Tag: myeloma

“The bone-marrow niche in MDS and MGUS: implications for AML and MM.” Part 2.

/ Margaret / 2 Comments

Back to the Dana-Farber study that I wrote about a couple of days ago.

The section titled “Therapeutic opportunities” is interesting. How to prevent progression, that is. As you can imagine, the chef’s daily special consists only of conventional treatments. For example, the authors make a reference to the Spanish study (Mateos et al) that I have repeatedly condemned here on the blog. The Spanish researchers–some with strong ties to the big pharmaceutical companies (hello???)–tested lenalidomide and dexamethasone on a group of SMM patients. The study claims to have prolonged progression-free survival and even overall survival in those patients…without ever taking into consideration QUALITY OF LIFE. Sorry, but I have no patience for statistical studies that play with people’s lives…

That said, the trend toward early intervention is clearly taking off, as the Dana-Farber study points out. Very unfortunate, IMO.

And there is no way to stop it, except that we, the patients, can say just say NO. Of course, if you have CRAB symptoms, that’s another matter. But, in the absence of the CRABs, WHY TAKE THE CHANCE OF WORSENING YOUR QUALITY OF LIFE?

Makes zero sense.

And there’s another thing that bothers me: where’s the proof that the overall survival of someone with SMM was extended thanks to these conventional treatments? Do the Spanish researchers have crystal balls that give them the exact times of death for their patients, both with AND without treatment? Oh, right, no, that’s what their STATISTICS tell them. Based on the patients’ “high-risk” data (see yesterday’s post).

I’m not saying that statistics can’t be useful in certain circumstances, mind you. But in these cases, when someone with no CRABs is deciding on whether to agree to early treatment, or not!, they can be harmful. If I had agreed to begin conventional treatments in 2005, I don’t know where I would be today (according to my former hematologist, I’d be dead…would have died in 2010…didn’t happen, OBVIOUSLY!!!…I’m still here, still splendid 😉 , still no CRABs, still no conventional treatments…).

Sorry for the rant. Okay, let’s calm down and try to understand the rationale of early intervention from the Dana-Farber study perspective. The researchers say that if the number of osteoblasts (bone-forming cells) can be increased in the early stages of myeloma, myeloma cells cannot proliferate. That’s good to know. There are non-toxic ways to do that, btw, but let’s keep to the study…

Mice that were injected with nanoparticles loaded with bortezomib before being contaminated with MM cells lived longer than non-injected mice. The researchers give another example in which early treatment of an antiangiogenic antibody was used on mice. Okay, but we’re talking about mouse models here. The reality, as the researchers themselves admit at the end of this paragraph, is that “…the use of antiangiogenic agents other than thalidomide and other immunomodulatory agents has not been shown to be successful in patients with MM.”

Not successful in patients.

So much for that.

Then there’s immunotherapy, which we have heard and read a lot about in the last few years. You may have heard about the anti-CD38 antibody known as daratumumab, which activates the immune system.

Anyway, it’s in this paragraph that I found a remarkable admission.

But first, let me say that ever since I joined online myeloma support groups, one of the key issues we discussed was what how to deal with our immune system. Should we stimulate it, thereby possibly stimulating our myeloma cells, too? Or should we avoid anything that stimulates the immune system? The consensus usually drifted toward the former approach. I wrote a post about this in 2013: http://margaret.healthblogs.org/2013/10/20/long-term-survival-in-myeloma-is-finally-linked-to-a-robust-immune-system-and-my-new-discovery/

I’ve had mixed feelings about it throughout the years, but my gut has always told me that it makes no sense to keep our immune system weak.

And here, in this paragraph, I finally have my answer (vindication!!!): “Indeed, trials involving these antibodies provide the first proof of concept that activation of the immune system has therapeutic benefits in patients with MM.”

After years of not knowing what to do, we finally know that having a strong immune system is GOOD.

Quelle surprise…not.

“The bone-marrow niche in MDS and MGUS: implications for AML and MM.”

