( yes /no)
Yes, there is a difference.
The BCR-ABL hybrid gene, the main product of the t(9;22)(q34;q11) translocation, is found in the leukaemic clone of at least 95% of CML patients. The fusion protein encoded by BCR-ABL varies in size, depending on the breakpoint in the BCR gene. Three breakpoint cluster regions have been characterized to date: major (M-bcr), minor (m-bcr) and micro (mu-bcr). The overwhelming majority of CML patients have a p210 BCR-ABL gene (M-bcr), whose mRNA transcripts have a b3a2 and/or a b2a2 junction. There is apparently no significant difference between patients with a 5' or a 3' M-bcr breakpoint, except maybe for a slight predominance of b3a2-expressing cases among those with increased platelet counts (ET-like syndrome). The smallest of the fusion proteins, p190BCR-ABL, (m-bcr breakpoint) is principally associated with Ph-positive ALL. Rare cases of CML are due to a p190-type of BCR-ABL gene and, in these, the disease tends to have a prominent monocytic component, resembling CMML. CML resulting from a p230 BCR-ABL gene (mu-bcr breakpoint) is also rare, and has been associated with the CNL variant and/or with marked thrombocytosis. Exceptional CML cases have been described with BCR breakpoints outside the three defined cluster regions, or with unusual breakpoints in ABL resulting in BCR-ABL transcripts with b2a3 or b3a3 junctions, or with aberrant fusion transcripts containing variable lengths of intronic sequence inserts. The reciprocal ABL-BCR gene found in the derivative 9q+ chromosome of the t(9;22) is transcriptionally active in nearly two-thirds of CML patients but has not been shown so far to have a functional role in CML. 'Ph-negative CML' comprises cases of typical CML in whom the BCR-ABL gene can be detected by molecular methods and others who are genuinely BCR-ABL negative and usually have an atypical disease phenotype.
One more question (Only information purpose)
After 3 years diagnose
(Gene copies / ABL Gene copies) :0.25 %
This report means???
DRUG NOT WORKING GOOD???
MY DOCTOR INCREASE MY DOSE 400 IMTINIB TO 600 MG
AFTER ONE YEAR
BCR-ABL - UNDERTACTABLE..
(Last 8 years all report undertactable
Last report end of 2019 - UNDETACTABLE...)
( Why doctors change dose??
After diagnosed 3 years 0.25% drug not working good??)
Only information purpose....
In 2018 news
This is could be a major breakthrough for people who are in remission for CML because there is always a concern that the disease will come back if TKI treatment is stopped,” Zhang said. “Miristen could be the drug that sends the disease into permanent remission.”
( mice trials )
After 2018 news....
No update... No news..
(no human trials)