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bcr-abl prevalence in non-CML patients

https://www.ncbi.nlm.nih.gov/pubmed/24535287

While the bcr‑abl p190 transcript was not detected, the p210 transcript was detected in ~10% of samples. Notably, the incidence of p210 translocation was higher in males (12.2%) compared with females (7.7%) and males were 2.4 times more likely to have the translocation.

 

Fascinating. I knew BCR-Abl could be seen in otherwise healthy people - but I never expected it could be even close to 1%, never mind 10%. 

The number nine and number 22 chromosomes are bound tightly in the nucleus right at the bcr, abl breakpoints. It's any wonder that CML is not more prevalent. But I suspect that despite 9;22 translocations being extremely common in 10% of the population; only a few contract CML. Our immune system routinely keeps 9;22 in check. Easily in fact. There is something about our immune system in CML patients, however, that fails. That is key here - not that the translocation takes place, but that after the translocation and production of bcr-abl proteins, nothing happens. No CML. I believe the translocation is normal. Normal in the sense that it can't be prevented, it just occurs naturally because of the tight packaging in the nucleus. What is likely happening involves the P53 gene and other genes failure to produce protein antibodies in response to the translocation error and fix it or keep it in check.

We don't know how many of the "10%" who show bcr-abl develop CML. It does seem to be a prerequisite to getting the disease. But there are a lot of people walking around with bcr-abl and never get CML. And they never know it.

Interesting. Putting this in perspective, you can argue that BCR-ABL is a symptom, or one of the symptoms, rather than the cause of CML. Maybe, TKI treatment is a symptom suppressor.

Here is the research I return to repeatedly, relating the poor function of P53 to CML, and the potential remedy through Misoprostol (ProstaglandinE1 kick-starts the P-53). 

I just finished another 14 day round of robust dose Misoprostol, looking forward to my next PCR in mid-August.  Fingers crossed, I’ll keep you posted. (Guinea pig, I am.) 

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“We found that by treating the cells with the J3 compound, we turn on the p53-dependent cell death pathway, which causes not only the leukemia cells to die, but the leukemia stem cells to die as well.”

https://agsci.psu.edu/magazine/articles/2012/summer-fall/a-cure-for-leuk...