I was exploring some posts to understand why 13q deletion is good when it occurred to me that I don't know why any mutation would be good. Why is "being mutated", which I am, considered good? Thanks in advance. Just curious
why is mutated good?: I was exploring some posts... - CLL Support
why is mutated good?
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Vlaminck
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lankisterguyVolunteer
Hi Vlaminck,
The short answer to your question is that statistics have shown that having a single clone of CLL cells with 13q Mutated results in a slower growing population of cancer cells than having "Normal" UnMutated CLL cells. The exact reason is not well understood.
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Here is a (moderately challenging to read) paper that digs into what and how these are tested, but the why is elusive: ncbi.nlm.nih.gov/books/NBK5...
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And another view of the Mutated vs UnMutated and other genetic factors in CLL as measured by the speed of progression to needing first treatment: ashpublications.org/blood/a...
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If your eyes have not glazed over yet, here is a third study result: nature.com/articles/s41375-...
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Sorry, I cannot provide a simpler clearer synopsis.
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Len
Len, you're great. I look forward to giving this reading a try,
Thanks, Len. Trying to read these articles reinforces my gratitude to you and all those on this site who volunteer and share their knowledge and understanding with us. I couldn't make head or tail of them!
Hello Vlaminck. I think with respect to FISH mutations, 13q mutated is “good” only in a relative sense. It’s “good” compared to the other type chromosomal mutations associated with cll that are known to act more aggressively. It would of course be better to have no chromosomal mutations, including no 13q. Some people get offended when cll is called the “good” leukemia. That just means to me that among the types of leukemia we can get, Cll is more treatable with longer average survival than the other types.
All chromosomal deletions involved the deletion of certain genetic material on a specific chromosome. The genes we have on the q arm of the 13th chromosome are not as critical cancer fighting genes as the gene located on the q arm of the 11th chromosome (the ATM gene) and the gene on the p arm of the 17th chromosome (the TP53 gene). 11q and 17p cll tend to be more aggressive because of the important cancer fighting genes lost in the deletion.
What can get really confusing is when they talk about people with IGHV mutated cll doing better than those with unmutated cll. To me, and I don’t understand it really well, this type of mutation is much different than a chromosomal mutations. Chromosomal mutations create abnormalities in genes that stop them from working correctly.
An IGHV mutation might be better understood as a B cell going through normal evolution during its life cycle. Our cll typically starts with one bad b-cell which makes a trillion copies of itself. Cll cells that go bad later in their life cycle have had time to have more changes (mutations) in the ighv region of the cell, which for reasons not fully known make treating mutated ighv cll easier than unmuated. I could have this entirely wrong, but I think the “mutations” in IGHV are just normal evolution in the life of the cell, while chromosomal mutations are abnormal mutations. Thats why being IGHV mutated is good, and having chromosomal mutations is not. Among the main types of cll, some mutations like 13 q tend to be less aggressive than others, like 17p, because of the genes involved.
thank you, cajunjeff. Never ever knew what you said re 13 q because when first diagnosed and did the whole testing thing, my doctor said I had 13q deletion "which is good." So I thought somehow this deletion actually made things better. I didn't quite follow you about the IGHV mutation, but haven't yet read the links Len has attached.
I remember reading a long post some years ago (pre-pandemic) that was like 'CLL For Dummies', which I really appreciated! Pretty sure that post was by you, Jeff?
Anyway, the clearest note I remember from it was a description of 'mutated' and unmutated' in the context of the lifecycle of antibodies. The upshot was that 'unmutated' antibodies hadn't developed the hooks for latching on to foreign bodies in the bloodstream, which rendered them ineffective, whereas 'mutated' antibodies do have the hooks and behave normally.
Highly simplistic, but very useful for a novice CLLer, I thought! Don't know about 13q, though.
Was it you, Jeff? Did I remember it correctly?
thanks, interesting way to put it and to think about
I am 13q mutated. Very good to have. Was on W&W for 12 years & now 6 years remission. 3 chemo treatments. Uneventful. Good question.
I think this article is discussing ighv mutations on b-cells. Mutated ighv is better than unmutated ighv cll.
Thats very different from a 13q mutation, or deletion, where genetic material is deleted at the q arm of the 13th chromosome.
