abelson virus.

Neonatal and adult BALB/c mice were investigated in a longitudinal study for the acquisition of leukemia-associated inhibitory activity (LIA) interactions after inoculation with Abelson virus in vivo. Within 2 to 4 days after virus infection, the granulocyte-macrophage colony-forming cells from the bone marrow and spleen of the infected mice became insensitive to inhibition by LIA, even though colony morphology appeared normal. Shortly after, or simultaneously with, the detection of the colony-forming cell resistance phenomenon, LIA was found in bone marrow, spleen, and thymus cells. The abnormal interactions appeared to be related to induction of lymphoma in BALB/c neonates and to a lymphoproliferative disease in adult BALB/c mice. In contrast, normal cellular interactions were noted in adult C57BL/6 mice which were not susceptible to the Abelson disease after virus inoculation and in untreated neonatal and adult BALB/c and adult C57BL/6 mice. Their colony-forming cells were sensitive to inhibition by LIA, and no LIA was detected in their bone marrow, spleen, and thymus cells. The abnormal cellular interactions are similar to those noted in human leukemia, lymphoma, and "preleukemia." This suggests that Abelson virus-infected mice can serve as a model for the study of LIA interactions.

Abelson murine leukemia virus↗
PubMed1984

Study of erythrocyte mean corpuscular volume during cytotoxic therapy as a predictive parameter of the risk of secondary leukemia in Hodgkin's disease.

Erythrocyte mean corpuscular volume (MCV) evolution was studied during cytotoxic therapy in 12 patients with Hodgkin's disease who developed secondary acute leukemia and in 83 patients with Hodgkin's disease without secondary leukemia as control group. Significant differences were observed in the maximum MCV and in the MCV maximum increase during therapy between the two groups of patients. These differences remained significant between the patients treated with chemotherapy alone and those treated with chemotherapy and radiotherapy. MCV maximum increase greater than 23.9 fl was observed in all patients with secondary leukemia and in only 20% of those without secondary leukemia; it was reached 46.3 months before the first sign of preleukemia. Its value in predicting the leukemic risk in Hodgkin's disease is discussed.

Antineoplastic Agents↗
PubMed1978

Deletion of the long arm of chromosome 20 [del(20)(q11)] in myeloid disorders.

Detailed clinical and cytogenetic studies were performed in five patients who had abnormal hematopoiesis and an acquired deletion of an F-group chromosome. Cytogenetic analyses, with banding techniques, of cells from bone marrow, spleen, or unstimulated peripheral blood showed a partial deletion of the long arm of one chromosome 20 [del(20)(q11)] in all five patients. Three patients had myeloproliferative disorders of uncertain classification, the fourth had possible preleukemia, and the fifth had acute myelomonocytic leukemia. Although the five cases showed certain similarities, the clinical and hematologic findings seen with the 20q- abnormality were not specific. None of the patients showed evidence of polycythemia vera or idiopathic acquired refractory sideroblastic anemia, two diseases previously associated with the 20q-. Our studies indicate that the 20q- abnormality is not limited to diseases primarily affecting erythropoiesis but that it can be found in the broader spectrum of myeloid disorders. In polycythemia vera, the 20q- has sometimes been regarded as a possible result of previous therapy with cytotoxic agents; however, four of our patients were untreated when the deletion was first noted.

Aged↗
PubMed1981

Defective neutrophil migration in monosomy-7.

The migration in vitro of neutrophils from six patients with monosomy-7 or partial deletion of the long arm of chromosome 7 was studied by two methods: the Millipore filter assay and the migration under agarose assay. Four of the patients had preleukemia, one had subacute myelomonocytic leukemia, and one polycythemia vera. In four patients, chemotaxis (migration towards a higher concentration of chemoattractant) and chemokinesis (stimulated migration without a gradient) were shown to be defective by both methods. In the remaining two patients, this defect could be demonstrated only by the Millipore filter assay or by the agarose assay. Under agarose, random locomotion (no chemoattractant present) of the patients' neutrophils was less than that of the control subjects in four patients, whereas no clear difference could be shown by the Millipore filter method. This study demonstrates that the previously described defect of neutrophil migration in monosomy-7 involves not only chemotaxis but all stimulated migration and, at least in some patients, random locomotion as well. Defective migration in two patients with an apparently terminal deletion of the long arm of one chromosome 7 indicates that the distal half of 7q carries genetic material important for neutrophil locomotion.

Adolescent↗
PubMed1980

Development of giant granules in platelets during prolonged storage.

