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Mounting evidence dasatinib discontinuation is safe

Questions to ask about the study:

1. What was their definition of "deep molecular response" EXACTLY? (In numbers)

2. What was their definition of "sustained" deep molecular response?  How long was "sustained"?

3. What was their definition of "remission" EXACTLY?  (In numbers)

Success rate of about 50% - what is new about this study?

I can’t find a full copy of the study, but here’s the DOI.

Just continuing added evidence that patients who reach deep molecular remission ("undetected" for 3 years) have a greater than 50% chance of treatment free remission.

50-50 are good odds to try when one reaches this milestone.

As important - the "risk" in trying is safe. So if it doesn't work out, you back on drug and resume where you left off.

We seem to know two things about TFR:  About half of DMR CMLers can sustain TFR for an as-yet undetermined time, and that almost all "failures" are able to return to TKIs and regain safe status.

Meanwhile, CML research seems to fall into two categories:  the search for a cure via taking out the stem cells responsible for the genesis of CML and second, even more closely targeted treatments to improve patients' necessarily lifelong dependence on them.

I wish, instead, research would center on these two questions:  One is, find the real reason(s) not everyone reaches "undetectable," and two, what are the crucial differences between those who can successfully attain TFR and those who fail.  Up until now, the effective research has been about what we all have in common; but I think research going forward needs to look at how each patient's CML is different.  This is going to come from the benches of basic science.  I'm getting a little tired of a zillion studies that just show AGAIN that it's OK to try TFR and that about half will make it and you can always go back on your TKI.  Enough already!  Let them continue, for sure, and let's get data on how long the TFR lasts, but I think it's been adequately shown that it's certainly OK to try.

I admit to sour grapes coloring my irritation.  I have been at 0.005% IS for well over two years (what you call "undetected" Scuba, but my onc calls "detected") and below 0.05% IS for six.  But each time I have stopped Sprycel for a pleural effusion, I have had a steep and swift return - within a few weeks - to MMR or lost MMR.  I meet all the current criteria for attempting TFR, but I fail each time - QUICKLY. I'm clearly in the 50% that can't (ever? that's another question) get to TFR.

I just really, really, really want to know WHY.  What is different about me?  This is where I wish research would focus.  OK, rant over.

Hi Kat - I can appreciate your frustration .... You apparently have very active CML stem cells that hide away and wait for a shot to get back in business once treatment stops. The daughter cells are very susceptible to your TKI, but your CML stem cells not so much. I have a working theory ...

As long as CML stem cells do not divide, they are "hidden" from a TKI and capable of re-starting disease. Two things have to happen to get rid of them. One - they need to be dividing when a TKI is around so their number gets greatly reduced. Second, the immune system needs to be primed to attack CML when CML is in its infancy so it never gets started again.

My approach to one above has been to fast (3 days minimum several times a year) in order to coax stem cell division and expose them to TKI attack. It is my attempt at upping the odds of reducing the CML stem cell population. My approach to number two above has  been to increase my vitamin D status to high normal (70 ng/ml) as well as take selenium (200 mcg per day) in the hope my immune system is strengthened to attack CML. I also take Curcumin which is a known down regulator of the NfKb pathway necessary for cancer progression and interferes with cancer cells preventing their own apoptosis.

I suspect people in the successful 50% had a natural set of circumstances that enabled them to cross over into not needing their TKI anymore (at least for now). Not knowing the reason, I call them lucky. Their stem cells may have just been out in the open at the right time when they started therapy! Lucky them.

I have no idea if my approach above works, but on paper it seems reasonable and its good for my overall health in any event - so worth trying. When I do try cessation again (this year) and cessation were to take hold, I would not be able to say it was because of my approach. But maybe. Only a scientifically designed clinical trial would be more definitive.

I strongly believe a true cure lies in targeted therapy which greatly increases our immune response to CML naturally (T-cell chimera's). It will come. Hopefully sooner rather than later.

I'm rooting for you Kat - you'll get there. One way or another.

I know TFR / without treatment chance cml comeback....

50 % rate TFR 3-4 year UNDETACTABLE..... (50% UNDETACTABLE without tki..)

Any chance of cure? (few CMLer cure??)
Any data available???

Fully cure chance (today)??? 0%???

