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At least 19 recordsLinked to original sources
PubMed1991

Genotypic and cytogenetic study of acute myelocytic leukemia and chronic myelocytic leukemia in blast crisis: specific delta rearrangement pattern does not involve J delta gene locus.

We have analysed the configuration of immunoassociated genes and the karyotypes of 30 patients with acute myelocytic leukemia (AML) and 10 with chronic myelocytic leukemia in blast crisis (CML-BC). In AML, the frequencies of T-cell receptor (TcR) beta, gamma, and delta chain and immunoglobulin heavy and light chain gene rearrangements were 4.2%, 19%, 8%, 10.7% and 10.5%, respectively. In CML-BC, they were 10%, 20%, 40%, 50% and 0%, respectively. Nine patients had abnormalities in chromosome 2, 7 or 14, upon which immunoassociated genes are located. There seems to be no apparent relationship between these chromosome abnormalities and gene rearrangements. In all patients but one (5/6), the delta rearrangement was accompanied by other immunoassociated gene rearrangements. Molecular size analysis revealed specific delta rearranged band(s) (19.5 kb-BamHI and/or 6.9 kb-EcoRI), as commonly detected in B-acute lymphocytic leukemia (ALL). All the patients with the delta rearranged band, however, had a germline configuration of J delta gene loci, suggesting a DD or V(D)D (probably V delta 2(D)D) pattern. This study also indicates that the delta rearrangement is specific in AML or CML-BC and distinct from that in early T leukemia/lymphoma.

Blast Crisis↗
PubMed2004

Deletion 6p23 and add(11)(p15) leading to NUP98 translocation in a case of therapy-related atypical chronic myelocytic leukemia transforming to acute myelocytic leukemia.

A NUP98 gene translocation occurring with a del(6p23) and an add(11)(p15) was determined in a 61-year-old patient with therapy-related atypical chronic myelocytic leukemia after complete remission from acute promyelocytic leukemia that eventually underwent clonal evolution and transformed to CD56-positive acute myelocytic leukemia (French-American-British classification M0). Precise chromosome analysis by G-banding, spectral karyotyping analysis, and dual-color fluorescence in situ hybridization showed this abnormality as 46,XY,del(6)(p23),add(p15). ish del(6)(NUP98-,D6Z1+),der(7)(NUP98+,D7Z1+),der(11)(NUP98+,D11Z1). A split signal of NUP98 was observed in 68.4% of the 117 cells analyzed, which clearly indicated that the NUP98 partially translocated to chromosome 7. However, the potential fusion partner of the NUP98 was not HOX family or DEK. The fusion gene has not been found by a differential display method. The significance of simultaneously combined del(6)(p23), which also has been reported with secondary leukemogenesis, has not been elucidated. Additional karyotype abnormalities evolved increasingly, and leukocytosis with blasts with more complex karyotypic abnormalities appeared 5 months later. Careful and continuous analysis of karyotype change clarified the process of the clonal evolution after NUP98 translocation. Further investigation of molecular characterization of this NUP98 translocation and interaction with 6p23 abnormalities might be worthwhile for understanding leukemogenesis.

Chromosome Deletion↗
PubMed1998

[Proliferation and differentiation of leukemic cells in acute myelocytic leukemia].

Acute myelocytic leukemia is characterized as a malignant disease with excessive accumulation of leukemic cells and deterioration of hematopoiesis. We studied the mechanism by which leukemic cells proliferated in patients. The indefinite growth of leukemic cells is supported by leukemic blast progenitors with a self-renewal capacity. Hematopoietic growth factors, such as granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3) or stem cell factor (SCF), have been revealed to stimulate the growth of leukemic blast progenitors. Furthermore, leukemic cells themselves produce and secrete hematopoietic factors that stimulate leukemic blast progenitors. The so-called autocrine growth mechanism has been postulated to play an important role in the pathophysiology of acute myelocytic leukemia. Leukemic cells show terminal differentiation under certain circumstances. For example, leukemic cells differentiate to neutrophils or macrophages in suspension culture. Leukemic cells of erythroleukemia (FAB M6) differentiate to granulocytic and erythrocytic lineages. The mechanisms involved in the proliferation and differentiation of leukemic cells in acute myelocytic leukemia are discussed in the article.

