A recent article. 27 Dec 2024
Somewhat surprising findings, but the trend in SLL inclusion in CLL clinical trials is improving. I suspect some of this is driven by the need to have active disease in the peripheral blood at adequate levels for trial participation.
BigfootT -
I think the move toward MRD tracking for SLL is also an issue, in my opinion. Since there's less CLL in the blood, uMRD status for an SLL patient will probably miss some significant CLL. Yet, the trial I am on at M.D. Anderson does not call for additional bone marrow samples from SLL patients.
ClonoSEQ allows lymph node samples for some diseases, but not for CLL or ALL:
ous.clonoseq.com/wp-content...
I don't know if a lymph node sample would be a full biopsy or if it could an aspirate.
=seymour=
Thanks Seymour. I would think one of the challenges of MRD via a lymph node excision would be that disease burden is not evenly distributed in the lymphatic system. My PETs have shown various hot spots and the largest node is considered inoperable due to its proximity to major arteries. So the node you'd like to excise for MRD may not be accessible.I would think a blood sample has a uniform burden is that also true for bone marrow? Bigfoot
BigfootT -
I was hoping a fine needle aspiration sample could do it. ClonoSEQ ma6 need more of a sample than Flow Cytometry. I think multiple nodes should be checked.
I wonder how much research has been done on the variability of clones in SLL, even FiSH types. I met a person with SLL on Facebook who had a lymph node biopsy that showed a TP53 deletion. They got a second opinion, and a blood FiSH found no TP53 deletion - not even a mutation. So, are they an exveption, or do we all have unique clones or So clones in lymph nodes?
=seymour=
Problem with bi-clonal and poly-clonal CLL is the minor clone can harbour poor genetics that aren't detected or reported.
Example major clone 85% of cells, minor clone 5% and normal B-cells 10%.
If the minor clone has 50% TP53 mutated the overall sample has 2.5% TP53 deleted and this gives a diagnosis of TP53 undeleted. There are still many countries that will treat first line TP53 undeleted with FCR, after treatment the TP53 mutated is the major clone.
I was told by a hematologist regarding my BMB 9 years ago with a 90% infiltration result that bone marrow is fatty and the CLL may not be evenly disbursed. I went 8 years before the doctor started seriously talking about treatment, so the high % of infiltration, I feel must have been localized at the sample site. You could ask your specialist about that.
Yes, I did not qualify for a trial because of limited lymphocyte presence in my peripheral blood. Often it was in the normal range during W & W. Now in cycle 3 of standard V & O treatment.
How interesting! I was DX w/SLL in 2016 at the age of 61 years. After 3 years of W&W, participated in EA9161 (NCT03701282) clinical trial for CLL/SLL (18 month fixed duration, 18 cycles ibrutinib 12 cycles venetoclax & 6 cycles obinutuzumab). Peripheral bloodwork registered in normal ranges by week 9 of treatment (treatment was 78 weeks). Before and after treatment, trial protocol called for bloodwork, bone marrow biopsy &aspiration CT scan, ClonoSEQ ( results were uMRD!). Using different methods of testing, I would think would encourage clinical trials to address both CLL & SLL.
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