It’s not good to have a deletion of genetic material at 13q, that means we have a type of blood cancer. Its only good in the sense that 13 q cll is more treatable than other types.
It gets confusing when some people with cll have a “normal” FISH test and it is said 13q is better than normal.
The issue there is that someone who is positive for Cll on flow cytometry and then normal on FISH still has a genetic mutation causing Cll somewhere, it’s just not a common mutation that FISH can detect.
Put another way, if I have 13 q cll and my wife has no cll at all, who is better off? She is. I would rather have 13 q cll than other types of cll, but I’d much rather have none of the cll genetic mutations that cause cll.
Thats different from ighv mutations.
Oh, I have been under the misunderstanding, of there being more than just the one mutated/unmutated status. Can you or anyone else point me to an article that explains this?
I'm going to have to get very remedial on this subject with myself. I mistakenly thought all CLL B-cells were either growing as a bunch of mutated/unmutated cells, and that the genetic breakdown 13q, 17p, etc. were just like different flavors of degenerate B-cells.
So, if I have this correct from re-reading your comments, there is IGHV mutated /unmutated status, and then chromosomal mutation happening in CLL?
First, I want to thank you cajunjeff and I also want to apologize for any confusion first to Vlaminck for any confusion I may have mislead you, and the rest of the readers of this post, my interpretation of the mutated/unmutated status and how it applies to CLL is in error.
I think you are right in that with cll we have an ancestor b-cell gone bad which then divides and multiplies. B-cells create antibodies to fight illness. As I understand it, b-cells have to go through a growing process to learn how to create antibodies.
The thinking is that if that b-cell turns cancerous in its early stage, before it has learned its function, that is an unmutated cll cell. All divisions from this cell will be unmutated as well. IGHV is the area on the receptor of a b-cell that undergoes change as the cell matures. That maturation is called a mutation, which is more an evolution of the b-cell. Call the cells evolved, mature or mutated, it just means the cells was more functional as will be all cells divided from this cell.
The author of the original post was talking about 13q, which is a chromosomal defect. The question was whether 13q mutated is a good thing. It’s really semantics. I dont think too doctor was implying 13 q is good in the sense that this mutation fights cancer. The doctor I would think was rather saying that if you have to have cll, 13q is best.
Thats different from ighv. While most people who have 13q cll as their only defect also have mutated ighv cll, some do not. You can be 13q and have unmutated cll. They are both different markers. I think even with unmuated ighv cll, that being 13q is still the best. If one has 13q cll, however, and acquires 11q or 17p cll, I think the benefit of 13q gets trumped. FiSH status can change over time, IGHV status usually does not.
"You can be 13q and have unmutated cll".
Which is what I think I've understood it to be for me. The Dx report put my range of mutation at 0% and in the next statement it said 0% -2% is considered unmutated. So at that point, if I understand what I'm reading they were saying, "here's the gene aberration...there are less than 2% mutations to it". Not, "you have B-cells that are (not ?) un-mutated regarding working as protectors in my immune system".
Maybe it's just me, tomorrow I'm getting these two kidney stones removed, I'll re-read this all as I rest up the following day and maybe I'll be clearer.
Thank you, cajunjeff for your kind reply. Time for me to shut down for today.🙂
Hello Spark_Plug
I for example am 13q deleted and IGHV unmutated at 0%. The percent of 13q deleted will change as your CLL progresses. My first FISH testing showed 13q deleted 38%, then 53% and right before treatment it was 87%. Yes, IGHV is considered unmutated if testing revels less than 2% mutation. I am going to call them helper mutations. 2% and above is considered mutated, however when tests show 97% and above it is called hypermutated. It is my understanding that hypermutated is being studied to determine if it is advantageous or not. Doctors consider 1% to 4% mutation a guessing game. Due to my 0% unmutated status, I have very aggressive CLL, I doubt that 13q deletion was much help. My first treatment was B+R. Being unmutated gives average remission of 3-3.5 years and mutated gives average 5-year remission.
Hey, Cajunjeff, you say that 13q deletion means blood cancer. So do people who undergo treatment and, for a limited time, become cll free -- do they still have 13Q deletion?
Vlaminck, to my understanding, some people can get such a deep mrd undetectable remission that this FISH test becomes negative for any chromosomal defect associated with cll, including 13q.
