T-Cell Cytogenetics in Chronic Granulocytic Leukaemia

Kearney, Lyndal; Orchard, Kim; Hibbin, Jill; Goldman, John M.

doi:10.1016/s0140-6736(82)91912-2

Cited by 22 publications

(8 citation statements)

References 5 publications

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“…Similar results for T lymphocytes were achieved using CD4 or CD8 antibodies. These results do not support the hypothesis that T cells are not, or only in a very small number, involved in the malignant transformation because of their long life-span (MacKinney et al, 1993;Kearney et al, 1982;Bartram et al, 1987). Due to their rarity in CML, we were able to investigate only a few plasma cells with the combination of MGG and FISH or with FICTION using CD38 þ cells with the typical morphology of plasma cells.…”

Section: Discussionmentioning

confidence: 80%

“…The same is true for T cells. Some authors showed that T cells were neoplastic (Allouche et al, 1985;Fauser et al, 1985;MacKinney et al, 1993;Tefferi et al, 1995;Kearney et al, 1982;Garicochea et al, 1993), but others were unable to confirm this (Nitta et al, 1985;Schmitz et al, 1991;Bartram et al, 1987). So far, unmanipulated or unsorted B or T lymphocytes have not been investigated with respect to the presence of the Ph translocation.…”

Section: Discussionmentioning

confidence: 99%

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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: 80%

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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“…Although T lymphocytes derived from the malignant clone are found in some patients, the majority of circulating T lymphocytes are cytogenetically normal [13, 15, 16]. Therefore, the Th and Tc profiles in CML patients are considered to represent those of normal T cell clones.…”

Section: Discussionmentioning

confidence: 99%

Type I and Type II T Cell Profiles in Chronic Myelogenous Leukemia

Tsuda

Yamasaki²

2000

Acta Haematol

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T cell immunity is considered to play an important role in the control of cell growth in chronic myelogenous leukemia (CML) although information regarding the characteristics of T lymphocytes in CML patients is limited. Using flow cytometric analysis of intracellular cytokine expression at the single-cell level, we analyzed helper T and cytotoxic T subsets in 8 CML patients. The percentage of interferon-γ (IFN-γ) single-positive CD4 cells (Th1) and that of interleukin-4 (IL-4) single-positive CD4 cells (Th2) was markedly decreased in pretreated CML patients compared to normal controls. In addition, the percentage of IFN-γ/IL-4 double-positive CD4 cells (Th0) was also reduced. Consequently, the percentage of IFN-γ/IL-4 double-negative CD4 cells was markedly increased. Similarly, a reduction in IFN-γ single-positive CD8 cells (Tc1) and IFN-γ/IL-4 double-positive CD8 cells (Tc0) and an increase in IFN-γ/IL-4 double-negative CD8 cells were observed in pretreated CML patients. Imbalance of these parameters was markedly improved following cytoreduction therapy. Our findings directly indicate anergic states in CML patients. Determination of the factors that affect Th and Tc profiles may lead to further understanding of immunological states and the development of effective immunotherapy.

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“…The analyses of clonality have provided evidence that not only mature myeloid cells, but also their immature precursors, erythoid precursors, megakaryocytes and B lymphocytes, belong to the malignant clone (Fialkow et al, 1977;Martin et al, 1980). In the majority of studies, the direct analysis of T cells has failed to establish evidence of the Ph chromosome (Kearney et al, 1982;Nitta et al, 1985;Bartram et al, 1987;Schmitz et al, 1991;Jonas et al, 1992;Garicochea et al, 1994;Tsukamoto et al, 1996;Takahashi et al, 1998). The clonal nature of T lymphocytes in CML cells has been controversial because of the limited sensitivity of Southern blot analysis and the lack of pure T-cell preparations obtained through E-rosetting.…”

Section: Discussionmentioning

confidence: 99%

Ontogeny of natural killer cells and T cells by analysis of BCR-ABL rearrangement from patients with chronic myelogenous leukaemia

Cho¹,

Heo²,

Seol³

et al. 2000

Br J Haematol

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Chronic myelogenous leukaemia (CML) is a haematological malignant disorder characterized by the Philadelphia chromosome (Ph) and BCR-ABL gene rearrangement. This abnormal fusion gene can be considered to serve as a marker for the transformed cell clone in CML and is found in all cells arising from the same malignant precursor cell. It has been detected in CML cells of the myeloid, monocytic, erythroid and B-lymphocytic lineages. However, it is still arguable as to whether T lymphocytes or natural killer (NK) cells carry this marker. Answering this question would clarify the ontogenic relationship between NK cells and T cells. We examined 12 CML patients and studied the expression of BCR-ABL rearrangement by fluorescence in situ hybridization (FISH) in both NK cells and T cells sorted by flow cytometry. The purity of T cells was 95.6-99.8% and that of NK cells was 95.3-99.3% after sorting. Neither NK cells nor T cells showed any positive BCR-ABL signal with the exception of one patient who recovered from a lymphoid blastic crisis. We speculate that T cells and NK cells originate from BCR-ABL-negative stem cells.

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T-Cell Cytogenetics in Chronic Granulocytic Leukaemia

Cited by 22 publications

References 5 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

Type I and Type II T Cell Profiles in Chronic Myelogenous Leukemia

Ontogeny of natural killer cells and T cells by analysis of BCR-ABL rearrangement from patients with chronic myelogenous leukaemia

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