“Pre-B” phenotypes in blast crisis of Ph1 positive CML: Evidence for a pluripotential stem cell “target”

Greaves, Melvyn F.; Verbi, Winston; Reeves, Brian; Hoffbrand, A. V.; Drysdale, H. C.; Jones, LaQuita M; Sacker, L. S.; Samaratunga, I.R.

doi:10.1016/0145-2126(79)90041-9

Cited by 69 publications

(8 citation statements)

References 23 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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“…In contrast, in lymphoid blast crisis only a single Ig type was found in the few patients in whom the blast cells expressed Ig. [58][59][60] Therefore, there is an evolutionary step between the Ph-positive B cells in chronic phase and those in blast crisis.…”

Section: Chronic Myelocytic Leukemiamentioning

confidence: 99%

Clonal development of myeloproliferative disorders: clues to hematopoietic differentiation and multistep pathogenesis of cancer

1998

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In November 1996, word reached the University of Washington that Philip Fialkow and his wife, Helen, had died while trekking in Nepal. Over a 30-year period, Dr Fialkow and his colleagues used the cellular mosaicism resulting from X-chromosome inactivation in females as a marker system to investigate the clonal development of human hematopoietic disorders. This review discusses the impact that these studies have had on our understanding of hematopoietic stem cell relationships and the pathogenesis of human neoplasia in general. To appreciate the special role played by studies on clonality, it is necessary to consider how little was known about the origin of leukemias and myeloproliferative disorders and the limited techniques available for their study in the early to mid 1960s. Dr Fialkow and his coworkers were the first to show that myeloproliferative disorders and acute myelogenous leukemias (AML) are clonal diseases at the time of diagnosis and to elucidate the level of differentiation manifested by the originating cell type. Although the myelodysplastic disorders were found to involve a pluripotent stem cell, heterogeneity was found in the level of stem cell involvement in AML. Evidence was obtained to support a multistep pathogenesis of these diseases as well as a clonal but cytogenetically normal stage in some cases of Ph-positive chronic myelogenous leukemia, AML, acute lymphoblastic leukemia and myelodysplasia.

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“…the majority of these cases appear to be lymphoid. The results of several studies identify characteristics of these lymphoid blasts which are similar to those of the blasts of common ALL and rarely to 'pre-B' lymphoid cells (Vogler et al, 1979;Greaves et al, 1979;LeBien et al, 1980). Despite these findings, the nature of the blasts in CML lymphoid blast crisis and Phl-positive ALL remains enigmatic.…”

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confidence: 99%

Philadelphia chromosome‐positive blastic leukaemia: ultrastructural and ultracytochemical evidence of basophil and mast cell differentiation

1982

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Ultrastructural, ultracytochemical, immunologic and biochemical studies were performed on leukaemic cells from 41 patients with Philadelphia chromosome-positive blastic leukaemia; 28 patients were in blast transformation of chronic myelogenous leukaemia and 13 patients presented with 'acute' leukaemia. The patients were divided into two morphologic groups, lymphoid (16 cases) and myeloid (25 cases), on the basis of light microscopy and cytochemistry. All lymphoid cases studied for the presence of CALLA (10 patients) and TdT (11 patients) were positive. Two of 13 myeloid cases studied were TdT positive. The blasts from 10 of 16 lymphoid cases contained immature basophil/mast cell granules on ultrastructural examination. Peroxidase-positive 'lymphoid' blasts were noted in three of seven patients studied by ultracytochemical techniques. The reactivity was primarily confined to granular structures. Of the 25 cases in the myeloid group, blasts from 14 cases showed basophil/mast cell differentiation, nine cases showed neutrophil/monocyte features, and two cases were megakaryoblastic. Distinct patterns of ultrastructural peroxidase positivity were seen in the seven myeloid cases studied. In basophil/mast cell precursors the reactivity was primarily confined to granules; neutrophil precursors showed reactivity in the nuclear envelope, rough endoplasmic reticulum (RER), golgi and granules; in megakaryoblasts, only the nuclear envelope and RER were positive while the granules were consistently negative.

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“Pre-B” phenotypes in blast crisis of Ph1 positive CML: Evidence for a pluripotential stem cell “target”

Cited by 69 publications

References 23 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

Clonal development of myeloproliferative disorders: clues to hematopoietic differentiation and multistep pathogenesis of cancer

Philadelphia chromosome‐positive blastic leukaemia: ultrastructural and ultracytochemical evidence of basophil and mast cell differentiation

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