Mrd undetectable just means that with the most sophisticated testing means they have to look for cll, it can’t be found. Unfortunately even with such promising mrd results, our cll often remains with us and will eventually return. Then again, despite the narrative that cll is not curable, some people do stay in such long remissions that they are very arguably cured. That result has been more likely with people with mutated cll who have undergone fcr chemo. Fcr is nevertheless being phased out in some parts of the world because of its harsher side effects.
Mutation of IgHV is considered good as it has a slower proliferation rate. It's thought to be an older B-cell. Being old it progresses like a geriatric.
Unmutated IgHV has a faster proliferation rate and is thought to originate from a younger more vigorous cell.
All the clones retain the memory and age of the original, they aren't reborn or rejuvenated by the cell division.
At diagnoses there is about a 50/50 split between IgHV mutated and unmutated. At first treatment this becomes 35/65, for R/R trials it can become 20/80. Most of those that never need treatment but remain in W&W for life are IgHV mutated.
It has been found (FLAIR and GLOW trials) that IgHV mutated is harder to treat with fewer getting to or taking much longer to reach uMRD4 and complete response. While IgHV unmutated respond quicker and deeper. To confound this the lack of response has little bearing for IgHV mutated as they have longer treatment free remissions than unmutated after short duration treatments. This is such a strong effect that IgHV mutated nearly nullifies a bad TP53 mutated Dx (CLL14 and CAPTIVATE FD trials).
(At first line treatment about 7% of IgHV mutated are TP53 mutated v's 15% of IgHV unmutated.)
Some interesting points Skyshark.
Can you ref the data from those trials, illustrating M-CLL (mutated IGHV) to be harder to treat? People may find that surprising, as U-CLL (unmutated IGHV) is regarded as a negative prognostic factor.
I read somewhere a theory that M-CLL is more indolent because, compared with U-CLL, its modified BCR binds less well to auto-antigens that promote CLL progression. I guess the difference in binding could explain the difference in response to (some) treatments?
FLAIR trial, appendix Figure S4, B&C overlaid. u-CLL is the upper line with more patients reaching uMRD earlier and discontinuing V+I sooner than the m-CLL lower line. As the protocol was continue on V+I for double the time taken to reach uMRD about 55% of u-CLL reach uMRD in 12 months (13 cycles) compared to 40% of m-CLL. Ratio 1.37 in favour of u-CLL. This demonstrates u-CLL responds better to treatment than m-CLL.
FLAIR report and supplementary appendix. (nejm is free to sign up and these are free reads)
nejm.org/doi/full/10.1056/N...
nejm.org/doi/suppl/10.1056/...
Finding from GLOW for 15 cycles fixed duration V+I. 71% of u-CLL (40/(40+16)) reached uMRD4, 54% m-CLL ((58-40)/(58-40+31-16)). Ratio 1.3 in favour of u-CLL and quite similar to FLAIR. Reports that m-CLL don't need to reach uMRD to have a good progression free survival time. While for u-CLL reaching uMRD on V+I is a very strong prognostic for progression free survival time. Using MRD m-CLL don't actually respond to treatment as well but do better than u-CLL which has led to m-CLL being considered "easy to treat".
In the Ibr+Ven arm, for patients with unmutated IGHV (uIGHV; n = 67) and mutated IGHV (mIGHV; n = 32), 54-month PFS rates were 58% and 90%, respectively.
Also in the Ibr+Ven arm, PFS rates at 3 years post-treatment were 82% in patients who achieved uMRD at 3 months after end of treatment (EOT+3; n = 58) and 73% for patients with dMRD (n = 31). Among patients with uIGHV, PFS rates at 3 years post-treatment were 81% for those achieving uMRD at EOT+3 (n = 40) and 56% for those with dMRD (n = 16). In patients with mIGHV, PFS rates at 3 years post-treatment were ≥ 92% regardless of MRD status at EOT+3. Overall, at 38 months after end of treatment (EOT+38), 32.1% of patients had uMRD in the Ibr+Ven arm. Of the patients who achieved uMRD at EOT+3 (n = 58), 53.4% sustained uMRD status at EOT+38 in the Ibr+Ven arm.
ashpublications.org/blood/a...