Cell Differentiation↗
PubMed1992

Rearrangement patterns of immunoglobulin heavy chain (IgH) and light chain genes in acute lymphoblastic leukemia and chronic myelocytic leukemia lymphoid crisis cells showing oligoclonal IgH gene rearrangements.

We investigated leukemic cells with multiple immunoglobulin heavy chain (IgH) gene rearrangements from nine B-precursor cell acute lymphoblastic leukemia (ALL) patients and three chronic myelocytic leukemia lymphoid crisis (CML.Ly-BC) patients in order to determine detailed recombination patterns of the variable (V), diversity (D), and joining (J) region genes. Southern blot study, using DNA probes for DQ52 and 5'D region genes, was useful to distinguish VDJ recombination from DJ recombination at the level of each allele. Leukemic cells from seven out of eight CD10-positive ALL patients showed biallelic VDJ recombinations. Rearrangements of Ig kappa genes were found in only one case. Leukemic cells from all of the CML.Ly-BC patients had a DJ/(V)DJ IgH genotype. These findings suggest that the multiple IgH gene rearrangements in B-precursor cell ALL occurred as a consequence of continuing V-(V)DJ rearrangements after neoplastic transformation, and were closely related to the stage of bone marrow B-precursor cell differentiation. Multiple IgH gene rearrangements in CML.Ly-BC might take place earlier in the process of IgH gene rearrangements than is the case in B-precursor cell ALL. In this sense, the genotypic oligoclonality observed in ALL and CML.Ly-BC should be regarded not as 'true', but as 'pseudo' oligoclonal leukemia.

Blast Crisis↗
PubMed2004

Development and progression of a Philadelphia-chromosome-negative acute myelocytic leukemia clone in a patient with Philadelphia-chromosome-positive chronic myelocytic leukemia.

We report a patient with typical Philadelphia-chromosome-positive chronic myelocytic leukemia who developed Philadelphia-chromosome-negative acute myelocytic leukemia following autologous stem cell transplantation. The implications of this observation for disease monitoring and treatment are discussed.

Antineoplastic Agents↗
PubMed1976

Human B-lymphocyte antigens expressed by lymphocytic and myelocytic leukemia cells. I. Detection by rabbit antisera.

A previously uncharacterized human B-lymphocyte antigen has been detected by rabbit antisera raised to papain digests of spleen cell membranes. The unabsorbed sera reacted in both cytotoxicity and immunofluorescent tests with normal B lymphocytes and cultured B-cell lines but not with normal T lymphocytes or cultured T-cell lines. The cytotoxicity titers against B cells were as high as 1:32,000, whereas the same sera undiluted were negative against T cells. By immunofluorescent staining 6-14% of unfractionated normal lymphocytes and 48-85% of B-rich lymphocyte preparations were positive. Normal peripheral blood granulocytes, platelets, erythrocytes, and phytohemagglutinin blasts were negative. The antisera reacted with the same high titers against leukemia cells from approximately 70% of the patients with acute lymphocytic leukemia, acute myelocytic leukemia, chronic myelocytic leukemia, and seven of eight cases of chronic lymphocytic leukemia. From absorption studies it appeared that the same antigen was being expressed by leukemia cells and normal B lymphocytes. Using immunofluorescent staining the anti-B-cell antisera were able to detect positive leukemia cells in the bone marrow of patients with advanced leukemia and to monitor the elimination of these cells after chemotherapy. Soluble B-cell antigen was found in the serum of some leukemia and lymphoma patients do but not in normal serum.

