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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the clinical, cytological, immunophenotypic, and cytogenetic findings in one patient with acute erythroblastic leukemia. Blast cells were identified by their reactivity with the early erythroid antibodies FA6-152 and carbonic anhydrase I. The leukemic blasts had no specific differentiating features identifying them as erythroblasts even at an ultrastructural level. Cytogenetic studies revealed multiple chromosome aberrations: 45,XX,i(11q),-16,-17,-21,+der(21)t(21;?)(q22;?),+mar 1.
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PMID:Acute erythroblastic leukemia. Cytological, cytogenetic and phenotypic studies in one case. 250 92

Ultrastructural and ultracytochemical studies were performed on blast cells from 12 Down's syndrome neonates with transient myeloproliferative disorder (TMD) and 13 Down's syndrome patients with megakaryoblastic leukaemia (MKL), in order to clarify the cytological characteristics of these cells. Average platelet peroxidase-positivity in blast cells of TMD patients was similar to that found in cases of MKL. Blast cells from subjects with TMD contained a number of different granules, namely, alpha granules, those that were myeloperoxidase (MPO)-positive, electron-lucent or basophil-like, and those containing membrane components or ferritin particles. On the other hand, granules found in the blast cells of MKL patients with Down's syndrome included the electron-lucent variety, those with membrane components and a few that were basophil-like, but not alpha and MPO-positive granules nor those containing ferritin particles. A demarcation membrane system was observed in blasts from the TMD group, but not in the MKL group. These findings suggest that blast cells in TMD patients differentiate to megakaryocytes, neutrophils, basphils and erythroblasts, while those in cases of MKL show limited differentiation to immature megakaryocytes, erythroblasts and, sometime, basophils. Such results correspond well with those of culture studies, in which TMD blasts were found to be precursors of various types of blood cells.
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PMID:Ultrastructural and ultracytochemical differences between transient myeloproliferative disorder and megakaryoblastic leukaemia in Down's syndrome. 253 35

DNA probes to both the joining region (JH) of the immunoglobulin heavy chain gene (IgH) and to the beta chain of the T-cell antigen receptor complex (TCR) have been used as tumour-specific markers to monitor the rearrangements of the IgH chain gene and the TCR beta gene in the blast cells of children presenting with acute lymphoblastic leukaemia (ALL) of B or T cell origin. Blast cells from 68 children with early B cell ALL and eight with T-ALL were examined at presentation, at day 28 after commencement of therapy and at varying times thereafter. An additional 43 patients (42 with B cell ALL, one with T-ALL) were studied both at presentation, at completion of their 2-year treatment course and 3 months later. Twelve patients, drawn from both these groups, were studied at relapse as were a further eight patients in whom an extramedullary relapse had occurred. Persistence of clonally-derived cells as a predictor of early relapse was seen in the day 28 bone marrows of 11/76 newly-diagnosed children (nine early B and two T-ALL) followed by rapid, overt relapse in four of the early B ALL cases. No minimal residual disease (MRD) was detected in bone marrows from any of the 43 patients completing their 2-year treatment course, but six of these subsequently relapsed at varying time periods thereafter. Identical patterns of rearrangement at both presentation and relapse were seen in most cases. Oligoclonality, or multiple IgH chain gene rearrangements was seen in the blast cells of 15% of patients with early B cell ALL. No correlation between oligoclonality, high white count, unfavourable phenotype or abnormal karyotype could, however, be ascertained.
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PMID:The use of DNA probes to monitor minimal residual disease in childhood acute lymphoblastic leukaemia. 255 52

A patient whose leukaemic cells carried the rare t(7;11)(p15;p15) was diagnosed as having acute myelomonocytic leukaemia (AML-M4), and supports the association of this specific translocation with forms of acute myeloid leukaemia showing differentiation. Blast phase chronic myeloid leukaemia was excluded by lack of involvement of the ABL and BCR genes. Chromosome in situ hybridization studies showed that both the HRAS1 and INS genes were present on the terminal part of chromosome 11p which was translocated to chromosome 7p. Neither HRAS1 nor INS were structurally rearranged. Field inversion gel electrophoresis showed that a 400 kb fragment encompassing HRAS1 was structurally entire in leukaemic DNA. Because the INS gene, which was also translocated, is probably located proximal to HRAS1 on chromosome 11p, it is unlikely that HRAS1 was near the chromosome 11 breakpoint or involved in this leukaemia.
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PMID:HRAS1 and INS genes are relocated but not structurally altered as a result of the t(7;11)(p15;p15) in a clone from a patient with acute myeloid leukaemia (M4). 271 71