(LINKS FIXED)
FLAIR I+V discontinuation = 2x time to uMRD
Fascinating detail, many thanks. But Fig S4 ??
Fig S4 A is on page 29, B&C are on page 31 of the linked to supplement appendix.
Now I see the problem. Your two links are not for the FLAIR study so I was looking at a different Fig S4.
Seem to have the wrong tags on my bookmarks. Edited the links, should work now.
Thanks
I just wanted to add this - I’m 13q and needed treatment within 5 years. So if/when you hear from many you may never need treatment or it may be decades, it isn’t always so. I also had so many side effects/adverse events from Ibrutinib, Acala and Zanu that I stopped my first treatment after 1.5 years. Not all of us with 13q do better than so many others.
Very true and fully agree.
To your original question re why is mutated better than unmuted - I was given a very simplistic explanation early on. When you are mutated, you know what has happened or how your disease has changed. When you are unmutated, this has not happened but could at anytime, thus the “fear of the unknown”. While I cannot always understand the intricacies of this topic, this explanation makes a bit of sense to me. Probably not technically correct , but it works for me. I am 13q unmutated. 13 q status is a good thing, while the unmuted status shows we don’t know how or when it might mutate.
BeckyL USA
When I was first dx'd in 2015 and my CLL specialist had my various labs & test results, I asked him to explain things as simply as possible.
He said unmutated means the CLL cells in question finished "cancer school" and were primed and ready to do their dirty work. The mutated cells were cancer school dropouts and most likely not as strong or efficient.
After I was diagnosed and found a CLL forum, a member called CLL the stupid cancer. It was in comparison to other types of blood cancers. Your CLL specialist's explanation confirms mutated CLL as the poster blood cancer for stupid, in this context.
Other way around 
The confusion about whether mutation is good or bad is arguably because of sloppiness in terminology:
1) FISH testing checks for gross mutations - deletions, additions (trisomy 12).
2) IGHV somatic hypermutation, measures whether the genes responsible for the immunoglobulin incorporated in the B Cell Receptor (BCR) on chromosome 14, have gone through deliberate somatic hypermutation to produce a different BCR to that produced from the lymphocyte stem cell. Somatic hypermutation occurs in the germinal centres in our nodes in response to infections or vaccinations. It's how we make the mature B cells (plasma cells) that are able churn out all the thousands of different immunoglobulins to counter all the bugs we've been exposed to in our lifetime. So 'mutated' IGHV is theoretically more mature. To complicate this, in the last 5 or so years, another theory has become prominent; that the degree of IGHV mutation is a measure of the ability of CLL to properly correct DNA mutations that have occurred during CLL cell division.
TP53 is a finer check to see if the CLL TP53 is wild type, that is, as inherited, or has had some mutation.
Neil
To further complicate things I remember being told by a hemotoligist that I have the good 13q on my side right now but that can also change after treatment so that is also a reason not to treat until totally neccessary? I seem to remember that we could lose that 13q fighter after treatment?
13q cll is not a fighter of cancer, its just a less virulent strain. It’s definitely not on our side, my 13q cll caused all sorts of problems for me.
It is true that over time we can have worse types of cll evolve, and that can happen with or without treatment.
Some people who took fcr as a treatment did see more difficult to treat types of cll develop, so yes, that’s one reason we wait to treat. There is another school of thought out there with the newer drugs. That would have people treating earlier with combinations of drugs like venetoclax and ibrutinib with the theory that our cll can be hit early with a one-two punch before it evolves.
I think there are some trials looking at that, but as of now, watch and wait is still the standard. Here is a dummy post I did on clonal evolution. Cll cells are alive, and just like most everything else that lives, they will resist being killed and evolve or mutate to stay alive .
Vlaminck,
My interpretation of the data on 13q mutated is that 13q shows better outcomes and response measures across all metrics.
A Cll diagnosis is never good, calling a bad thing good is just part of the numb prognostic linguistics that the profession has become used to stating.
ncbi.nlm.nih.gov/pmc/articl...
Yet as we know, there are no absolutes with cll and each one of us is an individual with individual measures.