Antigens↗
PubMed2002

Partial deletion of chromosome 1 in a case of acute myelocytic leukemia.

Acute myelocytic leukemia (AML) is a malignant disease characterized by the proliferation of immature myelocytic precursor cells causing the disruption of normal bone marrow function. Many chromosomal aberrations have been described in AML including translocations, inversions, deletions, and additions. Here we describe a novel deletion of chromosome 1, del(1)(p34p36) in a case of AML, French-American-British classification M1, in a previously healthy 33-year-old male. This isolated cytogenetic abnormality occurred in 33% of the myeloblasts examined at diagnosis. Subsequent cytogenetic analyses conducted on marrow following induction and consolidation therapy demonstrated a normal male karyotype in all cells examined. The patient remains in clinical and hematological remission 22 months following diagnosis. The presence of 1p abnormalities in AML and other malignancies is reviewed, as are candidate tumor suppressor genes in the 1p34 approximately p36 region. The implications of chromosome 1p abnormalities on clinical outcome are also discussed.

Adult↗
PubMed2005

Advances in understanding the biology and genetics of acute myelocytic leukemia.

Acute myelocytic leukemia (AML) is a malignant neoplasm of hematopoietic cells characterized by an abnormal proliferation of myeloid precursor cells, decreased rate of self-destruction and an arrest in cellular differentiation. The leukemic cells have an abnormal survival advantage. Thus, the bone marrow and peripheral blood are characterized by leukocytosis with a predominance of immature cells, primarily blasts. As the immature cells accumulate in the bone marrow, they replace the normal myelocytic cells, megakaryocytes, and erythrocytic cells. This leads to a loss of normal bone marrow function and associated complications of bleeding, anemia, and infection. The incidence of AML increases with age, peaking in the sixth decade of life. In the United States, there are about 10,000 new cases of AML and 7,000 deaths in those with an AML diagnosis per year. Current molecular studies of AML demonstrate that it is a heterogeneous disorder of the myeloid cell lineage. This paper will discuss the most recent understanding and research of the cellular origin of AML and associated common genetic mutations that fuel the neoplastic process. Also discussed are how these advances have impacted the classification, selection of therapy, and definition of complete remission in AML. Promyelocytic leukemia will be discussed in detail as this AML subtype reveals how our understanding of the biology and genetics of the disease has led to targeted therapy that results in a cure in up to 80% of patients.

Cytogenetics↗
PubMed1988

Immunoglobulin and T-cell receptor gene rearrangement in blast crisis of chronic myelocytic leukemia.

Chronic myelocytic leukemia (CML) displays a wide repertoire in its terminal phase, with blast cells showing characteristics of myeloid, B-lymphoid, or T-lymphoid cells in some patients. Blast crisis (BC) cells from 14 patients were studied for immunoglobulin (Ig)- and T-cell-associated gene rearrangements. Five myeloid BC patients had no Ig- or T-cell-associated gene rearrangement. In contrast, all eight patients with pure lymphoid BC displayed C mu rearrangement and two also showed kappa-light chain rearrangement. One patient with mixed (lymphoid and erythroid) BC, however, showed neither Ig- nor T-cell-associated rearrangements. One patient displayed both Ig- (C mu) and T-cell-associated (T beta and T gamma) rearrangements. These cells expressed CD9, CD10, and CD24 surface antigens, but no T-cell antigens. Although most lymphoid blast crises appear to represent an early stage in B-cell differentiation, some cells have undergone apparently inappropriate gene rearrangements during differentiation. Such cells may have been immortalized while undergoing normally occurring nonproductive rearrangement or may, due to their malignant nature, display abnormal genotypic characteristics.

Antigens, Surface↗
PubMed1998

Chromosome band 1p36 contains a putative tumor suppressor gene important in the evolution of chronic myelocytic leukemia.

