Hi everyone.
I would like to update all the data that we all provide and summarize it. Last week I had a meeting with a CLL teacher and we discussed Ricther's behavior.
That is what my doctor thinks but I am not satisfied. It is only his hypothesis and without any study.
He thinks that as long as the CLL is active, Ricther will never come out, but that doesn't mean he isn't there. Our Ricther is in our DNA from the beginning of the disease. When treated with treatments like Ibrutinib or Venetoclax that act so fast, the CLL goes away and that's when the RT comes out aggressively. He means that it does not mutate over time, if not that we already had it since the beginning of CLL, only that they get to see it in biopsies and the transformation is not declared until we enter CLL remission. He also thinks that the Pseudo Ricther does not exist when there are studies that affirm it. I'd like to share his opinion with you, but he doesn't mean it's true..
During the two and a half years that I have been in contact with RT patients like myself, I can see that it affects people who have had a very aggressive CLL and shortly after being diagnosed with CLL they had to be treated. If it is true that we already have RT in our DNA from the beginning, it may make sense that when LLC disappears, the door is already open to develop RT.
Why is it so difficult to cure? Doctors see it as a large cell lymphoma, but in reality it is not. CLL has no cure, so you can understand why RT is so resistant to treatments. I do not understand medicine and I am based on logic and what we are seeing is that doctors can treat it as what they see in biopsies, as a lymphoma, but what if they started to see it as a small cell that changes its appearance and becomes it behaves like a large cell, multiplying rapidly, but in reality it is still a small cell.
We see that whenever RT is treated with combinations of CLL treatments, they are working well. The Car-T are also a good alternative since it also works for both cases giving good results.
If the doctors say they cannot see the RT, only when it comes out, my theory is that they may not see it because it is not there. Why are there RTs that work differently and some are aggressive and others don't develop? Everything is very confusing and that 5% who say that there is RT but I wonder if there is not more, but you never know. There are cases where, if not through a biopsy, doctors do not even find out that there is a Ricther transformation, and where the disease has not developed, but they have continued with treatment for CLL and large cells, they returned. very small.
In Ricther's transformation group, few people have died and two of them had bone damage and two other people had the same problem. They had the disease practically all over their body and died shortly after. By this I mean that despite the poor prognosis of the disease, we must look at all cases with a magnifying glass and carefully.
The scientific community shares their studies and little by little more positive information is updated than years ago. With the new treatments and with a different vision of what this transformation is, I think the prognosis could change.
During these two and a half years, I have seen cases where they gave little hope of recovery from the beginning, but have come through and are still in complete remission. Some with cell transplantation, others with combinations of treatments such as Venetoclax and Ibrutinib, others with Car-T and very few have died, but they were diagnosed very late, because the disease was very advanced.
By this I mean that an early diagnosis of the disease has good results and in other cases I think that the 5% that doctors talk so much about, actually there are more, but they have not been discovered because they have not been biopsied and they have continued. with your usual CLL treatments.
