hello. I'm new to all this.
I had CLL with anemia, neutropenia and felt like death but no night sweats at age 42.
then it went into remission, asymptomatic, normal blood counts.
has anyone had this happen and then have it come back?
Were there any lingering symptoms in between?
How does it exhibit when it returns? Are there signs before it reveals itself in blood work?
Hi B12life,
There have been 8 previous posts on Spontaneous Remissions see:
healthunlocked.com/cllsuppo...
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Not certain you will find much about CLL then re-emerging, but if you do, please post it as a reply to this discussion.
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Len
In this UK study of 20 people who experienced spontaneous remission, subject CLL20's CLL returned.
ashpublications.org/blood/a...
Neil
The report calls it "regression", I'd style it as "CLL in abeyance". Just as your charts of ALC shows some can trend downwards.
"All spontaneously regressed tumors were IGHV-mutated", 11/20 were what would be classed as "highly mutated", <94% match to germline.
They all still had and have CLL cells, with the median 92% of ALC. This high proportion of CLL cells means the normal B cell population is very small <10% of normal.
13 have complete regression to normal ALC, 6 have a partial regression to ALC <25. Only one has "relapsed" after 14 years regression.
Good question. I thought that a spontaneous remission is a "miracle happened" and the person is cured. Unfortunately it looks like he isn't. The study shared by Neil mentions
"genetic and microenvironmental interdependency".
I'd add the macroenvironment to this.
This is called epigenetics.
We might have certain genes but they don't necessarily determine our fates.They can be switched on/off and express themselves or not.
Evolution as a consequence of mutations goes like this :
Genotype+environment+stimulus+random chance=phenotype (quote from "Gene", by Siddhartha Mukherjee).
I guess we are a phenotype!
That didn't answer your question but at least I did my morning mental exercise 😀.
Can we change the phenotype by changing some of its deciding factors?
We can change the environment and the stimulus, plus hope for a favorable random chance.
Hi
What do you mean when you say ,”change the environment and the stimulus “?
Thanks
Hi, what I mean is that a change of environment can mean a change of stimulus. Less smog- better quality air-less chance of a random mutation due to inhaling a carcinogen causing lung cancer, for example. Same steps: less alcohol and fructose lead to lower chance of cirrhosis. Genes can be influenced by the inhalation and ingestion of toxins. Which can cause mutations. They can be influenced by the avoidance of toxins and the ingestion of nourishing foods that contain essential nutrients. Then, radiation exposure is more likely than not a bad thing. Etc.
CLLpa -
> "change the environment and the stimulus “
Have you ever wondered how muscle cells can be so different from blood cells or nerve cells, etc.? They all have the same DNA in the nucleus. What makes them different is which genes are turned on and how much they express certain proteins.
There are 2 types of genes - those that ultimately produce protein and those which control the turning on or off of the ones that produce proteins. The latter have multiple types - promoters, enhancers, silencers, and insulators.
medlineplus.gov/genetics/un...
There's also multiple pieces of RNA floating around inside the cell like screw drivers, spanners, wrenches, and hammers to be used at just the right (or wrong) time.
In addition, as the cell type is established during development after conception, molecular tags (methyl and acetyl molecules) are added to sections of DNA, rather like bookmarks, that make those sections of DNA easier or harder to be unwound, copied to RNA, and then expressed. Those tags begin the process of epigenetics.
medlineplus.gov/genetics/un...
As cells get stressed or receptors on the surface signal a change of conditions, epigenetic changes happen to that cell and probably cells surrounding it. Those receptors and conditions around the cell are the microenvironment. There may be some links between the microenvironment and the environment outside the body, but they are by no means obvious or predictable in most case.
For CLL, the microenvironments in lymph nodes, spleen, and marrow are intensely studied to find out why the cells like to hang out there and what stimulates growth or death. This is not something we can do via blood tests. It requires biopsies and analysis of multiple kinds of cells besides the blood cells. It boggles my mind that anyone can keep track of all the Rube Goldberg chains of reactions.
smithsonianmag.com/history/...
Much begins with the CD's we see on Flow Cytometry, which determine the fate of each type of cell starting with stem cells in the marrow, and let us sort the cell types easily. Then the cells begin to interact, signal each other by grabbing receptors, emitting or sensing cytokines in response to infections and our own biome.
pmc.ncbi.nlm.nih.gov/articl...
A physical wiring diagram for the human immune system
Nature. 2022 Aug 3;608(7922):397–404.
In the end, CLL cells can differ from each other, depending on where they are and what other cells they come close to, plus all those cytokine molecules that let the system signal that a particular type of infection has reached a certain point. I visualize it as weather systems in my body, which is itself a planet. Clouds and rain and snow make things grow or go dormant for awhile. Some changes become permanent - mutations that ultimately lead to our FiSH type, among other things. and the rate of replication and resistance to other parts of the immune system and to drugs.
=seymour=
Spontaneous remissions do occur for a variety of malignancies. I've personally seen it in three people, two with metastatic renal (kidney) cancer and one with prostate cancer. There are scattered reports in the medical literature of this in many other tumors, Whether it is an activated immune response (tumors have the ability to avert the immune response) that eventually recognizes the tumor as foreign and destroys it, or some other process is unclear. The immune response theory is held by many and is consistent with current approaches to cancer treatment using reprogrammed cells, or antibodies, or small molecules to enhance or activate our immune responses.
yes. I had FCR, then BR, then Ibrutnib, then V&O. After a year on V&O I was in remission that lasted just a short of 1 year. I had V&O again but it didn’t work. Now on Brukinska. So only achieved remission once and it didn’t last a year.
My 2 cents: remission is a bit overstated. Our numbers may suggest “remission” but in reality our disease is call Chronic Lymphocytic Leukemia for a reason. It’s a chronic disease that we hopefully control.
I've been on Ibrutinib for 6 years and have recently been taken off due to some other issues. I'm doing well so far, but my oncologist tells me I may be fine for months or even years, but it will come back at some point.
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Anyone gone off Acalabrutinib and experienced lasting remission?