Chronic myelocytic leukemia (CML) is a common neoplasm of hematopoietic pluripotent stem cells. Although the evolution from chronic phase to blast crisis (BC) in CML patients is an inevitable clinical feature, little is understood about the mechanisms responsible for the transformation. We have previously performed allelotype analysis in CML BC and have detected frequent loss of heterozygosity (LOH) on the short arm of chromosome 1. To know the common region of LOH where a putative tumor suppressor gene may reside, deletional mapping was performed using 33 microsatellite markers spanning chromosome 1 in 30 patients with CML BC (21 myeloid and 9 lymphoid). DNA was extracted from slides of bone marrow smears or from bone marrow mononuclear cells. In each patient, DNA from chronic phase was analyzed alongside DNA from either their BC or accelerated phase. Allelic loss on 1p was observed in 14 of the 30 individuals (47%): 10 of the 21 myeloid and 4 of the 9 lymphoid BC cases. Serial cytogenetic information was available in 10 cases with LOH on 1p; interestingly, deletions in this region were not detected. Two samples showed LOH at all informative loci on 1p, whereas the other 12 samples showed LOH on at least one but not all loci on 1p. The common region of LOH resided proximal to D1S508 and distal to D1S507 (1p36). Our results suggest that a tumor suppressor gene that frequently plays an important role in the evolution to BC resides on 1p36 in CML.

Adult↗
PubMed1990

The BN acute myelocytic leukemia (BNML) (a rat model for studying human acute myelocytic leukemia (AML)).

Even if animal models have many properties in common with the human disease, as is the case for the BNML and human AML, they have their limitations with respect to the extrapolation to the clinical situation. This also holds for the BNML; thus, conclusions should only be drawn with great caution. Nevertheless, the studies in the BNML model have added considerably to the understanding of various processes that occur during the development of leukemia, e.g., the interaction of leukemic cells and normal hemopoietic stem cells in relation to the microenvironment. The methodology developed in the BNML model allows the quantification of the relative effectiveness of any given treatment with regard to the antileukemic activity compared with the toxicity for normal host tissues. Furthermore, the cell kinetic studies performed in the BNML as a consequence of timed sequential chemotherapy has been helpful in designing an approach to take advantage of this phenomenon in the treatment of acute leukemia. The comparison of the various treatment modalities, employed for the conditioning prior to bone marrow transplantation, made it possible to determine the relative effectiveness of the various approaches. The fractionation of total body irradiation for conditioning purposes was supposed to have a negligible effect with regard to a reduced antileukemic effect. Detailed studies that were conducted in the BNML model did not confirm this hypothesis indicating that (hyper-)fraction of TBI results in a reduced antileukemic effect. The in vitro purging studies in the BNML aimed at the elimination of residual leukemic cells in autologous bone marrow transplantation contributed to the introduction of this method in clinical practice. However, extended studies in the BNML model also indicated that the contribution of the residual leukemia cell in the patient contributed to a much greater extend to the recurrence of leukemia then did the residual cells in the autologous marrow graft. A major contribution of the BNML was achieved in the study of the area of so-called "minimal residual disease" (MRD). A number of so-far unknown aspects of relapsing leukemia could be identified and studied. A new concept of discriminating locally relapsing leukemia and a delayed occurrence of generalized spreading of leukemia formed the basis for the explanation of the observed heterogeneity in the distribution of leukemic cells during the remission and the subsequent relapse phase. In conclusion, it is obvious that proper comparison of the human disease as well as the counterpart in the animal model requires a detailed knowledge of both.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1978

Acute lymphoblastic leukemia followed by chronic myelocytic leukemia.

Second hematologic malignancies occur rarely in patients previously treated for leukemia. This report describes a patient with acute lymphoblastic leukemia who remained in complete remission for 5 yr and then developed chronic myelocytic leukemia (CML). The original lymphoblasts were associated with a partial deletion of chromosome 21, while CML was associated with a classic Philadelphia marker, indicating the independent origin of the two leukemias.

Acute Disease↗