Fairly new here and curious... If I am 13q and mutated, is it still possible to also acquire 17p down the line? Or does the mutated help?
Possibility of gaining 17p: Fairly new here and... - CLL Support
17p deletion can occur at any time, but is more likely to develop with chemotherapy treatments, due to selective pressure (termed clonal evolution). The IGHV mutation status doesn't protect against it, but I believe it is more likely to develop while on watch and wait if you have a complex karyotype (multiple deletions).
I expect you are right. IGHV mutated CLL should correlate with a slower progression time, even with 17p deletion. The 17p deletion becomes relevant should treatment be needed, as chemo based treatments are unlikely to work.
Adfendum: See the 2013 paper referenced by Chris below for a study confirming that on a small number of cases.
Here is a good look at IGHV mutation and aggressive FISH markers 11q and 17p.
Yes, I would imagine that the results for the research would be different now with the new therapies.
About a year ago, my husband's FISH test showed him having 17p along with a potpourri of abnormal chromosomes; however, he was tested later as being IGHV mutated. Trying to sift through the information and understanding how it applies to him has always been a challenge since very often information is generalized.
I had to smile when I read the opening statement of the article, which says 'Limited outcome data exist for patients with chronic lymphocytic leukemia (CLL) with a poor-risk cytogenetic profile and a good-risk (mutated) immunoglobulin heavy-chain variable (IGHV) sequence.' That pretty much captures the problem!
Even though the article pre-dates novel agents, it does help a lot regarding his iGHV status but it is important to remember the treatments have changed a great deal and so would the results, which I believe would be improved.
I had a FISH in September last year which showed no abnormal markers (IGHV not tested) prior to chemo immunotherapy treatment, as it turned out the treatment had to be postponed due to developing a serious osteomyalitis condition in my tibia just a week before starting. I was on high dose antibiotics for the next 6 months by which time I was badly in need of treatment for the CLL, another FISH was conducted which came back with a TP53 mutation marker and as a result I was able to access Ibrutinib. So it is possible for this marker to develop during the course of the disease progression and why it is important to have an up to date test prior to treatment even if a previous test has been done.