Giant granules are uncommon in normal human platelets but are frequently observed in platelets from patients with the Chédiak-Higashi syndrome, some case of May-Hegglin anomaly, and individuals with chronic refractory anemia (preleukemia) or myelomonocytic leukema. However, the numbers of platelets containing the giant granule anomaly are so low that it has been impossible to isolate them in sufficient quantity to identify the mechanisms involved in their formation. Recently conditions were found that foster the long-term preservation of functional platelets in vitro. Ultrastructural examination of samples of C-PRP stored for 15--21 days revealed the presence of giant granules in 10--20% of the cells. Although factors involved in large organelle development were not determined in the present study, the new in vitro system for platelet storage may provide a useful approach for investigation of giant granule formation in normal and abnormal platelets.

Blood Platelets↗
PubMed1997

Fatal gastrointestinal bleeding as the primary manifestation of granulocytic sarcoma in a patient with myelodysblastic syndrome.

Granulocytic sarcoma (GS), or chloroma, is a rare extramedullary tumor composed of immature myeloid cells. It most commonly involves bone, soft tissue, lymph nodes and skin and develops during the course of or preceding myelogenous leukemia (ML). Involvement of other organs has been rarely reported including ovary, uterus and cervix, lung and the gastrointestinal tract; however, GS presenting as upper and lower gastrointestinal (GI) bleeding from ulcerated gastric mass and concurrent bleeding vaginal mass is an unusual rare manifestation of GS. We describe a case of GS in a 70 year old black woman who presented with a bleeding "lump" in the vaginal wall and suffered fatal GI bleeding from an ulcerated gastric lesion. She was diagnosed with myelodysblastic syndrome a few months earlier. From the review of the available English literature, this is a unique presentation of GS. It is important to include this entity in the differential diagnosis when encountering GI bleeding particularly in a patient previously diagnosed with myeloid leukemia or preleukemia. The importance of Naphthol Chloracetate Esterase (NCAE) stain and lysozyme immunoperoxidase stain in establishing the diagnosis is breifly discussed.

Aged↗
PubMed1977

[Prognosis of hematopoietic dysplasia (author's transl)].

90 patients with hemopoietic dysplasia (preleukemia) have been studied with iron kinetics for the mechanism of the anaemia, 23 patients had a bone marrow autoradiography and 18 a bone marrow culture in semi-solid medium. The death was caused in half the cases by acute myeloblastic leukaemia transformation (LAM) and in half the cases by complications of pancytopenia (infection, haemorrhage) or hemochromatosis. Three data give prognostic factors at short or long term: the bone marrow hypoplasia, no patient with major bone marrow hypoplasia (ratio of 59Fe fixation in liver and sacrum of more than 2) lived more than 2 years after the examination. The low labeling index of myeloblasts and promyelocytes, the mean LI is 0.20 patients having lived less than one year after the study and 0.35 for those who lived more than two years. The bone marrow culture of the macroclusters type, no patient whose bone marrow grew with macroclusters and no colonies survived more than 8 months after the study. These three data seem to be essential in the regular survey of the patients with hemopoïetic dysplasia.

Autoradiography↗
PubMed1997

Antiplatelet drugs induce apoptosis in cultured cancer cells.

In order to understand if antiplatelet drugs possess direct antineoplastic property, we tested the apoptotic effect of 5 popularly marketed antiplatelet drugs in Taiwan in 6 cultured cancer cell lines (Hep 3B hepatocarcinoma, U87-MG malignant glioma, PC-3 prostate adenocarcinoma, HeLa cervical adenocarcinoma, HL-60 preleukemia and K-562 chronic myelogenous leukemia). While acetylsalicylate and flunarizine exerted no effect on these cancer cells, pentoxifyline (PTX), dipyridamole (DYA) and ticlopidine hydrochloride (T. HCl) displayed a time and dose-dependent apoptotic effect on them except for HL-60 and K-562 cells. PTX induced apoptosis in U87-MG, Hep 3B and HeLa cells, DYA in HeLa cells, while T. HCl in U87-MG, Hep 3B, PC-3 and HeLa cells. Adriamycin also provoked apoptotic effect in all 6 cell lines but neither PTX, DYA nor T. HCl acted synergy with adriamycin to HeLa cells, implicating that they may share a similar pathway for inducing apoptosis. Therefore, our results show that the antiplatelet drugs do possess antineoplastic property in vitro. A co-administration of antiplatelet drugs is noteworthy for an alternative adjunctive therapy in cancer patients.

Antineoplastic Agents↗
PubMed1998

[Relationship between the occurrences of AL, MDS and AA and abnormal BM proliferation of patient's parents].

