I have shared my father's second treatment of CLL with BR over a year ago.
His case was interesting and i would like to share what happened and if anyone can comment or shed some light on it.
He was diagnosed with CLL in 2007. W&W till early 2011. He was supposed to do the regular 6 session of FCR. He only did the FIRST chemo session, day 1 Rituximab, then half a dose of Fludarabine before a severe tumor lysis syndrome kicked in that almost costed him his life. He stopped the treatment and was on a partial remission for 8 years! till Feb 2019. all his blood was much better, gained his weight back , everything went back to normal from half a dose of Fludarabine in just one session.
on Feb 2019, he relapsed. He used Bendamustine/Rituximab. Again, the recommended treatment of 6 cycles. He did cycle 1 with no issues, cycle 2 with no issues except a severe neutropenia where all white cells dropped to 0. The doctor advised us to stop. A month later, all his blood levels restored to levels not seen even during the first treatment. He has low gamma globulin and low platelets, 120K. but he regained his weight, and all his vital signs are great. So this time, only 2 cycles out of 6 and he is on a complete remission. I hope this lasts forever.
*He has no mutations or deletions.
But just wondering if anyone of you heard of case like this and can explain it maybe.
All the best.
Written by
mkawass
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He has CLL. He sees a specialist in Morocco. I personally had opinions from MD Anderson hematologists. i never heard that you cant use BR after FCR. FCR was out of stock when his time came for treatment so we opted for BR.
Ummm, how did he get a diagnosis with no cell abnormalities? No mutations or deletions? My understanding is, there has to be at least changes in CD38 or ZAP70. I mean, there has to be some kind of cell abnormality to get the diagnosis, right?
Right, but 17p is only one deletion that gives a CLL diagnosis. There are other markers that are mutated, missing, only weakly present on cell, or absent from cells, that would still give a diagnosis of CLL. Thats's why they do FISH & Flow Cytometry. It's great he isn't 17p del, that's usually the toughest to treat. If he has only a small percentage of cells of a single DNA allele (we have one from each parent) that's defective, he could be "borderline" diagnosed, but still diagnosed, and that might logically (to me, anyway) make him much more responsive to treatment. People can have both alleles affected in a high percentage of cells. While I have the dreaded 17p del, even though it's 77% of cells, it's only on one allele, the other doesn't have the deletion. Which may explain why I respond to some treatments. When I had my first FISH a decade ago, I don' recall my onc talking about percentage of cells affected, or one vs both alleles, but the FISH I had last year definitely had that information.
Sofia, A CLL diagnosis is the result of an Immunophenotype Flow Cytometry test showing the presence of clonal B-lymphocytes expressing CD5, CD19, CD20(usually dim), and CD 23. In countries other than the USA, FISH testing is hopefully done prior to treatment, to check if 17p del is present. TP53 testing should also be done, but sadly, these tests aren't even done regularly in the USA, hence the CLL Society's much needed "Test before Treat" campaign. This testing means the patient can be given a more appropriate non-chemo treatment, IF that is available, which may not be the case in Morocco. Many of us have FISH test results reporting a 'Normal Karyotype', which just means that the cause of the CLL wasn't picked up in the limited number of probes used in the FISH testing kit used.
Mkawass,
It appears that your father's CLL is particularly sensitive to treatment, hence the Tumour Lysis Syndrome with his first CLL treatment with FCR. Without having more information on his prognostic markers, we can only speculate on why he responded so well to treatment. One possibility is that your father may be in the small percentage of people with CLL that brightly express CD20 on their CLL cells, which means that they respond brilliantly to anti-CD20 drugs such as Rituximab. As GMa27 touched on, it is now usual to give a non-chemo treatment after a first chemo treatment (of, for example, BR or FCR), but that's only a recent change and only possible in some countries, where the more expensive non-chemo treatments are becoming available. It's otherwise quite standard to repeat the same chemo treatment, particularly after a remission lasting 8 years, even more so when only one cycle was given in the first treatment. So your father's doctor followed well accepted practice for his second treatment. If remission after FCR only lasted up to a couple of years or so, then a different treatment would be tried.
While your father has done very well on just a few cycles of FCR and BR in total, we know from decades of statistics that remissions from BR do eventually end, but that could be five or more years away. If your father gets to the point of needing further treatment, do see if you can again get some input from M D Anderson doctors. If his platelets don't recover, it could indicate that he would not do as well on FCR or BR in a future treatment. If I am right about him having bright CD20 CLL, he could do very well on just Rituximab.
Thanks for sharing the encouraging news about your father. It will give hope to many members approaching treatment in the many countries where BR, FCR and other, older chemo treatments are all that is available.
Thank you folks for the input. My father has been approved for Ibrutinib from his insurance but he is not using it right now since he is in remission. We do have Ibrutinib, acalabrutinib and Venetoclax...The FISH test also showed no TP53 mutation. FISH testing at least in Morocco and France, is always done prior to treatment.By saying "brightly express CD20 on their CLL cells", you mean he has more than average CD20 on the CLL cells?
More and more patients in Morocco now are on Ibrutinib. The insurance over there fully pays for it, no copay nada. But my father could not get on it immediately due to some insurance bureaucracy that would have taken time to get it approved while his lymphocyte count was rising and rising.
" it could indicate that he would not do as well on FCR or BR in a future treatment. If I am right about him having bright CD20 CLL, he could do very well on just Rituximab." I will get in touch with his doctor and see what kind of tests we can do to verify this. If you know, please let me know.
In response to your questions, yes bright CD20, as opposed to dim CD20, means a higher expression of CD20 on the CLL cell walls, so that they are more strongly targeted by Rituximab or newer generation anyi-CD20 treatments, such as Obinutuzumab or Ofatumumab. Obinutuzumab is approved for use with Chlorambucil by the USA's FDA, but Chlorambucil is a very old chemo treatment. Some US specialists use "off label" Rituximab or Obinutuzumab monotherapy for CLL
The Immunophenotype Flow Cytometry test used to diagnose CLL reports how much CD20 is expressed by CLL cells. Repeated use of anti-CD20 drugs selects for dimmer CD20 expressing CLL, so the effectiveness of this treatment may reduce over time, but it could have the attraction of a limited treatment time, compared to the other approved treatments in Morocco. It's good to hear that France and Morocco both recognise how important it is to repeat FISH and TP53 mutation testing directly before any future treatments. The TP53 test is a separate test to FISH testing.
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