This study is about 6 months old, but I'm posting this very good article about epigenetic changes discovered in CLL...that drives this cancer.
Originally researchers thought there were 1000 changes, but this study has found a million changes...
The complexity and number of DNA changes in CLL is staggering... what was believed to be 'junk' DNA has found out to be encoded.
Really interesting Chris, so it's not just the identifiable genomic mutations of DNA but also the areas described previously as junk DNA in combination with the possible epigenetic mutations in the programs that implement this genetic information that effects how CLL performs?
It's a massive picture and all of a sudden a lot of avenues to explore were revealed (that's a lot of questions). Am I right in believing that it is the study of these epigenitic functions and mutations that is aiding research into therapies that target pathways in autophagy for example. Resulting in discovery of novel agents such as the the small-molecule Sirtuin inhibitor Tenovin-6 recently being developed by Scottish researchers? cllsupport.healthunlocked.c... .
The scale of all this is so enormous, perfect and of such unimaginable complexity it is amazing that this all came about through evolution. we are trying to unlock this in a passing moment of time.
Think of a million light switch on a wall...OK a very long wall. Some are switched on and some are switched off... There is probably a number of correct patterns of which switches are on and off, but in CLL these switches could be on and off at random. Something changes the pattern. Perhaps we inherit changes, perhaps gamma radiation turns switches off and on, perhaps viruses set up shop and 'play' with the switches, make patterns that fool our immune systems...maybe plastics and our chemical soup disable switches?
From this it is not hard to believe that each CLL patient has their own version of CLL.
Then...we know we have telomere shortening...these are the, 'junk' ends of chromosones, but now the question arises...are the ends really junk? So if the ends are shortened, what negative effect does this have...??
Combinations and permutations that boggle the mind...
A massive game of naughts and crosses with potential many players playing and changing the game together and the game is always altering shape and the rules keep changing,
Not only do we have our own version of CLL it also evolves.
Dr Chris Pepper of the Cardiff CLL research group discussed his work with Telomeres at the Cardiff CLLSA meet in January.
Telomere length can identify prognosis of CLL patients. CLL patients that have shorter telomeres have more progressive or aggressive CLL. As telomeres shorten the chromosome ends fuse together dislocating information. this is clearly visible when a genome is sequenced.
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Yes. A lot of questions! It's getting harder and harder to explain to others, just what CLL is......sparkler x
Good job we have some of the greatest scientific brains in the worlds cancer research communities on the case and they are making headway. there is much to be hopeful about.
Happy Easter. 
Science rules.........and Easter Eggs too!!!! X
Its only this type of research that will provide answers but the more researchers find out the more there is to know.
For people just now finding this thread, AussieNeil started a new thread on epigenetics based on another excellent article from The Conversation:
healthunlocked.com/cllsuppo...
It has further links to resources of interest.
Following LeoPa's “On CLL, diet and possible connections.”
Real-World Study Shows Limited Implementation of Reccomended Biomarker Testing in CLL
CLL Tracker - Patient Data
in our discussions about cause of CLL 