After studying of familial leukemias, Myelodysplastic Syndrome (MDS) and aplastic anemia (AA), we observed and analysed bone marrow (BM) cells hematologically and molecular-cytogenetically in 36 persons who are first degree relatives (FDRs) of patients with acute leukemias (AL), MDS and AA. The peripheral blood (PB) lymphocyte chromosome fragility sensitive to folic acid and unstability was also analysed in 18 FDRs. The abnormal BM megakaryocystic/erythroid cellularity and the rearrangement of c-erbB were found in 66%-86.1% of parents and siblings of patients. The associations of dysplastic megakaryopoiesis, including the presence of lymphoid small megakaryocytes, with the chromosomal monosomy or/and the rearrangement/amplification of C-erbB, were found in a few parents and siblings. These results were consistent with those of MDS, Fanconi Anemia (FA) and AL. The normal karyotype and SCD positive of BM cells and PB lymphocytes, and PB lymphocyte chromosomal fragility and unstability were found in most of patients' parents, while familial chromosomal monosomy of BM cells and PB lymphocyte chromosomal fragility were found in parents and siblings of familial leukemia patients. Based on the studies of a large family with 7 cases of acute erythroleukamia and relative myeloleukemias in three consecutive generations and a family with 3 CAA and 1 AML, the rearrangement of c-erbB might be inherited. The rearrangement/amplification of c-erbB and its PCR detected results could be the indicators of gene diagnosis of preleukemia and might be useful in genetic conselling of leukemias. The common origin of AL, MDS and AA was discussed.

Anemia, Aplastic↗
PubMed1996

Leukemogenic risk of hydroxyurea therapy in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.

In polycythemia vera (PV), treatment with chlorambucil and radioactive phosphorus (p32) increases the risk of leukemic transformation from 1% to 13-14%. This risk has been estimated to be 1-5.9% with hydroxyurea (HU) therapy. When compared with historical controls, the risk with use of HU does not appear to be statistically significant. The leukemogenic risk of HU therapy in essential thrombocytosis (ET) and in myelofibrosis with myeloid metaplasia (MMM) is unknown. HU remains the main myelotoxic agent in the treatment of PV, ET, and MMM. We studied 64 patients with these three disorders, seen at our institution during 1993-1995. The patients were studied for their clinical characteristics at diagnosis, therapies received, and development of myelodysplasia or acute leukemia (MDS/AL). Forty-two had PV, 15 ET, and 6 MMM, and 1 had an unclassified myeloproliferative disorder. Of the 42 patients with PV, 18 were treated with phlebotomy alone, 16 with HU alone, 2 with p32, 2 with multiple myelotoxic agents, and 2 with interferon-alpha (IFN-alpha). Two patients from the phlebotomy-treated group, one from the HU-treated group, and 1 from the multiple myelotoxic agent-treated group developed MDS/AL. In the larger group, 11 received no treatment or aspirin alone, 18 were treated with phlebotomy alone, 25 with HU, 5 with multiple myelotoxic agents, 2 with p32, 2 with IFN-alpha, and 1 with melphalan. Study of the entire group of 64 patients showed that only one additional patient (total of 5 out of 64) developed MDS/AL. This patient had been treated with HU alone. Statistical analysis did not show any association between clinical characteristics at diagnosis, or HU therapy, and development of MDS/AL (P=0.5). Thus, our data provide no evidence suggestive of increased risk of transformation to MDS/AL with HU therapy in PV, ET, and MMM. Larger, prospective studies are needed to study this issue further.

Acute Disease↗
PubMed1999

CD3xCD19 bispecific antibodies and CD28 bivalent antibodies enhance T-cell reactivity against autologous leukemic cells in pediatric B-ALL bone marrow.

Bispecific CD3xCD19 antibodies and CD28 co-stimulating antibodies were used to activate T cells in bone marrow aspirates (n = 8) of children with B cell-derived acute lymphoblastic leukemia. Bone marrow specimens were incubated for 10 days with CD3xCD19 bispecific and CD28 antibodies. Changes in the numbers of T lymphocytes and tumoral B cells as well as surface expression of T cell-activation markers were determined by flow cytometry, and cytokines (human IFN-gamma, IL-2, IL-4 and IL-12) were measured in the cell culture supernatant. In 7 of 8 bone marrow samples, an increase in the number of CD4- and CD8-positive T lymphocytes was found, which correlated with an up-regulation of T cell-activation markers. Additionally, we demonstrated a decrease of tumoral B cells in 3 samples and enhanced cytotoxic T-cell activity against autologous malignant B cells. ELISpot analyses in an autologous Epstein-Barr virus model showed that bispecific antibodies (CD3xCD19+CD28) were more potent at generating T-cell responses against autologous and allogeneic tumoral targets than a combination of monospecific antibodies (CD3+CD28). Thus, T-cell targeting by CD3xCD19 bispecific and CD28 antibodies may be used to eliminate leukemic B cells ex vivo and reconstitute immunological control of residual malignant disease by the induction of anti-tumoral T-cell responses.

