Two gadolinium-based contrast agents are banned in Italy

Wellwellwellwellwell! WELL!

I just read a bit of welcome (or, wellcome!) news in Italian. If you understand Italian, here’s the link: In a nutshell, beginning today, yes, TODAY!, two contrast agents used in MRIs have been banned in ITALY. And, quelle surprise (not), they are gadolinium-based.

Remember the study that came out some years ago about how much myeloma cells simply LOVED gadolinium, and proliferated at mad rates when placed in it? If not, just do a search of my blog for “gadolinium.” Gadolinium can also have a bunch of not-very-nice side effects…

The reason for this ban isn’t, however, because of that important gadolinium-myeloma study. No, what’s happening today in Italy is mostly a precautionary measure, based on the July 2017 recommendations of the EMA, the European Medicines Agency, which in turn are based (!) on the findings of its Pharmacovigilance Risk Assessment Committee, which is Europe’s equivalent to the U.S. FDA. Basically, small quantities of gadolinium have been shown to accumulate in the brain, and there is no way of proving that those quantities do not cause any damage in the long term.

Hence the ban.

Does that mean that gadolinium has been completely banned? Unfortunately not.

In some cases–when there is no other way to reach a diagnosis, e.g.–the smallest dose possible will be used. But there will be no more widespread use of this crap. Oh sorry, did I say “crap”? Oh dear, so I did. 😉

Another thing: the gadolinium-based contrast agents gadoxetic acid and gadobenic acid will continue to be used in liver scans.

But that is IT. Gadolinium is on its way out (at least, that’s what I hope!).

We need to focus on finding non-toxic or at least not-so-toxic contrast agents. There must be another way to do this…there must be…

Ah, speaking of which, I just read about potentially safer manganese-based contrast agents in an article titled “U.S. patients left fending for themselves with gadolinium safety risks”:

And this is where I am going to stop today, with the hope that a non-toxic contrast agent can be found…

P.S. I’ve been having difficulty accessing the Internet in the past few days…It’s on, then off, then on again…a real drag. I want to publish this post before I lose Internet again, so I’m not going to reread it, as I usually do…pazienza!

Off I go…Need to feed the cats and have lunch! Ciao! 🙂

Andrographolide and parthenolide kill myeloma stem cells

My andrographolide-researching blog reader also sent me the link to a 2011 U.S. study on the effects of parthenolide (remember PTH? Remember DMAPT? Yeah, I haven’t written about it in a long time…making mental notes right now…) and andrographolide on myeloma stem cells:

That’s right…on MYELOMA STEM CELLS.

Problem: only the abstract is available for free online. With the help of a fab friend, however, I was able to read the full study, but I have to be careful about copyright issues, even though it irks me that you have to pay for studies that could be of vital importance to us. Of course, I DO understand that journals need to survive. And so…well, let’s have a look, without going into too much detail. Compromises…

Incidentally, this is the first study discussing “a natural product with anti-CSC activity in myeloma” (CSC = cancer stem cell).

As we all know, the main problem with myeloma is RELAPSE. Relapse is caused by the tough myeloma stem cells, the cells that can clone themselves, the really bad thugs that escape being killed by chemotherapy. The chemo drugs used in myeloma target the general plasma cell population, that is, the cells that cannot reproduce themselves, BUT they are NOT able to eliminate our myeloma stem cells. So no matter how many chemo bombs we throw at our myeloma, there will always be a handful of nasty ruffians in hiding, ready to come out and start proliferating again at some point.

This study shows that parthenolide AND andrographolide do just that: they go after the ruffians. The abstract calls them two “potent anti-MM-CSC agents.”

Potent…I like that!

Okay, I’m going to see if I can extract some gems from the full study.

As we’ve seen, it’s not enough to target the circulating plasma cells. If we want to get rid of the myeloma weed, we must go after the stem cells, the “clone troopers” (Star Wars, anyone? 😉 No, I’m not really a fan, but I do remember that expression…). The only way to prevent relapses is to kill the cloners!

