Elevated platelet count features the variant type of BCR/ABL junction in chronic myelogenous leukaemia

Yamagata, Tetsuya; Mitani, Kinuko; Kanda, Yoshinobu; Yazaki, Yoshio; Hirai, Hisamaru

doi:10.1046/j.1365-2141.1996.d01-1798.x

Cited by 40 publications

(30 citation statements)

References 6 publications

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“…A CML patient with thrombocytosis and a BCR exon c3, ABL exon 2 junction and poor response to therapy has been described. 15 However, our case differs in that the transcript was similar to the b2a2 transcript with an inserted sequence, the disease resembling ET due to the marked thrombocytosis, absence of splenomegaly, and normal LAP score. Early reports of ET with a Ph chromosome 1 have not included detailed molecular genetic studies but have indicated that the prognosis in ET was similar to that in CML.…”

Section: Discussionmentioning

confidence: 58%

A novel BCR-ABL rearrangement in a Philadelphia chromosome-positive chronic myelogenous leukaemia variant with thrombocythaemia

Rubinstein

1998

Leukemia

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Reverse transcription polymerase chain reaction was used to detect an unusual BCR/ABL transcript in a patient who presented with thrombocythaemia and was Philadelphia chromosome positive but weakly reactive to conventional BCR/ABL fusion probes. Sequencing revealed the presence of a 12 bp insert between BCR exon2 (b2) and ABL exon2 (a2). In such cases the use of conventional BCR/ABL probes may lead to false negative results. This is the first report of this transcript. Clinically the patient has responded well to therapy.

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Section: Discussionmentioning

confidence: 58%

A novel BCR-ABL rearrangement in a Philadelphia chromosome-positive chronic myelogenous leukaemia variant with thrombocythaemia

Rubinstein

1998

Leukemia

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“…Attempts by our group 7,8 and by others 9 to verify the expression of p230 protein in patients bearing the e19/a2 type BCR/ABL gene have been unsuccessful. Patient 6 had undetectable p230 protein in both peripheral blood and bone marrow 12 years after diagnosis and 6 years after discontinuation of IFN␣.…”

Section: Resultsmentioning

confidence: 99%

Neutrophilic‐chronic myeloid leukemia

Verstovšek

Lin

Kantarjian

et al. 2002

Cancer

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BACKGROUNDNeutrophilic‐chronic myeloid leukemia (CML‐N) has been described as a CML variant associated both with a distinctive molecular defect of the Philadelphia chromosome and with a more benign clinical course than classic CML. The translocation (9;22) in CML‐N results in the transcription of an e19/a2 type BCR/ABL mRNA that codes for a 230‐kD BCR/ABL protein (p230). The indolence of the clinical course of patients with CML‐N has been disputed.METHODSThe objectives of this study were to quantify and correlate with clinical outcome the p230 mRNA and protein in patients with CML‐N, to describe six new patients and the follow‐up (with molecular analysis) of five previously reported patients with CML‐N, and to review characteristics of all patients with CML‐N and p230 BCR/ABL reported to date in the literature.RESULTSQuantitative polymerase chain reaction assays on specimens from the great majority of patients with CML‐N revealed minimal numbers of molecules of p230 BCR/ABL transcripts per total RNA. This also was associated with a lack of detectable p230 BCR/ABL protein in patient specimens, even in one patient who was followed for 16 years after diagnosis. This may explain the milder leukemic phenotype in most patients with CML‐N. A review of all 23 patients who had an e19/a2 type BCR/ABL translocation suggested that the low level of p230 BCR/ABL mRNA and the lack of detectable p230 BCR/ABL protein in patients with no additional cytogenetic abnormalities may predict their indolent clinical course.CONCLUSIONSPatients with p230 positive CML‐N have indolent course, probably as a result of low p230 mRNA and protein levels. This supports the need to conduct additional molecular studies, even if cytogenetic studies have revealed t(9;22), because of the prognostic importance of the molecular findings. Cancer 2002;94:2416–25. © 2002 American Cancer Society.DOI 10.1002/cncr.10490

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“…To date, an e19a2 transcript has been observed in nine patients with CML in the chronic phase, [1][2][3][4][5][6] but also in four with CML rapidly evolving to the blastic phase, [7][8][9][10] and in one with acute myeloid leukemia (AML). 11 Moreover, patients in the chronic phase also presented characteristics of the classical type, such as pronounced leukocytosis and splenomegaly.…”

Section: The Editormentioning

confidence: 99%

The e19a2 BCR/ABL fusion transcript with additional chromosomal aberrations on a new case of chronic myeloid leukemia (CML) of mild type

Bertorelle

Bonaldi

Bianchini³

et al. 2001

Leukemia

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Elevated platelet count features the variant type of BCR/ABL junction in chronic myelogenous leukaemia

Cited by 40 publications

References 6 publications

A novel BCR-ABL rearrangement in a Philadelphia chromosome-positive chronic myelogenous leukaemia variant with thrombocythaemia

A novel BCR-ABL rearrangement in a Philadelphia chromosome-positive chronic myelogenous leukaemia variant with thrombocythaemia

Neutrophilic‐chronic myeloid leukemia

The e19a2 BCR/ABL fusion transcript with additional chromosomal aberrations on a new case of chronic myeloid leukemia (CML) of mild type

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