Antibodies, Bispecific↗
PubMed1996

Specific N-ras mutation in bone marrow within 48 H of 7,12-dimethylbenz[a]anthracene treatment in Huggins-Sugiyama rat leukemogenesis.

7,12-Dimethylbenz[a]anthracene (DMBA)-induced leukemias in Long-Evans rats consistently have an A --> T transversion at the second base of codon 61 in the N-ras gene. This mutation is also detected in the preleukemic stage. To determine when this specific N-ras mutation occurs in the early stages of leukemogenesis, we designed the mutant allele-specific amplification method, which was sensitive enough to detect one mutant cell among 10(6) normal cells. In the study reported here, N-ras mutation was found in bone-marrow cells 2 d after a single DMBA injection and thereafter throughout the preleukemic stage. These results show that DMBA induces a specific N-ras mutation soon after one DMBA injection and that this mutation is probably the first event in DMBA leukemogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Immunologic dysfunction in the myeloproliferative disorders.

Forty patients with various types of myeloproliferative disorders were evaluated immunologically. Serum immunoglobulin levels were within the normal range in most patients and no monoclonal gammopathies were detected. Serum C'3 levels were decreased in 19 of 40 (48%) patients. The response of peripheral blood lymphocytes to phytohemagglutinin was decreased in 26 of 40 (65%) and to pokeweed mitogen in 18 of 28 (64%) patients studied. Lymphocytes from patients with polycythemia vera were least affected. Unstimulated lymphocytes from some patients demonstrated markedly increased thymidine uptake activity. Despite the diminished mitogenic response, only 2 of 33 patients (6%) were anergic by intradermal skin testing. There was no association between depressed lymphocyte response and recent chemotherapy except in chronic myelogenous leukemia where 6 of 8 patients were receiving cytotoxic therapy when studied. These observations suggest that most of our patients with myeloproliferative disorders have abnormal cellular responses in vitro, but that delayed hypersensitivity and humoral responses are minimally affected.

Adult↗
PubMed1978

The preleukemic syndrome (hemopoietic dysplasia).

Retrospective analysis of patients with acute myelomonoblastic (or nonlymphocytic) leukemia has helped to clarify the early stages of the evolution of this disease, and a clinical picture has emerged that is sufficiently discriminating to permit prospective observations. The clinical and laboratory features of the hematologic disorder preceding overt, blast-cell leukemia (i.e., the "preleukemic syndrome" or "hemopoietic dysplasia") are described, and diagnostic criteria and approaches to management are considered. This hematologic syndrome appears to be a stage in a multiphasic panmyelopathy that involves all products of the marrow stem cell. Available data indicate that most of these patients develop acute leukemia within 24 months of the onset of the hematologic abnormalities, but longer courses are not uncommon. Prospective documentation in a large group of patients is needed before the natural course can be accurately defined; such studies are now being planned.

Adrenal Cortex Hormones↗
PubMed1979

Therapy-related leukemia: a panmyelosis.

Fifteen patients developed acute nonlymphocytic leukemia (ANLL) 31 to 182 months following chemotherapy and/or radiotherapy for various malignancies and one non-neoplastic disorder. The ANLL was commonly heralded by a brief preleukemic phase consisting of cytopenias and a variety of morphologic abnormalities. At diagnosis of ANLL, all of the patients had a panmyelosis with variation in the predominant abnormal cell line. Neutrophilic and erythroid abnormalities were most striking in 12 of the patients, megakaryocytic abnormalities predominated in 2 and monocytic abnormalities in 1. Pancytopenia, marked anisopoikilocytosis, normoblastemia, large hypogranular platelets, hypogranular neutrophils, pseudo-Pelger-Huet nuclei, low myeloblast counts and basophilia were the most common abnormalities in the blood. Bone marrows were hypercellular with increased myeloblasts and basophils, abnormal neutrophil precursors, occasional monocytoid blasts, dyserythropoiesis with PAS positive erythroblasts, ring sideroblasts and micromegakaryocytes. All of the 7 patients who had bone marrow chromosome studies exhibited major chromosomal abnormalities. Response to anti-leukemic therapy was poor. The morphologic and clinical findings of these 15 patients appear to define a clinical-pathologic entity.

Adult↗