/ Margaret / 1 Comment

Remember the post I wrote back in December 2014 about myeloma subpopulations and the bone marrow microenvironment? Probably not…so here’s the link: http://margaret.healthblogs.org/good-or-bad-for-myeloma/first-do-no-harm-myeloma-subpopulations/

The main point is that not much is known about the interactions between the myeloma subpopulations living in our bone marrow, how they compete for survival and so on…

Therefore, the only conclusion, in my opinion, is that going in with conventional bombs and blasting the heck out of this microenvironment doesn’t seem to be the best strategy for those of us with MGUS and SMM…certainly not until we know a LOT more about what goes on inside this complex and, I would add, delicate setting.

Luckily, there have been more studies on this topic since my 2014 post, including this recent Dana Farber one, titled “The bone-marrow niche in MDS and MGUS: implications for AML and MM.” A blog reader sent me the link (thanks!): goo.gl/Ew3K4A

The full study isn’t available for free online, but I was able to read it thanks to a good friend. Okay, let’s have a look at it…

We know that MM is preceded by MGUS and by an intermediate stage called SMM.

Progression, that is, the “clonal evolution” of myeloma, takes place between MGUS and MM. But, the researchers add, some of the characteristics of myeloma can be found, “at lower frequencies,” at the MGUS and SMM stages. For example, the gene deletions.

Therefore, they say, it is the development of neoplastic “subclones” in the earlier stages that probably leads to the progression to myeloma.

This development wouldn’t be able to take place without the help of the bone marrow microenvironment, which therefore must be targeted in order to prevent progression as well as increase the effectiveness of conventional treatments once the stage of MM has been reached.

As I was reading this study, full of technical jargon that I could barely grasp, I began imagining the bone marrow microenvironment as a marketplace where strong nasty myeloma hooligans live and operate in coexistence with other, not-so-harmful, silly myeloma characters, as well as a bunch of normal folks, our normal cells.

Problem: myeloma clones have the ability of turning the marketplace into a toxic environment that helps them grow and proliferate.

A lot depends on how the marketplace reacts to these attempted changes. If it is weak and yields to the MM hooligans, it will become full of “weeds.” If it resists, it will be full (well, perhaps not entirely!) of crowds of happy customers, what the researchers call a “physiologically useful crop of mature blood cells,” that is, normal blood cells.

Now, a NORMAL marketplace contains all sorts of custome…I mean, all sorts of cells, including osteoclasts, macrophages, endothelial cells and, don’t you love this one?, sympathetic neurons. Lots of different cells that live happily ever after in this lovely area of the body.

Too many details here…okay, we don’t need to know this stuff…skip skip skip.

Certain cells (the above-mentioned stromal cells, e.g., after they have gone over to the dark side) become responsible for helping myeloma develop. Furthermore, whenever myeloma cells initiate a disruption, things that should be sleeping (in technical terms: in a quiescent state) wake up (remember EBV?). Not good.

Disruptions also cause tumor suppressor genes, such as Rb1, to be…suppressed. Also not good!

The end result of all the disrupting and suppressing, without any reaction from the immune system, is that the BM microenvironment becomes myeloma-friendly, and MM stem cells can begin proliferating, helped along by processes such as angiogenesis (remember all my posts on VEGF?).

As you can imagine, the study doesn’t mention anything remotely non-conventional. But some of its findings are interesting, so let’s keep reading.

Ah, another thing occurs: immunosuppressive cells arrive in the marketplace and make such a ruckus that T cells and B cells are completely overwhelmed and can’t function properly. This means, of course, that myeloma cells are no longer being sought and destroyed by our immune system.

The study therefore gives us a lesson in progression. First and foremost, as we’ve just seen, myeloma cells learn how to avoid being annihilated by the immune system. They then create what the researchers call an “immunosuppressive environment” where the immune system defenders are no longer able to function normally. Other types of important cells present in this now-toxic environment are also affected, such as stromal cells.

When MGUS progresses to SMM and then MM, immunosuppression is one of the main culprits. In fact, I recently read a study that discussed this problem, concluding that patients with SMM whose other immunoglobulins—in my case, e.g., IgA and IgM—are suppressed are more at risk of developing myeloma. *

The questions are: can we stop this process? How? And…when?

In 2014 (and before), my opinion was to “watch and wait” for as long as possible. Until CRAB symptoms appear. My opinion hasn’t changed in all these years. Indeed, it hasn’t changed today.

