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.
Priss69, Have you seen any characteristics that RT patients have in common, such as unmuted IGHV, certain FISH abnormalities, tp53 deletion, 4-39 gene usage, stereotypes, NOTCH1 mutations, or complexed karyotype? I've never seen a profile for a RT candidate but would like to.
I couldn't tell you, but I can give you the information about my case. But what if I can assure you that there are cases of Ricther that have been diagnosed and have not been treated with R-CHOP, which is the treatment that they give to this transformation. The transformation did not develop it. I am going to pass your question to the Ricther Transformation group because I find it very interesting.
I finish seeing that in one of the cases of a Ricther patient, he has the tp53 marker.
I am going to review my reports of when I was diagnosed with CLL because I never saw it since I did not understand anything at all when I was diagnosed with CLL.
‘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.’
Being in this position of having just achieved remission on I&V, I’m wondering where this hypothesis comes from? Is there some research you can link to because without it, I think it’s important not to unnecessarily create anxiety about Richter’s in this patient group. To be honest, I found your post to be confusing though I appreciate you were trying to generate hope for RT treatment and outcomes. That’s what we all sincerely want of course.
This I did not say. It was what my doctor told me and I was very surprised. It is the first time I have heard that the Ricther is in our genetics from the beginning.
Can you reference the work of this specialist Priss because we are an evidence based site and would want to carefully study a hypothesis of such clinical significance.
It's what I'm trying to know. My Post was written to find out what other people think about the Ricther Transformation and its possible causes. I really think that nobody knows anything and they are only based on their experiences, but I know cases that have been transformed from Ricther and they have never been treated and the disease has not been developed.
My case is now led by a teacher specializing in CLL. In Barcelona they told me that it is transformed by 5%, but last week another doctor told me that this was not true. He says we've had Ricther since CLL started and that once we go into remission, the Ricther comes out. Maybe I didn't explain myself well in the message, but it was the doctor's opinion, not mine. He was very surprised.
Thank you for this update from your Richter's FB group and your own research.
I must admit to being confused by the second paragraph where you say
"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."
I'm not sure I've ever read anything that suggests that the Richter's never shows whilst the CLL is active. Some patients develop Richter's whilst on W&W prior to treatment so it's certainly not a disease of people with their CLL in remission. Many patients have long and durable remissions from CLL where it's inactive and do not develop Richter's.
It is true that some genetic markers and combinations of them, which we may have from the beginning of our CLL, do predispose some people to Richter's - is that what you mean by "we already had it since the beginning of CLL,"? However, I don't think it can be said that Richter's co-exists with the CLL from the beginning if that is what you are suggesting
Can you help with references of papers or presentations please?
It was the opinion of the doctor that I saw last week. Due to my medical history, they have changed my doctor and now a professor specialized in CLL is going to consult me. What he told me is that he is in our DNA the Ricther since the beginning of the CLL but they cannot see him in the tests and they do not know why. He told me that people who already have the Ricther in their DNA once you go into remission, leave room for the Ricther to come out. He also told me that while the CLL is active the Ricther never comes out. He left me totally confused, because in this adventure with the Ricther I met people with CLL and Ricther at the same time. What this doctor told me has created more confusion in me. My Post was to find out if anyone knew anything about this information. For me it is new.
With all respect to your doctor, I have never heard of this theory/opinion being expressed before, nor in any paper I have read. Is this publication any help to you? haematologica.org/article/v...
I'm going to read it. It also puzzles me because it was the first time I heard this. That is why I comment on it in this group in case anyone knows something. It may be that some patients are already predestined to have Ricther, but I don't think it is in our DNA. I had a genetic study done in another hospital and there was absolutely nothing in my DNA, just CLL and I had Ricther and my DNA didn't show up.
The information is very complete but it is scary to see it. Mortality in this study is very high and within the Ricther Transformation group there are people who have been in remission for six years and very few people have died so far. If it is true that for many they are resistant to treatments. The Car-T are working very well, but we do not know the long-term results.
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