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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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Chronic myeloid leukaemia as a model of disease evolution in human cancer.

TL;DR: Chronic myeloid leukaemia can be considered as a paradigm for neoplasias that evolve through a multi-step process and one of the best examples of a disease that can be targeted by molecular therapy; however, the success of new 'designer drugs' is largely restricted to the chronic phase of the disease.
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Chromosome aberrations and cancer

TL;DR: The association of consistent chromosome aberrations with particular types of cancer has led to the identification of some of these genes and the elucidation of their mechanisms of action.
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Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment.

TL;DR: Results indicate that inhibition of BCR/ABL tyrosine kinase activity by imatinib mesylate does not eliminate malignant primitive progenitors in CML patients.
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ErbB receptors: from oncogenes to targeted cancer therapies

TL;DR: Current therapy has not yet been optimized, allowing for opportunities for optimization of the next generation of targeted therapy, particularly with regards to inhibiting heteromeric ErbB family receptor complexes.
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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