“Watch and wait” doesn’t mean sitting around and moping and doing nothing but watch TV series all day long. It means being proactive, doing research, enjoying life, taking something that doesn’t have any toxic side effects and that has been shown at least in vitro to be anti-myeloma, such as curcumin. And so on. There’s lots of stuff we can do in this stage…

Okay, I think this is enough for one day. After almost falling asleepzzz myself, I decided to divide this post into three parts…or perhaps only two.

So…more on this topic tomorrow! Ciao!

P.S. The study also discusses the evolution from MDS to AML, but I didn’t really look at that part, of course, since it’s not my main focus…

* P.P.S.S. While it’s true that my IgA and IgM are suppressed (barely “alive,” in fact!), it’s also true that they’ve been pretty much at the same tiny level for years now. So yes, I am in the high risk category BUT I am still here, leading a normal life, no CRAB symptoms…

Living proof that being at “high risk” doesn’t have to be as scary as it sounds…right?  🙂 

EBV and myeloma stem cells. Chapter 3

/ Margaret / 3 Comments

Back to the Ph.D. thesis. Dr. Biswas tells us, on page 28, “that the tiny percentage of cells that harbor virus are [sic] stably maintained over months or years.” Years?

Could it be maintained for decades, too? Hmmm. At my request, I was tested a few years ago for EBV, but the only thing we found was that I had some anti-EBV antibodies…nothing at all useful…

Anyway, here’s something interesting on page 31: “EBV infects B cells both in vitro and in vivo.” In vitro, EBV makes these B cells immortal. What happens in vivo, however, isn’t that clear. In people who aren’t affected long-term by EBV, as mentioned previously, the virus doesn’t cause any real harm. What triggers it to wake up and initiate the development of different types of cancer?

On page 46 we find “that in myeloma, EBV persists in a latent form in the 47 CD19+CD138- B-cell progenitor population and undergoes lytic reactivation in tandem as the cell becomes a CD19-CD138+ plasma cell.” So something has to happen within the B cell, the CD19 positive cell that is, in order for EBV to wake up and jump into action.

It’s actually on page 46 where my brain almost exploded. Lytic reactivation? 😯  I had absolutely no idea what that meant, so I looked for an “easy” explanation, which I found, finally (if you are interested, have a look here: http://goo.gl/pg8Q6r ).

This study tells us there are two ways in which a virus, nothing more than a “parasite,” can infect its host cell: 1. actively, by causing “a lytic infection characterized by the release of new progeny virus particles, often upon the lysis of the host cell,” (lysis refers to the destruction of a cell, the host cell in this case), or 2. inactively, which occurs when the virus just sleeps, without reproducing itself.

“Reactivation” occurs when a sleeping virus wakes up and reproduces, stimulated by internal or external factors…but that gets into too much detail, so let’s skip that part.

Here’s another clue: in order to be reactivated, EBV needs the help of a protein called Zta, as well as a transcription factor called Rta (remember NF-kappaB?). Not easy to describe a process that I barely comprehend myself, but, in a few words, a transcription factor (XBP-1) activates this pesky Zta, which then rushes over to hug its buddy Rta. The two of them, fortified by their love, then activate other genes, in what is called a “cascade.” (Phew…wiping the sweat off my brow…)

At the end of this process, EBV gets reactivated, which means it’s fully awake and ready to do its evil deeds. And in fact this is discussed in the Ph.D. thesis, too, on page 13, if you want to have a look. Yes, I’m jumping a bit back and forth, but it’s inevitable, especially when things aren’t too clear. [I just hope I’m not making any mistakes…Please correct me if I am! Thanks!]

An important aside (p. 48): EBV doesn’t become a target of T cells because it hides its “viral gene expression during latency.” Aha!!!

Another aside: the EBV myeloma lines are different from those of Burkitt lymphoma and lymphoblastoid cell lines, but are similar to chronic lymphocytic leukemia or CLL cell lines. The EBV-infected CLL B cells, however, do not become immortal and only grow for a short time. Bit of a difference there.

