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Difference???

M-BCR-ABL

AND

m- BCR-ABL

Any difference???

( yes /no)

PLEASE reply...

Yes, there is a difference.

Abstract

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.

 

https://pubmed.ncbi.nlm.nih.gov/9376660/

Thanks for reply...

M - BCR-ABL (Only mentions).......

M-BCR-ABL.. AND m-bcr-abl

Which one is more dangerous??

M-BCR-ABL (ONLY MENTIONS IN REPORT)

One more question (Only information purpose)

After 3 years diagnose

1780 copies of M-BCR-ABL gene /ug RNA

(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??)

PLEASE reply....

After 3 years diagnose

Increase dose 400 to 600...

Early...???

Normal????

Only information purpose....

In 2018 news

Miristen 126

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..

Human trials??

Fail ??)

(no human trials)

Any information.....

PLEASE reply.......