4 replies to this topic

[survenant]

See New abstracts at EHA 2015

[kat73]

Interesting - thanks, survenent. 

 

Scuba - Look at the abstract on NK cell function and durability of TFR.  I wonder if you could get yourself tested for the KIR2DL2 inhibitory receptor?

[scuba]

Interesting - thanks, survenent. 

 

Scuba - Look at the abstract on NK cell function and durability of TFR.  I wonder if you could get yourself tested for the KIR2DL2 inhibitory receptor?

 

This is a related paper on the role of other cells and their association with CML. This has the attention of my Oncologist.

I'll ask about the KIR2DL2 IR as well. I suspect, however, that it would be a moot point since I am already in a cessation plan and time will certainly tell. Monthly PCR test next week. 

 

http://www.ncbi.nlm....les/PMC4432672/

Myeloid Derived Suppressor Cells in Chronic Myeloid Leukemia

[IGotCML]

Scuba,

 

Do the findings of the paper correlate to your idea that the 9,22 chromosome translocation is a frequent mutation among the general population but a normally functioning immune system is able to destroy the mutation and prevent it from developing into full blown CML?

[scuba]

Scuba,

 

Do the findings of the paper correlate to your idea that the 9,22 chromosome translocation is a frequent mutation among the general population but a normally functioning immune system is able to destroy the mutation and prevent it from developing into full blown CML?

 

Translocations of DNA between chromosomes are very common. I am not sure if the findings in the paper support my idea that 9;22 translocation is common in the general population. We do know that most translocations are benign and don't matter. The 9;22 translocation creates an oncogene that codes for tyrosine kinase that is always on and drives white blood cells to proliferate unchecked. It is estimated that a third of the population may very well have 9;22 translocated cells but do not develop CML disease. The cells either remain quiescent (non-dividing, but capable) or are senescent (not capable of division).

 

Our immune system is capable (with various cytokines and T-cells) of either producing an environment that causes these cells to die out, senesce or remain dormant. All of this happens.

 

What is unknown is why 40% of patients who developed CML and then succeed in taking a TKI and achieve MMR/PCRU are able to remain stable for years without disease returning. Dr. Druker suspects their immune system became "armed" during the disease/treatment process and is now able to keep the disease in check whereas this immune response didn't exist prior. No one knows.

 

There is a lot of debate in the literature as well as right here in this forum concerning this topic. I, for one, do not believe it is necessary or even possible to eradicate CML cells without the immune system playing a role. Drugs may be able to knock it down or even get rid of it at one point in time, but CML expansion will likely re-start as a new disease without some form of immunosurveillance to keep it in check.

 

Just like Measles. Once you are vaccinated - your immune system keeps you measles free - it doesn't mean measles doesn't get into your system form time to time - or chicken pox, or the mumps ... As long as your immune system is healthy, any growth in these virus' is checked. If your immune system is able to check CML in a similar way, then a patient for all practical purposes is functionally cured - or at least can live a life without a TKI. 40% of the people who are TKI free seem to be able to travel that road. Perhaps the results highlighted in this paper may help explain why.