So, okay, back to us: in myeloma, B cells get activated and become plasma cells, thanks to the help of transcription factors (Blimp-1 and the above-mentioned XPB-1, etc.). In this process of transformation, in this cascade of events, EBV disappears. That is, it is no longer present in the newly-created plasma cell. Since plasma cells cannot reproduce themselves, it doesn’t have to be. It has already done its damage.

And now let’s get to something that I thought could be very useful, potentially at least: if you interfere with the cascade, with the process of transformation, EBV cannot reactivate itself.

This is important because, as we can see on page 93, “The investigations presented here show that although the cells that harbor EBV are only a tiny percentage of the cells in culture, EBV is an important driver for the proliferation of the cultured cell population considered as a whole.”

Margaret’s simple (simplistic) solution: we need to block the reactivation of EBV…keep it asleep, like Fluffy, the three-headed dog in Harry Potter. We need to block these transcription factors.

Shortly after I began this umpteenth EBV-MM journey (but, THIS TIME, with PROOF of the association!), I went to see our family doctor, who is a real genius. I’d sent him the main EBV-MM association studies, which we discussed briefly. Then I asked him to prescribe an anti-EBV drug for me.

My idea was:  block the EBV = block the MM.

Well (I should have known it), my doctor told me it’s not that simple. Sure, he could prescribe a cycle of acyclovir for me, but:

  1. For how long?
  2. What should the dose be?
  3. Would it work?
  4. What about the side effects?
  5. Did I really want to take the risk?

Of course I had no good answers, except to question e. (I’ve taken risks before, so, no biggie). And so I gave up, but only for the time being.

I just have to do some more research. There must be a way, a non-conventional way. Any ideas?

Hmmm, I just read that bortezomib (Velcade) kills EBV. Not that that gives me an incentive to start conventional treatments, mind you! But 1. if you are already on Velcade, AND 2. if EBV might have initiated your myeloma, well then, two birds with one stone, right?

Anyway, proteasome inhibitors in general have an effect against EBV, including, tada!, curcumin.

Food for thought.

Okay, I think I have enough fodder for a Chapter 4, then I’m done with the Ph.D. thesis. Take care, everyone! Ciao!

EBV and myeloma stem cells. Chapter 2.

/ Margaret / 1 Comment

One thing Dr. Biswas discovered is that the subset of EBV-positive (as opposed to the EBV-negative) myeloma cells are the blasted stem cells, which have CD19 on their surface. What does that mean? Simply that we’re not talking about plasma cells here, but about B-cells that have the ability to REPRODUCE themselves, turning into plasma cells (which do not have that ability, btw).

Confused? Well then, let’s have a look at something different.

On page 12, Dr. Biswas discusses the 90% percentage that I mentioned in my previous post. While EBV “is benign in acute stages and latent in chronic stages […], in some cases, EBV has been demonstrated to be involved in the development of many malignancies, both hematologic and epithelial.”

So EBV doesn’t normally cause any terrible mischief. but remains inactive (quiescent) once it gets inside its host cell. But, in some cases, EBV doesn’t keep sleeping like Fluffy (Harry Potter reference: Fluffy, the three-headed sleeping dog)…That is the case with myeloma, as we have seen, but it happens in other types of cancers, too, such as Burkitt lymphoma, Hodgkin and non-Hodgkin lymphomas.

Even though it’s difficult to keep up with the technical gobbledegook, what is clear is that other factors have to be present in order for EBV to initiate the development of cancer (the image in my brain is of Fluffy waking up when the music stops…the music would be the “other factors”…). Anyway, that will be fodder for my third chapter, methinks.

So, summing up: 1. in MOST cases, EBV causes no long-term harm but simply remains dormant inside its host cell; 2. In some cases, unfortunately, it is associated with the development of cancer; 3. In myeloma, EBV DNA is present only in a small subpopulation of MM cells = the myeloma stem cells; 4. EBV doesn’t cause just one type of cancer, but quite a few, and 5. As for other types of cancer, EBV is present in EVERY SINGLE tumor cell, so myeloma really stands out in this group of EBV-associated malignancies. Yaaay, we’re special! Um.  🙄

A question just popped into my head (actually, it’s been in my head for a while now): would it make a difference if you took antiviral drugs such as acyclovir as soon as you receive an EBV diagnosis? Hmmm.

