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Journal ArticleDOI

Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining.

Janet D. Rowley
- 01 Jun 1973 - 
- Vol. 243, Iss: 5405, pp 290-293
TLDR
An unsuspected abnormality in all cells from the nine patients with chronic myelogenous leukaemia has been detected with quinacrine fluorescence and various Giemsa staining techniques, suggesting that there may be a hitherto undetected translocation between the long arm of 22 and thelong arm of 9, producing the 9q+ chromosome.
Abstract
CELLS from nine consecutive patients with chronic myelogenous leukaemia (CML) have been analysed with quinacrine fluorescence and various Giemsa staining techniques. The Philadelphia (Ph1) chromosome in all nine patients represents a deletion of the long arm of chromosome 22 (22q−)1,2. An unsuspected abnormality in all cells from the nine patients has been detected with these new staining techniques. It consists of the addition of dully fluorescing material to the end of the long arm of one chromosome 9 (9q+). In Giemsa-stained preparations, this material appears as an additional faint terminal band in one chromosome 9. The amount of additional material is approximately equal to the amount missing from the Ph1 (22q−) chromosome, suggesting that there may be a hitherto undetected translocation between the long arm of 22 and the long arm of 9, producing the 9q+ chromosome.

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Citations
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The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors

TL;DR: It is demonstrated that in CD34+ CML cells, FOXO1 and 3a are inactivated and relocalized to the cytoplasm by BCR‐ABL activity and TKI‐induced G1 arrest in C ML cells is mediated through inhibition of the PI3K/AKT pathway and reactivation of FOXOs.
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Resistant mutations in CML and Ph(+)ALL - role of ponatinib.

TL;DR: Mechanisms of resistance in CML are discussed, which provide insight and background into the need for this third generation TKI, followed by the molecular design and pharmacology of ponatinib, which lead to its success as a therapeutic.
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Clinical course and therapy of chronic myelogenous leukemia with interferon-alpha and chemotherapy

TL;DR: This article begins with a review of the natural history of chronic myelogenous leukemia, with an emphasis on prognostic features, and some potentially effective novel agents including homoharringtonine, decitabine, ATRA, and topotecan are described.
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The consequences of chromosomal aneuploidy on the transcriptome of cancer cells.

TL;DR: Gross genomic copy number changes, including aneuploidies of entire chromosome arms and chromosomes, result in a massive deregulation of the transcriptome of cancer cells.
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Leukemia stem cells: the root of chronic myeloid leukemia

TL;DR: Increasing evidence shows that leukemia stem cells are the root of CML and targeting LSC may offer a curable treatment option for CML patients, and a number of LSC-associated targets and corresponding signaling pathways have been identified over the past decades and various small inhibitors targeting L SC are also under development.
References
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Journal ArticleDOI

New Technique for Distinguishing between Human Chromosomes

TL;DR: It seems probable, therefore, that the darker staining with Giemsa of these regions, after denaturation and annealing, indicates the presence of highly repetitive DNA.
Journal ArticleDOI

Technique for Identifying Y Chromosomes in Human Interphase Nuclei

TL;DR: This work investigated the possibility of positively identifying male nuclei in interphase by virtue of this staining property of the Y chromosome using quinacrine dihydro-chloride.
Journal ArticleDOI

Clinical Implications of Cytogenetic Variants in Chronic Myelocytic Leukemia (CML)

TL;DR: The development of other chromosomal abnormalities in Ph1 positive patients presaged the terminal stage of the disease.
Journal ArticleDOI

Philadelphia-Chromosome-Positive and -Negative Chronic Myelocytic Leukemia

TL;DR: Chromosomal studies were performed on 61 adult patients with "typical chronic myelocytic leukemia" and the Philadelphia (Ph1) chromosome was found in 43 patients, with equal sex distribution a year after diagnosis.
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