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Imatinib&nilotinib failure ! Please advice !


Hello everybody , i’m new here and i’m kinda scared because of my sister who was diagnosed last year with CML in Viena . She began oral therapy with Imatinib for 6 months and then switched to nilotinib for better results of the treatment- she takes nilotinib since November til now  . Sadly the doctors aren’t thankful with the results of her BCR-ABL (between 20-30%) and now i think they want to make a transplant . She don’t have any mutation so we don’t know why she is not in remission yet . 

•Please tell me if someone from here was in the same situation ? What did you do ?

•is there another TKI better than Nilotinib ?

• if she does the transplant is she 100% cured? Or has she better chance to live ?


I'm really sorry to hear your sister isn't responding to her medication as well as had been hoped.

Mutations and CML can be quite complex. The one patients know most about is called "T315i" which in the table below is the one which is in red (i.e. bad) for all TKIs except ponatinib. But, you'll see there are also mutations which nilotinib is not so good at dealing with that other TKIs are. So it's not quite as simple as one TKI being "better" than the other.

So whilst in theory there could be another TKI that could work better for your sister, am I right in saying that they have done a mutation analysis on her bone marrow? If so, those "cytogenetic" tests can see (or not) any mutations so you don't need to guess by trying another TKI.

Unfortunately, it does seem that some people who don't show up as having mutations don't do so well on TKIs. I don't know if this is because of an undiscovered mutation, or another reason altogether which is not yet understood.

In these cases, transplant is a viable option. There are patients on this group who have had a transplant and are doing really well, and gone on to life a totally normal life freed from the daily management of CML. But it is not always so simple as it depends on the quality of the donor bone marrow and many other factors. A transplant should only be considered as a last resort as it is a very serious medical procedure. I have seen a few cases recently where the patient has taken ponatinib for a while, as it is the most potent TKI, to prepare for a planned transplant. 



David, my chromosome report shows t (9,22) and pcr shows transcript detected as p210.

I dont see any of these in mutation list of tki resistance. What would be my mutation?

Sorry if I wasn't very clear, most of us of course have the Philadelphia Chromosome which is in itself a mutation compared to a normal person. This mutation creates the BCR-Abl kinase, and the exact form most that most of us have is called P210. So, in the context of CML t(9;22) and P210 is "normal".

The table shown are further mutations of the BCR-Abl kinase.

Does that make sense?


Hi David ,

thanks for your response and Yes you did understand good , she doesn’t has any mutations but the Imatinib and Nilotinib didn’t brought her below from 20% BCR-ABL in fast 9 months .

should we try Bosutinib or directly transplant ? 

Hi - I don't often check or post on here now as I was diagnosed over fifteen years ago. I know that people have high expectations of a rapid response to TKIs and that this is generally the case. However not everyone follows this exact route. After diagnosis I had little response within six months and only a little more by nine months. No mutations were detected but I was sent to discuss transplant. I was not keen on transplant because of the risks especially given that at that time my family were very young. By twelve months after diagnosis, results had improved very significantly and the transplant was never needed. I am happy to say I have been on imatinib for fifteen years. So it sounds that the doctors are looking at all the options, which is very sensible but I certainly would not be rushing to transplant until all other options have been considered.