When my EBV infection was diagnosed, I was given nothing, e.g. Nothing. Just told to go home and rest…

But after going through all these new EBV-myeloma studies, I wonder if I would have ended up with MGUS (more than 18 years ago!) if I had immediately taken acyclovir or something similar? And I wonder this not just for myself but for all the people who have EBV-associated cancers.

Well, perhaps it’s because there wasn’t much research on this topic back then (the EBV-MM studies are quite recent, as we have seen). Perhaps EBV is too insidious to be targeted by any existing drug on the planet…even acyclovir has its limits, I have read. Perhaps it’s because nothing can be done once the process has begun, but I can tell you that I’d have been “relieved” (with lack of a better word) to have known the cause/s of my cancer. It would have eliminated all these years of wondering where I got this thing (well, not wondering obsessively…you know what I mean).

And another thing: with all we know about EBV now, it seems absolutely astounding that everyone diagnosed with MGUS, SMM, or MM doesn’t get immediately tested for EBV. I mean, NOW (not 20 years ago).

Or am I wrong? Was anyone here tested for EBV?

Okay, enough for today. I seem to have more questions than answers…

My next chapter is going to be a bit more technical. I’m sure you can’t wait, eh! 😉 I’ll try to tone it down…  😎 

Dieneke in the news

/ Margaret / 6 Comments

Well, well, I am so pleased for Dieneke! Her myeloma-curcumin story is still in the news, even after all these months (I first reported on it in August).

But what surprised me was to discover (today) that the Italian news has also picked up her story, as you can see here: goo.gl/sCKzkA

And the Times, too (in addition to many British papers, of course): goo.gl/bnefDA

Well done, Dieneke!

Mummy with myeloma

/ Margaret / Leave a comment

I just read a fascinating bit of news. After examining two Egyptian mummies (a man and a woman who had died, respectively, in 1800 and 2000 BC), an international team determined that they both had cancer…The woman had breast cancer…and the man had multiple myeloma.

These are the oldest known cases of breast cancer and myeloma…

So myeloma is NOT a relatively recent type of cancer…That’s incredibly interesting, don’t you think? I thought so, anyway…

Here’s the link to the Science Daily article: goo.gl/tkW8T4 

Well, well…

December test results

/ Margaret / 12 Comments

I had blood tests (and the Bence Jones 24-hour urine test) last week.

This afternoon I got my results. Here goes, in a nutshell:

  • My M-spike has gone down (it has actually been going down a wee bit for the past two tests, so this is the third “wee bit down”).
  • Total IgG is also down (for the second time, when compared to my last few tests).
  • My hemoglobin is in the normal range, even though my red blood cells are slightly low, but just slightly.
  • Everything else looks pretty much the same. Almost everything, certainly anything of importance, is a wee bit better compared to my most recent tests. For example, my monoclonal component hasn’t been this low since 2012. And my freelite chains have also gone down quite a bit.
  • No Bence Jones. Yaaaay!

You are probably curious to know what I’ve been taking. Not much, actually. I mean, in addition to using Nigella sativa in my food, I’ve been taking my usual 8 grams of C3 Complex curcumin a day, divided into two doses (4 grams at lunchtime, 4 at dinnertime). And, since last summer, I have been testing a Ganoderma lucidum supplement: 960 mg, twice a day (again, lunch and dinner, together with the curcumin). Well, the Ganoderma seems to have done something, for sure.

Or could it simply be the “kitten” effect (see photo of Pandora, left; Pixie, right)? Meow!!! 

Who knows? 😉

Anyway, whatever the cause, these results confirm that I’m stable…And to think that more than 12 years have passed since my SMM diagnosis…

Well, well, well! Stefano and I certainly have some celebrating to do this evening. 🙂

Ciao, everyone, and may the holiday season bring GOOD NEWS to you, too!!!

