"13q deletion (13q-) is the most common cytogenetic aberration in CLL and it is usually associated with the most favourable prognosis as a sole abnormality. However, recent
studies have shown that CLL patients carrying higher percentages of 13q- cells have more aggressive clinical courses"
New study looks at 13q deleted CLL and found two groups...
This follows on from research that looked at deletion size and RB1 gene involvement, which indicated a more agressive type of 13q deletion.
Now, Chronic lymphocytic leukemia patients with higher percentages of 13q- cells (>80%) showed a different level of gene expression as compared to patients with lower percentages (<80%, 13q-L).
This study found that cases with a high number of 13q- cells (13q-H) had both shorter overall survival and time to first therapy. The goal of the study was to analyze the genetic profile of 13q-H patients.
The study went on to find that apoptosis, proliferation as well as miRNA regulation are involved in cases with higher percentages of 13q- cells.
Not so much 'Breaking News' but yet more proof that some other similar research was correct. From memory this might be the third or fourth proof of this research and that of course is important as not all research stands up after more tests are done.
Importantly it goes to show that we must ALL have a FISH test performed so that we can have some ideas of our longer term prognosis. Remembering that a FISH test often changes due to clonal evolution.
Thanks for posting, useful confirmation of this research
Thanks for your reply. Yes your point is valid, I will change the Breaking News Blog title to CLL Research News Blog. I am pleased you found the post of interest.
Actually, this is fairly new. Certainly deletion size has been studied and miRNA15a et al involvement as well as RB1 gene, DLEU1 and DLEU2 gene continuity, single double alleles etc, but this is the first time to my knowledge, that high and low numbers of cells and an 80% cutoff has been asserted.
There is no indication this is clonal evolution....evolution is defined as secondary markers appearing, often 17 p, 11q, and possibly subclones like BIRC3, SF3B1, NOTCH1.
Certainly these are early days and further studies are required to confirm these findings, but it underlines the complexity of CLL, and that even 'good' markers can have a more aggressive side. Hopefully FISH testing will fade away soon to be replaced with whole genome testing on the clinical level.
Chris thanks for your explanation where this study is novel. So that different research materials can be discussed removing breaking news from the science blog will keep me out of deep water. ( :
The good markers may also be covering for others perhaps numbers are also very important to keep others at bay?.
There seem to be layers of complexity that are being unraveled,. Clever clinical scientists are busy working on the relationship between clonal mixes and competition keeping the disease at bay suggesting there is clonal interference when; “co-existing clonal populations may limit each other’s growth by mutual competition.” .
It is improved sequencing in the future that may be used to detect if a more aggressive clone may emerge after therapy that is present pretreatment at a low frequency. So it’s may not just be numbers that may be important but the mix?
We've been discussing the recent paper by Dr Anna Schuh this original paper, and a commentary describe and discuss evidence for, and implications of, multiple clones of CLL cells in a given patient.
COMMENTARY:
"CLL clonal heterogeneity: an ecology of competing
subpopulations"; Catherine J. Wu; Blood 2012 120:4117-4118
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