Forty-eight children with acute lymphoblastic leukaemia (ALL) who presented to the Oncology Department of Our Lady's Hospital for Sick Children, Crumlin, Dublin over a 52 month period were treated using a schedule modified from the BFM-81 protocol. All patients achieved remission within four weeks. With a minimum follow up period of 18 months, actuarial disease free survival was 68% and overall survival 75%. Mean hospital stay throughout the treatment period was 31 days. While these results represent an improvement in overall survival compared with historical controls, careful selection of risk categories will be the major aim of future studies so that more appropriate treatment can be instituted for high risk patients while minimising therapy for low risk disease.
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PMID:Recent experience with intensive combination chemotherapy for treatment of childhood acute lymphoblastic leukaemia. 275 13

The effects of human recombinant tumor necrosis factor type alpha (rTNF alpha) on the blast progenitors from 14 acute myeloblastic leukemia (AML) patients and 1 chronic myelogenous leukemia patient in blastic crisis were studied in methylcellulose and suspension cultures. Blast progenitors renew themselves and/or undergo terminal divisions. Plating efficiency of primary colony formation (PE1) in methylcellulose, which is considered to reflect the terminal divisions of blast progenitors, was suppressed by rTFN alpha in a dose-dependent manner in all cases. Plating efficiency of secondary colony formation (PE2) and the recovery of clonogenic cells in suspension culture, which are considered to reflect the self-renewal capacity of blast progenitors, were also suppressed by rTNF alpha in a dose-dependent manner in almost all cases. rTNF alpha also inhibited both PE2 and clonogenic cells in suspension culture, even in relapsed AML patients who were very refractory to intensive chemotherapies. The results demonstrate that rTNF alpha inhibits not only terminal divisions but also the self-renewal capacity of leukemic blast progenitors. The finding that rTNF alpha suppressed the self-renewal capacity of leukemic blast progenitors proposes the utility of rTNF alpha to AML therapy.
Leukemia 1989 Sep
PMID:Effects of recombinant human tumor necrosis factor on the self-renewal capacity of leukemia blast progenitors in acute myeloblastic leukemia. 276 17

Blast cells from ten patients (seven adults, three children) with acute lymphoblastic leukemias (ALL) contained immunoreactive cytoplasmic alpha-1-anti-trypsin (alpha-1-AT) and alpha-1-antichymotrypsin (alpha-1-ACT). Cytochemically positive reactions for block-like periodic acid-Schiff and a localized acid phosphatase suggested that the cells were of lymphoid origin rather than myeloid origin: negative for sudan black-B, nonspecific esterase, chloroacetate esterase, and myeloperoxidase. By surface phenotype, the leukemia showed positive reactions for both lymphoid (common acute lymphoblastic leukemia antigen, Ia, OKT-10) and myeloid (OKM-1, Leu M-1) antigens. Three of three patients tested portrayed the Philadelphia chromosome. Nine patients were Mexican-American and one was Japanese: all were of Asian ethnic derivation. Both myeloid and lymphoid treatment regimens were employed, with survival less than expected. Early granulocytic differentiation detectable by cytoplasmic alpha-1-AT and alpha-1-ACT in lymphoid blasts is discussed.
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PMID:Acute leukemias with both myeloid and lymphoid surface markers. Cytoplasmic alpha-1-anti-chymotrypsin and alpha-1-anti-trypsin as possible indicators of early granulocytic differentiation. 294 24