Dendritic cells, miR-29b, and multiple myeloma

/ Margaret / 1 Comment

Life is very complicated these days. This morning, after consulting with the vet, I discovered that our giardia-ridden kittens will have to undergo a second cycle of treatment, which will begin next week. This means that they will have to spend another month holed up in their luxurious quarantine, poor dears! I am spending almost all of my free time with them…playing with them, feeding them, holding them, cleaning  up, sterilizing, and being SUPER CAREFUL whenever I handle anything at all in the quarantine room.

Mind you, it may sound like it, but I’m not complaining. Not at all!!! I mean, just look at that face!  🙂 

Well, okay, I admit, I HAVE had a few frustrating moments in which I’ve asked myself, and/or Stefano, HOW and WHY did we get into this mess??? Agh!

But the truth is that we almost certainly saved the lives of our kittens, and probably the lives of their siblings, too (immediately after we received the giardia diagnosis, I got in touch with the woman who gave us the kittens…She had no idea…). So that is something to remember…

And besides, these two kitties are so incredibly adorable and funny and affectionate…They act like normal, playful, curious, crazy kittens that zoom all over the place and then crash and sleep until they have enough strength to go back into the crazy kitten mode…I mean, you can’t tell that there’s anything wrong with them…except for the huge quantity of smelly pooparoni (though it’s MUCH better than it was a couple of weeks ago, let me tell ya)! Yuck!

Okay, enough…It will only be another month, then they’ll be cured, and we’ll be able to let them out into the rest of the house…and meet their older siblings (yikes…a bit nervous about that). If we’re lucky, they’ll be well enough by Xmas. That would be a lovely present indeed!

But that’s not the reason I’m writing this post, even though, hehe!!!, it might seem that way. Nope, this evening I wanted to write (then I got derailed, sorry!) about a new myeloma study that I bumped into just this morning…a very interesting, and mostly Italian!, study on myeloma and dendritic cells (DCs, for short), which is fully available online and has been accepted for publication in “Leukemia.” Here’s the link: goo.gl/wFMjS1 I’ve written a few posts on dendritic cells and myeloma, btw, so you can use my “Search Box” to have a look through my blog, if you want.

The abstract begins with a good explanation of DCs: “Dendritic cells (DCs) play a key role in regulating tumor immunity, tumor cell growth and drug resistance.” The authors believe that MM cells may recruit and reprogram DCs in order to survive. They found a member of the microRNA family (a family of teeny tiny RNA molecules that regulate gene expression), called  miR-29b, which is is not downregulated in normal DCs but, drum roll!, is downregulated in most types of cancer, including myeloma.

Now, even though we may not understand (or care!) what exactly this little, hairpin-shaped miR-29b does, etc., the main thing is that it  is able to counteract “pro-inflammatory pathways, including STAT3 and NF-kB, and cytokine/chemokine signaling networks which correlated with patients’ adverse prognosis and development of bone disease.”

Translation: more miR-29b, less myeloma cell proliferation.

So, miR-29b is GOOD. From our perspective, of course, not from that of a myeloma cell. 😉

Now, it’s getting late over here in Italy, and I don’t have much time left. Stefano is on his way home (oh, oops, he just walked in the door…I have to go help him with dinner…He’s the chef tonight…). So I have to leave you with this study and all its complexities.

But do have e a look at page 23. There you will find that ASPIRIN and CURCUMIN “revealed a promising therapeutic activity in both MGUS and sMM patients.”

AHA!, so researchers ARE paying attention. This one sentence made my day…my week, even! 🙂

Oh, and guess what? Curcumin upregulates the expression of miR-29b. Tadaaaaaa!

I will have to keep my eye on these authors who are also looking into the role of this little molecule in the progression from MGUS to MM.

Good stuff, good stuff!!! Take care, everyone!!! Ciao!

Update on the viral connection to myeloma

/ Margaret / 3 Comments

A blog reader (thank you!) sent me the link to a French study that was recently published in JCI. It discusses the link between IgG myeloma and pathogens such as, ta da!, the Epstein-Barr virus, or EBV for short, the virus to which I was exposed while doing my doctorate at the University of Toronto and which I have always believed to be the underlying cause of my own, er, situation…

Before I forget, in all the excitement!, here’s the link to the (full) study: goo.gl/g73Sx8 And there, right at the end of the abstract, we learn that “a dysregulated immune response to infection may underlie disease onset and/or progression of MGUS and MM for subsets of patients.”