Parthenolide is the first extract to be discussed. In addition to being a powerful NF-kappaB inhibitor, parthenolide (PTH from now on) kills the stem cells of myeloma and of acute myelogenous leukemia, without killing the normal hematopoietic cells, the good guys, which produce red/white blood cells and platelets. One big problem has been PTH’s has low solubility in water (but remember DMAPT? It’s water soluble… but these researchers don’t mention DMAPT, except in their References…anyway…).

Andrographolide (AGR from now on) hasn’t been studied as much as PTH. However, it’s more soluble in water compared to PTH. That is very good news…

The researchers point out that melphalan and bortezomib “are not curative” (their words, not mine), because they don’t target the MM stem cells.

But, they add, that’s what PTH and AGR do…

One of the coolest things about this study, IMO, is that the researchers used a 3-D tissue culture of rBM, which is basically a reconstruction of a bone marrow microenvironment (rBM stands for reconstructed bone marrow). They also used 2-D cell cultures. They were able to confirm that the main target of PTH and AGR were the myeloma stem cells.

Clearly, more research is needed…more testing…but I’d say that this study shows how promising these two extracts are. We need to rip out the myeloma weeds…without harming ourselves in the process…

Testing promising natural extracts is a step in the right direction.

Are our official myeloma organizations going to do something about this very important study??? C’mon!!!!!!

Out in the cold

I just read an article mainly about the cost of Revlimid in the U.S.A. and the “games” that Celgene, the maker of Revlimid, has been playing in order to prevent it from becoming a generic drug.

The article tells the story of Pam Holt, a myeloma patient and retired educator, who pays $640 a month in order to take Revlimid:

Having myeloma is hard enough, but being forced to go into debt in order to have conventional treatments is simply OUTRAGEOUS.

The greed of these big drug companies has to be stopped…

I consider myself extremely lucky to live in a country (Italy) where nobody has to pay a cent for their conventional treatments. It should be the same in every country.

Does myeloma run in the family?

Ever since I began doing research on myeloma, one of my certainties–although with something like myeloma you can never be absolutely certain!!!–has been that myeloma is NOT a hereditary disease. Yes, of course, I’ve read about a few patients who had relatives with myeloma, but…only a few.

If you do an online search, you will find that not much is known about the causes of myeloma. A few known ones are things such as pesticide exposure, past exposure to radiation, genetic changes that turn our plasma cells into MM cells…stuff like that. The family connection seems to be a minor one…

Today, however, I read a Science Daily article that suggested otherwise. As you can see for yourself (, the article begins like this: “Researchers have identified two gene regions that contribute to multiple myeloma, an inherited cancer…”


The Science Daily article picked this up from a newly published gene mapping study that I won’t even try to read today (my brain is still reeling from that “inherited” business). If you’re interested and find technical jargon as fascinating as my kittens find me doing practically anything 😉 , go right ahead and have a look:

Still stunned, I immediately began digging and found a few relatively new studies on the apparent inheritance factor. A 2013 “Leukemia” study uses the expressions “familial clustering” and “genetic predisposition” in its abstract, but the full study isn’t available for free online, so I wasn’t able to check it out. For what it’s worth, here’s the link (to the abstract):

According to another study published in 2016 (see, full study available online, “Results from this pooled analysis provide compelling evidence to support hypotheses that genetic inheritance plays a role in the aetiology of MM.” The risk is greater if you have a first-degree relative with myeloma, non-Hodgkin lymphoma, Hodgkin lymphoma, or leukaemia.

But is that enough evidence? I mean, can we really define myeloma as an “inherited cancer”?

Of one thing I am certain: nobody in my family has MGUS, let alone MM. I’m the first (and last, since I don’t have any children, apart from the marvelous furry ones, of course!). Besides, based on my most recent readings, I am 100% positive that EBV started my myeloma.

I think there are too many potential causes out there, there’s too much we just don’t know (for example, the bone marrow microenvironment wasn’t even considered to be an important player in myeloma until a decade ago), for us to be able to define myeloma as a hereditary type of cancer. Or…am I wrong?

I’d be really interested to know how many of you have myeloma (or leukemia/lymphoma) in the family…

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

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:

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.”

Remember the post I wrote back in December 2014 about myeloma subpopulations and the bone marrow microenvironment? Probably not…so here’s the link:

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!):

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

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: ).

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.

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

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:

And the Times, too (in addition to many British papers, of course):

Well done, Dieneke!