JM
Vlaminck -
Mutation only means "changed," but it got a seriously negative connotation in the context of cancer as well as inherited mutations that cause disorders and diseases like Down syndrome and Cysitic fibrosis, Sickle cell anemia, Tay-Sachs disease, Huntington's disease, etc. Nobody thinks of the sudden appear of a new talent in a family that has few talents as being caused by a mutation. But it can happen. It's just hard to prove so far. So mutations are not inherently bad.
With CLL, usually the word "mutated" added to the end of a FiSH is short for IGHV mutated, and doesn't refer to the FiSH type itself.
We may have been taught in school (or our kids may have been taught - some of this was discovered after some of us grew up!) that every cell in the body has identical DNA. This is an oversimplification, and completely untrue for a variety of reasons that we learn about in biology classes.
One major reason it's untrue is that several genes in our B-cells and T-cells constantly mutate on purpose to try to match invaders (antigens). They call this repeated mutation, "hypermutation." Those mutations take time. If the B or T fails to match an antigen, or if it matches one of our own cells, it's supposed to die automatically. The mutations in B-cells are what eventually lets the plasma B-cells make serum antibodies in the blood. But before that, those antibodies are bound to the B-cell tightly, and they call it a BCR - a B-cell receptor.
One of the genes in the B cell that automatically mutates is the IGHV gene - the Heavy Chain Variable Region gene. There's other genes that automatically mutate as well, but it was simpler and cheaper to focus on just IGHV for the test. If IGHV has not mutated at all, we would call it "germ line," meaning it matches the copy in most of our other cells.
The test tries to calculate a percentage mutated figure by looking at each DNA base pair, and comparing it to a hypothetical germline copy. The cutoff is usually 2%, which is actually thousands of base pairs changed out of hundreds of thousands. The people who score right at the cutoff are a matter of study, because their outcome varies more. But a 2% mutated IGHV gene is actually very early in the hypermutation process, and the cells mutated that much don't make copies of themselves as fast as one that's, say, 10% mutated. So the CLL doesn't progress as fast. But there's other variables, too, like FiSH type.
=seymour=
It should be noted that IgHV is a cell surface immunoglobulin, not DNA. The various CD markers (cluster of differentiation) are cell surface proteins found by cytometry. While FISH for 11q, 13q, 17p, Tris +12 and NGS for TP53, ATM, SF3B1, NOTCH1 etc. are testing cell nucleus chromosome DNA.
This is an early report for CLL14. It found that for chemotherapy (Obinutuzumab and Chlorambucil) del(13q) was comparable in response to "normal" (no del() or Tris in chromosome DNA). Mutated IGHV was preferentially found in patients with del(13q) (Odds Rate, 3.20; P < .01). Many other markers (indicated by *) except for MYD88 are more associated with IgHV unmutated. The novel targeted therapies have removed nearly all poor prognosis for markers except for IgHV unmutated (not yet apparent in this report for 28 months) and del(17p)/TP53mut.
ashpublications.org/blood/a...
CLL14 trial incidence of genetic markers
To quote a Brave AI answer, IGHV testing "involves the amplification of the IGHV gene using polymerase chain reaction (PCR) and subsequent sequencing of the variable region of the gene. The sequencing analysis is used to identify somatic hypermutations in the IGHV gene, which are associated with a better prognosis and response to treatment."
The resulting immunoglobulin is expressed in the CLL B Cell Receptor, but that's not what's assessed.
Neil
Skyshark -
The genetic nomenclature is often confusing, because the proteins are often named the same as the gene. So we can speak of the IGHV part of the BCR (B-cell Receptor) chains of protein molecules, and show them in a diagram as the inner, top part of the Y shaped BCR. Or we can label the many (123? 129?) IGHV genes on a diagram of Q arm of Chromosome 14, and pick one to show how the process that DNA goes through to re-arrange (mutate) to match the zillions of possible antigens.
How they worked out all the locations and the process of how the DNA automatically and repetitively mutates is beyond me at the moment. It was surely a genius bit of research.
When I first got tested back in 2013, the nomenclature called the gene IGVH, with the V first. I think around 2019 most authors came around to calling it IGHV. See my reference below (albeit in mice and not humans).
There were also arguments about TP53 vs P53, and existing confusion about deletion of the entire TP53 that happens with del17p FiSH type vs. a mutation in TP53 that could be a deletion of as little as a single base pair out of thousands - or an insertion or a translocation of base pairs. I doubt that most hematologists can adequately explain FiSH plus cytogenic results. Textbooks have trouble keeping up.