Bingo!

This isn’t the only study I’ve read or glanced at in the past week on pretty much the same topic, which, um, to be honest, I haven’t looked at in years now. So yes, there are others. But first, let’s have a look at this one.

The abstract tells us of the association between B-cell malignancies and EBV (also, HCV and H.pylori): “Subsets of mature B cell neoplasms are linked to infection with intracellular pathogens such as Epstein-Barr virus (EBV), hepatitis C virus (HCV), or Helicobacter pylori.” First point.

And here is another piece of the puzzle (see Introduction): “…viral and bacterial infection in patients can lead to the production of oligoclonal or mc Ig.” (Note: mc Ig = monoclonal immunoglobulins or antibodies.) Our clonal plasma cells produce a lot of these antibodies that thus far had been thought “not to have functional activity.”

But wait!, that may not be the case. Perhaps these antibodies do have a purpose after all. In previous studies, the French researchers in fact found that in Hepatitis C-positive patients these antibodies “almost always target the virus…” Aha. And that is an important third point. I don’t remember ever reading anything about MM cells doing anything remotely useful, so this was a big, no, it was a HUGE discovery for me.

Let’s keep going.

Their conclusion is that “an abnormal plasma cell response to infection could be the initiating event of some MGUS, SM, or MM cases.”

I can’t tell you how this made me feel, after years of having myeloma experts tell me that there could NOT possibly be any link whatsoever between my myeloma and my EBV infection. Vindication? Yeah, I guess.

The article at one point refers to a study discussing the case of a patient with a  chronic HCV infection whose stage IIA MM regressed to MGUS.

Regressed to whaaat??????

Now that really caught my attention!!!!!!!! And so I rushed to read the case study, which is fully available online and is an Italian study, to boot: goo.gl/yeDwZvZ

This patient’s MM regressed to MGUS after just six months on an anti-HCV treatment. Six monthsssssss, that’s it???

I had to stop reading for a minute to let this all sink in.

How did I miss that 2013 Italian study???

Well, true, I can’t keep track of everything…I do have a life, after all!!! Besides, the important thing is that I finally did read it. Anyway.

So here’s the thing: IF transforming her MM back into MGUS was possible for an HCV patient, why couldn’t, theoretically, the same be possible for an EBV patient with SMM or MM? And even if a regression didn’t occur, what’s there to lose?

Get rid of the virus, get rid of the myeloma. Sounds simple. Too simple, probably. But…worth a try. (Important note: I don’t know how toxic the antiviral treatments are. More research AND my doctor’s advice needed, here, before doing anything too hasty…)

Now, as the authors suggest in the Discussion part, perhaps this could be feasible in the early stages of the “chronic underlying infection”…But they also add that it might even be effective in later stages of MM. Boy, that would really be something, wouldn’t it?

Here are some excerpts from the Discussion (my highlights): “Overall, our findings imply that chronic stimulation by infectious Ag may promote MGUS and MM in certain patient subsets. Importantly, some of the identified infectious pathogens (HSV, HCV, H. pylori) can be effectively treated. This observation has obvious clinical consequences, since the detection of MGUS or SM patients with an mc IgG specific for a treatable pathogen would allow the proposal of antiviral or antibiotic treatment for patients. If an underlying chronic infection were cleared early enough in disease progression, it could perhaps offer the tantalizing possibility to prevent MGUS transition towards SM and overt MM for the first time. In such cases, addition of antiviral or antibiotic treatment to current protocols might indeed induce disease regression and/or improve response to standard treatments, as reported for interferon-? treatment in HCV-associated MM.”

Hmmm, they say that “some of the identified infectious pathogens […] can be effectively treated,” but they don’t list EBV. Have to check on that one…

Okay, I’m stopping here for today. This is just the first part of a series of posts that I intend to write on this topic. I’ll re-read and, if I find something else of interest, finish writing about the JCI article in my next post…in any case, I have also downloaded a couple of other studies that might be of interest. Need more time, though…

Must rush off now. Ciaooooo!

Oh wait, let me leave you with some food for thought, hehe: curcumin inhibits EBV.

Bam!