(tki and after undetectable)

This 50% people... ( 3-4 year UNDETACTABLE after TFR) any CMLer fully cure....

UNDETACTABLE mean no cancer cell in 1,00,000 cell....test.... (0.0001)???
UNDETACTABLE men's no evidence of diseaseā€ right???

What's different healthy person and undertactable person report....?

Why some (50%) CMLer TFR SUCCESSFUL 3 + year some (50%) CMLer lost UNDETACTABLE status few months...?


Hi Kat.

Same here.

I stopped Sprycel for a little over 30 days last year for Plural Effusion ( was undetected for about 1 year prior to stopping!).

Numbers  spiked to over 1.16  in  very little time and it took me  6 months on Sprycel to get back to undetected. 

I'd sure like to know what is the factor/factors causing 50% success versus 50% failure and having to return to Meds.  




I have a working theory based on what we already know about CML stem cells.

1. Leukemia stem cells (as well as other normal stem cells) can remain quiescent for a very long time in a non-dividing state (years). The 50% of people who succeed in treatment free remission, just may have been lucky that they nailed many of their LSC's while in a dividing state. The other 50% were not so lucky.

TKI's only kill actively dividing CML cells including dividing stem cells (because it attaches to the ATP energy site) meaning that non-dividing stem cells live to divide another day when TKI is not present and re-start the disease.

2. Suppressed immune system is not available to attack re-emerging CML - so disease restart occurs.

In light of 1, and 2 above, an approach I have taken in order to "up" my odds of treatment free success is to:

a. Coax CML stem cells into dividing - thereby exposing more of them to my TKI while I am still taking it.

b. Improve my immune system function using nutrition to as high a level as possible.


I am now fasting regularly as a method to coax blood cell regeneration which induces stem cells to divide. I have no idea how many times I have to do this in order for it to work, but decided that 4 times a year (3 days no eating) is a good start. Data from Dr. Longo's research suggest a few times per year. I interpret that as four. Blood letting (i.e. pints of blood) is another way to 'induce' stem cell division, but I need my blood (i.e. anemia).

I increased my vitamin D status significantly in order to maintain blood levels around 70 ng/ml. In fact, I strongly believe that if I had maintained a high normal vitamin D level in the first place, I might have avoided CML altogether. Data shows high normal D levels (70 ng/ml) may strengthen our immune system in terms of cancer prevention. Not a cure, just an added boost. Help tip the odds in my favor. (and I have not been sick with cold or flu once since doing this).

I take Curcumin which data shows has a strong down regulating effect on critical cancer cell pathways (NFkB) causing spontaneous apoptosis. Another quiver in the arsenal attacking CML.

If after I try treatment free remission and it fails (I lose PCR undetected status), I will just assume, my genetics puts me in the unlucky camp.

Hey Chuckster, did you WBC increase when your bcr-abl measured above 1%??

i am asking because i cut my tasigna doze in half for a month an my WBC went up from 9,5 (my normal level on tasigna) to 10,5, then for another month before doctor apointment i took the full doze, now i am waiting for the bcr-abl result and i'm litlle bit woried. 

Here are my Bcr/Abl1 and WBC  numbers from May 2019  to Jan.30th 2020


MAY15th-2019 :  Bcr/Abl1:  NOT DETECTED and WBC: 7,400.

July 19th-2019:   Bcr/Abl1:  1.1457% and WBC: 7,900.  ( Went up 500 after being off of Meds for over 35 days)

Aug 30th- 2019:  Bcr/Abl1:  .3861% and WBC: 6,600. Back on meds but at lower dosage of 20 MG daily from 50 Mg of Sprycel.

Nov 1st- 2019 :   Bcr/Abl1:  .1314% and WBC: 7,200.

Jan30th- 2020 :  Bcr/Abl1:  NOT DETECTED and WBC: 7,600.

 Hope this helps you.


Thank you Chuckster, it seems that your WBC was not affected by BCR-ABL growth to 1,3.


 Could it be  "Something" is different in the actual composition of the  BONE MARROW that is having a pronounced effect on

who can be  DRUG FREE/ CML FREE  and who CANNOT????

Food for thought or AKA: Throw it at the wall and see if it sticks (LOL)