1984
DOI: 10.1016/0092-8674(84)90077-1
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Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22

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Cited by 1,503 publications
(578 citation statements)
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“…For myeloproliferative neoplasms (MPN) and leukaemias, this stem cell population has been associated with deregulated protein tyrosine kinase (PTK) activity (for review see Mitelman 10 ), including FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukaemia (AML) 11 , Janus kinase 2 (JAK2) in erythroid neoplasia 12 and BCR-ABL in chronic myeloid leukaemia (CML) 13,14 . Tyrosine kinase inhibitor (TKI) therapy using imatinib mesylate (IM) has been shown to inhibit PTK activity in CML [15][16][17][18] .…”
Section: Introductionmentioning
confidence: 99%
“…For myeloproliferative neoplasms (MPN) and leukaemias, this stem cell population has been associated with deregulated protein tyrosine kinase (PTK) activity (for review see Mitelman 10 ), including FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukaemia (AML) 11 , Janus kinase 2 (JAK2) in erythroid neoplasia 12 and BCR-ABL in chronic myeloid leukaemia (CML) 13,14 . Tyrosine kinase inhibitor (TKI) therapy using imatinib mesylate (IM) has been shown to inhibit PTK activity in CML [15][16][17][18] .…”
Section: Introductionmentioning
confidence: 99%
“…This gene was shown to be present in the Ph chromosome in CML cells (Bartram et al, 1983;Groffen et al, 1983;Canaani et al, 1984;Stam et al, 1987). Breakpoints along the Ph chromosome were found to occur within the breakpoint cluster region (BCR) gene, suggesting that BCR is also be involved in the translocation that creates the Ph chromosome (Groffen et al, 1984). Hybridization of both BCR and ABL probes to the unique mRNA product of the Ph chromosome, demonstrating that Ph chromosome mRNA was composed of BCR-ABL (Shtivelman et al, 1985;BenNeriah et al, 1986;Stam et al, 1987).…”
Section: Philadelphia Chromosomementioning
confidence: 99%
“…The fusion of BCR to ABL during the translocation increases the tyrosine-kinase activity of ABL, and brings new regulatory domains/motifs to ABL, such as the growth factor receptor-binding protein 2 (GRB2) and SH2-binding sites (Li et al, 2001). Depending on the precise breakpoints in the translocation and RNA splicing, different forms of BCR-ABL protein with different molecular weights can be generated in patients, such as P190, P210, and P230 (Groffen et al, 1984;Fainstein et al, 1987;Saglio et al, 1990).…”
Section: Bcr-abl Tyrosine Kinasementioning
confidence: 99%
“…This rearrangement results in the formation of a chimeric fusion oncoprotein defined as p210 kDa BCR-ABL, whereas p185 kDa and p230 kDa proteins can also exist in CML depending upon differences in breakpoints [2]. This encoded BCR-ABL1 is a constitutively activated protein tyrosine kinase caused by excess activation of some famous signaling pathways like RAS/RAF/MAPK, PI3K-Akt, JUN, MYC, and Janus kinase/signal transducers and activators of transcription (JAK/STAT) [2,3].…”
Section: Introductionmentioning
confidence: 99%