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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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Journal ArticleDOI

LMO T-cell translocation oncogenes typify genes activated by chromosomal translocations that alter transcription and developmental processes

TL;DR: The scientific challenge of the last decade has been to define the contribution of the genes activated by translocations to the course of tumor development and to ascertain whether any general principles can be determined about these ‘translocation’ genes.
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Kinome-wide Decoding of Network-Attacking Mutations Rewiring Cancer Signaling

TL;DR: Six types of network-attacking mutations (NAMs) are identified, including changes in kinase and SH2 modulation, network rewiring, and the genesis and extinction of phosphorylation sites, and mutant molecular logic gates and kinase-inactivating hotspots in cancer are discovered.
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Chromosomal translocations in cancer

TL;DR: In this review, the well-studied chromosomal translocations in cancer are summarized and the mechanism of formation of most of these translocations is still unclear.
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Heterogeneity of chromosome 22 breakpoint in Philadelphia-positive (Ph+) acute lymphocytic leukemia.

TL;DR: In this paper, the authors investigated the chromosome breakpoints in several cases of ALL carrying the t(9;22) translocation and found that the breakpoints on chromosome 22 occur within a 58-kilobase segment of DNA referred to as breakpoint cluster region.
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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