Chronic Myeloid Leukaemia Blast Crisis With T‐cell Features

Hernández, P; Carnot, J; Cruz, Conrad Russell Y.

doi:10.1111/j.1365-2141.1982.tb07302.x

Cited by 44 publications

(15 citation statements)

References 9 publications

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“…Although involvement of B lymphocytes (Bettelheim et al, 1985;LeBien et al, 1979;Greaves et al, 1979;Bakhshi et al, 1983) or T cells (Allouche et al, 1985;Hernandez et al, 1982;Griffin et al, 1983;Sun et al, 1991;Kuriyama et al, 1989) in CML blast crisis is well known, direct evidence of involvement of B or T lymphocytes in the chronic phase of CML is inconclusive. Some authors were able to demonstrate the involvement of B lymphocytes (Martin et al, 1980;Bernheim et al, 1981;Nitta et al, 1985;Fauser et al, 1985;MacKinney et al, 1993;Tefferi et al, 1995), whereas others were not (Ferraris et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Which compartments are involved in Philadelphia‐chromosome positive chronic myeloid leukaemia? An answer at the single cell level by combining May‐Grünwald‐Giemsa staining and fluorescence in situ hybridization techniques

et al. 1997

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Summary. Chronic myeloid leukaemia (CML) is believed to represent a stem cell disorder involving all three cell lineages. The typical chromosomal aberration, the Philadelphia chromosome, is the translocation (9;22)(q34;q11). Several studies with cytogenetics, fluorescence in situ hybridization (FISH), or polymerase chain reaction have investigated the presence of the t(9;22) in different cell compartments. However, questions still remain. In six cases of CML we combined the standard May-Grü nwald-Giemsa staining with FISH at the single-cell level and were able to demonstrate that not only all maturation stages of granulopoiesis, erythropoiesis, and megakaryocytes, but also plasma cells, eosinophils, basophils and monocytes carried the Philadelphia chromosome in 53-98% of samples. Using immunological identification of single cells we were able to demonstrate that the t(9;22) is detectable in 34% of CD3-positive T lymphocytes, in 32% of CD19-positive B lymphocytes, and in 82% of CD34-positive precursor cells. The results give new insight into the biology of CML and may have implications for future therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Which compartments are involved in Philadelphia‐chromosome positive chronic myeloid leukaemia? An answer at the single cell level by combining May‐Grünwald‐Giemsa staining and fluorescence in situ hybridization techniques

et al. 1997

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“…These clinical findings are similar to those reported in 17 previously described cases of Tcell blast crisis. [5][6][7][8][9][10][11][12][13][14][15][16][17][18] In our three patients, the T-cell blasts had an imma- lanes 1 and 2) or the T-cell receptor 8 locus (lanes 3 to 5). Lanes 1 and 2 reveal presence of normal 11-, 10-, and 9.3-kb genomic bands hybridizing to the T-cell receptor P1/P2 probe, with no additional, rearranged bands seen in the patient sample (lane 2).…”

Section: Discussionmentioning

confidence: 99%

“…4 Only rare cases of CML blast crisis w i t h a T-lymphoblast immunophenotype have been reported. [5][6][7][8][9][10][11][12][13][14][15][16][17][18] The characteristic cytogenetic finding in CML, observed in 90% to 95% of cases, is the Ph' chromosome, representing t(9;22)(q34;qll) translocation of the abl oncogene on chromosome 9 to the breakpoint cluster region (bcr) on chromosome 22.…”

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confidence: 99%

T-Cell Blast Crisis in Chronic Myelogenous Leukemia:Immunophenotypic and Molecular Biologic Findings

et al. 1997

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T-cell blast crisis in chronic myelogenous leukemia is rare. We examined three patients (ages 35 to 72 years) in whom T-cell blast crisis developed 11 to 36 months (mean, 25 months) after diagnosis of chronic myelogenous leukemia and who died 4 to 12 months (mean, 7 months) thereafter. Two patients had diffuse lymphadenopathy, and the third had marked lymphocytosis (white blood cell count 217,000/uL, with 90% circulating blasts). In all three patients, neoplastic cells had the appearance of lymphoblasts and were immunoreactive for T-cell markers by immunohistochemical or flow cytometric analysis or both. Chronic myelogenous leukemia (CML), one of the chronic myeloproliferative disorders, typically is diagnosed in an indolent phase of disease of 3 to 4 years' duration, which, after conventional therapy, is followed by an accelerated phase of 12 to 18 months' duration and a fatal, blast phase (blast crisis) of 3 to 6 months' duration.1,2 Blast crisis is defined as the presence of 30% or more blast cells in the blood or bone marrow or a focus of blast cells at an extramedullary site.3 ' 4 Blast cells in CML exhibit a myeloid phenotype in 70% of cases and a lymphoid phenotype in 30%. 4 In most lymphoid blast crises, the blast cells have LI or L2 lymphoblast morphologic features, are positive for terminal deoxynucleotidyl transferase (TdT), and have the immunophenotypic profile of pre-B cells4 Only rare cases of CML blast crisis w i t h a T-lymphoblast immunophenotype have been reported. 5-18From the Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston The characteristic cytogenetic finding in CML, observed in 90% to 95% of cases, is the Ph' chromosome, representing t(9;22)(q34;qll) translocation of the abl oncogene on chromosome 9 to the breakpoint cluster region (bcr) on chromosome 22.

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“…Although the surface membrane markers and cy togenetic analysis was not done simultaneously [22,23], the immunological characterization of the blasts in blood and liquor was clear [24], In contrast to other reports [25,26], no T cell and myeloic markers were found. Thus the blasts in our patient could not be Dis tinguished from childhood common ALL blasts, for which Philadelphia chromosome [27] and hyperdip loidy [3,28] are described.…”

Section: Discussionmentioning

confidence: 67%

Hyperdiploidy of 54 Chromosomes with Double Ph<sup>1</sup> Chromosome in Lymphoid Chronic Myelocytic Leukemic Blast Crisis

Clemm¹,

Thiel²,

Riess³

et al. 1985

Acta Haematol

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Cytogenetic analysis of bone marrow cells in a 40-year-old man revealed a mosaic of two cell lines during blast crisis: one diploid with typical Ph1 chromosome (46 XY Ph¹) and one with hyperdiploidy of 54 chromosomes with double Ph¹ chromosome, trisomy 4, 6, 8, 18, 21 and duplication of the sex chromosomes X and Y. Immunological characterization showed common acute lymphoblastic leukemia antigen in 90% of the blasts. In spite of intensive chemotherapy the patient died in a third blast crisis 15 months after the first blast crisis, 3 months after successfully treated central nervous system relapse.

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Chronic Myeloid Leukaemia Blast Crisis With T‐cell Features

Cited by 44 publications

References 9 publications

Which compartments are involved in Philadelphia‐chromosome positive chronic myeloid leukaemia? An answer at the single cell level by combining May‐Grünwald‐Giemsa staining and fluorescence in situ hybridization techniques

Which compartments are involved in Philadelphia‐chromosome positive chronic myeloid leukaemia? An answer at the single cell level by combining May‐Grünwald‐Giemsa staining and fluorescence in situ hybridization techniques

T-Cell Blast Crisis in Chronic Myelogenous Leukemia:Immunophenotypic and Molecular Biologic Findings

Hyperdiploidy of 54 Chromosomes with Double Ph<sup>1</sup> Chromosome in Lymphoid Chronic Myelocytic Leukemic Blast Crisis

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