Nine cases of early erythroblastic leukemia, unidentified by usual criteria, have been diagnosed using a panel of antibodies. Three cases arose in patients with Down's syndrome, one in a patient with therapy-related leukemia, and four patients were in blast crisis of chronic myeloid leukemia; only one case arose de novo. Blast cells could be assigned to two main stages of erythroid differentiation: presence of all erythroid-specific proteins in two patients, a phenotype corresponding to an immature erythroblast; absence of the erythroid markers such as glycophorin A and spectrin in the presence of carbonic anhydrase isoenzyme I, ABH group antigens, and the antigen defined by FA6 152 monoclonal antibody in six patients, a phenotype related to a late erythroid progenitor (CFU-E). One patient had an intermediate phenotype. All patients except one demonstrated a megakaryocytic component. In three patients, chromosomal abnormalities were present, detected both in blasts and in erythroid colonies. In conclusion, these findings indicate that most "cryptic erythroleukemias" are blocked at a "CFU-E-like" stage of differentiation, it may be a frequent event in Down's syndrome and chronic myeloid leukemia, and these erythroleukemias are phenotypically heterogeneous.
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PMID:Phenotype of early erythroblastic leukemias. 294 4

The cellular origin of acute undifferentiated leukemia (AUL) is still a matter of controversy. We report on two cases in which the diagnosis of AUL was established according to restricted criteria. Blast cells of both patients showed phenotypic conversion during the course of disease. In one case, within 24 days from starting treatment, the leukemic phenotype changed from AUL to acute myelomonocytic leukemia (FAB L1, TdT+ to FAB M4, TdT-). The initial phenotype of this acute leukemia was characterized by the co-expression of both B-lymphoid and myeloid markers on the same cell. Moreover, analysis of esterase isoenzyme pattern showed the whole spectrum of isoenzymes typically seen in myelomonocytic leukemias already at diagnosis, yet blast cells additionally contained all three isoenzymes of beta-hexosaminidase typically seen in AUL. However, examination of immunoglobulin (Ig) heavy chain gene rearrangement initially and after conversion revealed an identical monoclonal configuration of Ig heavy chain sequences in both samples. The second AUL patient relapsed after allogeneic bone marrow transplantation with common ALL-antigen (CALLA) positive acute leukemia. Subsequent Southern blot analysis showed a novel rearranged Ig fragment compared to the analysis before transplantation indicating that the leukemic clones prior to and after transplantation were not identical. No chromosomal abnormalities were observed in both cases. These data support the view that AUL cells originate from a pluripotent stem cell that is capable to differentiate in the myelomonocytic lineage (patient 1), and confirm the value of Ig gene analysis as marker for cellular clonality.
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PMID:Conversion of acute undifferentiated leukemia phenotypes: analysis of clonal development. 294 79

Blast cell populations from 32 patients with acute non-lymphoblastic leukaemia of various morphological types have been examined for their ability to stimulate allogeneic T lymphocytes from normal donors in one-way mixed leucocyte culture (MLC). At the same time, these leukaemic cell populations were examined for the amounts of major histocompatibility complex Class I and Class II antigens they expressed, and their ability to release interleukin 1 (IL1) in culture both with and without stimulation by lipopolysaccharide. The abilities of the leukaemic cell populations to stimulate in MLC, and to produce IL1, were found to be associated with the expression of morphological characteristics of monocytic differentiation, and correlated significantly. In contrast, no correlation was observed between the extent of Class I or Class II expression and MLC stimulatory ability. Many myeloblast populations of immature phenotype were unable to stimulate allogeneic T cells despite their strong expression of these antigens. This lack of stimulatory ability was not overcome by the addition of exogenous IL1. We therefore conclude that the correlation between the production of IL1 and MLC stimulatory ability does not necessarily imply a cause/effect relationship, and that the interaction between allo-antigen and the T cell receptor together with a supply of lymphokine 'co-stimulator' is not sufficient to activate resting T lymphocytes. The failure of some Class I and II antigen positive leukaemic blasts to stimulate in MLC even in the presence of exogenous IL1 may be due to the lack of other differentiation-associated cell surface molecules necessary for stable cell-cell interaction.
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PMID:Requirements for the stimulation of allogeneic T lymphocytes by acute non-lymphoblastic leukaemia cells. 296 Apr 48


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