Arguments about gene naming started back in the 60s or early 70s, and continue at this very moment. I think this confusion holds back science a lot, because we cannot easily do a search for all the possible variations in a gene name. AI will surely stumble over this!
The document that tries to make sense of the names and notations is the ISCN (International System for Human Cytogenomic Nomenclature), which used to be called the International System for Human Cytogenetic Nomenclature. The latest was published in 2020, I believe:
en.wikipedia.org/wiki/Inter...
I couldn't afford a recent copy, so I bought a used copy of the 2013 edition to try to understand my NGS report from M.D. Anderson. Even then, it's still a challenge.
=seymour=
References:
ncbi.nlm.nih.gov/pmc/articl...
Nomenclature for Cellular and Genetic therapies: A Need for Standardization
Transplant Cell Ther. 2022 Dec; 28(12): 795–801.
---
ncbi.nlm.nih.gov/pmc/articl...
A Proposed New Nomenclature for the Immunoglobulin Genes of Mus musculus
Front Immunol. 2019; 10: 2961.
Skyshark -
Your points about the association of unmutated vs mutated IGHV with particular FiSH types or outcomes of therapy are valid.
More than Unmutated vs Mutated, I think the IGHV families are getting more focus. Some of us do not receive info about the IGHV family (the 120-130 different IGHV genes on chromosome 14).
ncbi.nlm.nih.gov/pmc/articl...
Association of Cytogenetics Aberrations and IGHV Mutations with Outcome in Chronic Lymphocytic Leukemia Patients in a Real-World Clinical Setting
Glob Med Genet. 2024 Jan; 11(1): 59–68.
"IGHV3 was the most frequently used IGHV family (46%), followed by IGHV1 (30%) and IGHV4 (16%). IGHV5-51 and IGHV1-69 subfamilies were associated with poor prognosis, while IGHV4 and IGHV2 showed the best outcomes. The prevalence of CK was 15% and was significantly associated with U-CLL. In the multivariable analysis, IGHV2 gene usage and del13q were associated with longer TTFT, while VH1-02, +12, del11q, del17p, and U-CLL with shorter TTFT. Moreover, VH1-69 usage, del11q, del17p, and U-CLL were significantly associated with shorter OS."
Notice how the authors bounced around with shorthand - first talking about IGHV3, IGHV1, and IGHV4 families, then about IGHV5-51 and IGHV1-69 subfamilies, then later just VH1-02 (and not IGHV1-02).
At some point, we'll just use NGS for everything that's currently done via FiSH, and then report on how many different clones have which "FiSH" type. We sort of get that now on some FiSH reports, where they may report a percentage of a FiSH type blood sample. But FiSH itself is often limited to only looking as 20 to 200 total cells. ClonoSEQ looks at several million total PBMC's (Peripheral Blood Mono-nuclear Cells - White cells other than Neutrophils, Eosinophils, and Basophils - those 3 have multi-lobed nuclei, which are harder to sort and count). I have tended to say ClonoSEQ finds 1 out of a million WBCs, to avoid explaining the exceptions.
en.wikipedia.org/wiki/Perip...
ClonoSEQ has it's own IGHV test report, by the way. But they only report it on the initial test. I may have mentioned before that there's a possibility that I had both an IGHV Mutated clone and an IGHV Unmutated clone, because my initial test showed Mutated and my long W&W seemed characteristic. Most of us never get a second IGHV test, because the dogma is that it never changes. The assumption is that there was only the original sentinel mutational event. Maybe I was hit by the alien UFO ray on more than one cloudy night!
=seymour=
Bluesinthenight, when referring to IGHV mutation status it is the number of nucleotide changes in the IGHV gene, not the number of cells that carry a IGHV mutation. Take a look at the gene sequences below for the IGHV region in a germline sequence (before hypermutation) and after hypermutation in a clonal CLL cell. The letters in the sequence refer to the DNA nucleotides A = Adenine, T = Thymine, C = Cytosine and G = Guanine.
The sequence I am using as an example is from ncbi.nlm.nih.gov/nuccore/LM...
Nucleotide sequence of IVHG3-7 before and after hypermutation
Thanks for the correction. My post deleted.
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