Your help is needed for the FIRST large-scale survey on MGUS and SMM patients’ experiences and quality of life

About a week ago I was contacted on my blog’s Facebook Page (see: goo.gl/FQrMQ9) by a Ph.D. student at Queen’s University in Belfast. He asked for my help in getting SMM and MGUS folks to participate in a survey focusing on premalignant conditions, which will be part of his thesis. In a nutshell: he needs to reach as many SMM and MGUS patients as possible.

He is mainly interested in SMM and MGUS patients’ quality of life, how we were diagnosed, what is our level of care, and how we reacted upon receiving our diagnosis.

He wrote: “This is the first large-scale survey on patients’ experiences with premalignant conditions and the plan is for it to be published as a research paper and a component of my PhD. We also plan to produce a summary of the findings for patients to read when we finish.”

He and his team hope that this information will be able to help medical staff to provide the best standard of care possible. That would be really super. I remember being so confused at diagnosis (both MGUS and then SMM), not really understanding what was going on, and so on. It would have really helped to have gotten a bit more information, solid information…

And another thing: when some of the top myeloma experts in the world told me that there was nothing I could do to stop or even slow down progression to full-blown myeloma, except sit back and WAIT, I really did lose hope for a while. Luckily for me, I’m an optimist, so I soon decided the experts were WRONG and began doing a lot of research.

More than 12 years post-diagnosis, things are completely different…for me…But I’m afraid they are not so different for a lot of patients who receive a premalignant diagnosis and are left with no hope…

Of course it would be negative for doctors to give patients false hopes (“oh, everything is going to be fine”…that sort of hogwash). But to take away their hope is equally as bad…Remember David Servan-Schreiber and “false hopelessness”? Exactly.

In a premalignant condition, there is definitely HOPE. And, as I think I have proven throughout the years, there are also a lot of things we can DO. We do NOT have to sit back and fret. No…We can be proactive…in a natural way…I mean, c’mon, we just found out that meditation might have an impact on our progression genes! So much is changing…so much is going on…It’s rather exciting, I must say…

Anyway…

Sorry, I got a bit carried away there. Back to the Queen’s University survey now. I took a few days to think about Blain’s request, since I’ve never publicized anything like this on the blog.

The first thing I did was take the survey myself. I’ll warn you: it takes a while…or at least, it took ME a while, since I had a lot to say (imagine that! 🙂 ). But if you aren’t interested in writing entire dissertations the way I did, practically, all you have to do is say yes or no to the various questions, and that should cut your time in half, at least.

Besides, it’s worth it…It’s an interesting survey…

Okay, enough said! Let’s give Blain a hand, shall we?

The results of this survey could be very IMPORTANT for future patients, but if we don’t take the survey, Blain and his team will have very little to go on, right?

Besides, it’s FREE…won’t cost you anything!

Here’s the link to the surveygoo.gl/EsT7Ki

If you are connected to Facebook, you can follow the study/survey’s progress here: goo.gl/v32Es2 

Okay, that’s it! Thanks for your help!!! And please don’t forget, TAKE THE SURVEY!!!!!! 🙂

A MGUS and SMM patient study on the possible impact of meditation in myeloma progression

A recent Patient Power video caught my attention a few days ago, but I was caught up in my andrographolide research, so I ignored it until today. It’s titled “Can smoldering myeloma progress to full-blown myeloma?” The obvious answer is yes, it can, of course. We know that.

Here’s the link to the video, which has other interesting things, too: goo.gl/e3ksk1

At one point, Dr. Raje talks about a Harvard project, called the , during which MGUS and SMM patients used meditation and mindfulness to try to stop progressing to full-blown myeloma. The study’s main purpose is to look at the genomic profile of these patients to ascertain if meditation could actually change the genetics of myeloma progression. Isn’t that something?

Dr. Raje adds, don’t worry too much about your disease…makes common sense. And perhaps, with the data they are collecting from patients right now, we will soon have actual proof that stress can have an impact on our progression genes….Wowsie.

We know that stress plays a big role in myeloma. We’ve known that for quite a long time (remember the 2008 Ohio State study on myeloma progression and norepinephrine, = one of the stress hormones? Exactly…). Certainly at times it isn’t easy to reduce stress levels, and I myself am not always successful (life complications, you know!). But I try! And meditation really does help…It helps even to just close your eyes for a few minutes and visualize a beautiful country or place you’ve visited, an event that made you happy, whatever.

You don’t necessarily have to follow a course to learn how to meditate (I never have)…although you could, of course! I’ve found my own meditation method, mainly based on watching online videos, and it works well for me. Anyway…

But this is the first time I’ve heard a conventional myeloma doctor mention MEDITATION as a possible way of avoiding progression. And I didn’t know about this project…Something to keep an eye on, for sure…

Dr. Raje  added that their results would be presented at ASH later this year. So we have a while to wait. However, I did find this abstract, published in the Journal of Clinical Oncology in May of last year: goo.gl/68nYeq

This link informs us that the experiment has been going on for a while now, and that this meditation program REDUCED STRESS, indeed DISTRESS, “in participants with intermediate or high-risk MGUS and SMM…”

Boy, I’d love to participate in something like that. A slight, er, obstacle is that I live across the pond…! Oh well!!! I’d also love to hear from someone who might be in the program…

Time for dinner…Have to rush off…Take care, everyone! 🙂

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: goo.gl/3e6Nk5

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!!!!!!

A new anti-myeloma substance: andrographolide

A blog friend (thank you!!!) sent me the link to a few studies on andrographolide, extracted from a medicinal plant called Andrographis paniculate, native to South Asian countries and also known as the “king of bitters.” The leaves and underground stems of this plant are used for about a million purposes: to prevent and treat colds and the flu, to treat digestive disorders (diarrhea, colic, stomach pain and so on), liver conditions (jaundice, liver damage caused by medications), infections (all sorts, from pneumonia to rabies, even HIV/AIDS), and skin conditions.

The list is seemingly endless and even includes snake bites, loss of appetite, kidney problems, hemorrhoids, worms (ugh). It has antibacterial, anti-inflammatory, antiviral, anti-tumor, anti-fungal, and immune regulatory, properties. It also protects the gallbladder and the liver. Oh, and apparently it is good for the heart, too!

But the main reason I’m writing about this seemingly amazing substance today is because it has ANTI-MYELOMA properties. What I really like about this new (new to me!) substance is its “low toxicity and low cost.” 

Luckily for us, the main andrographolide-MM study, published in 2015, is available for free online, so you can read it, too. The whole shebang can be found here: goo.gl/Z9CaVF

Incidentally, this is the first study to discuss the effect of andrographolide on myeloma cells…

According to the abstract, these two Chinese researchers showed that andrographolide reduced the proliferation of MM cells and increased their death rate (apoptosis) by inhibiting the NF-kappaB pathway that we’ve learned so much about in all these years.

Results: as mentioned in the abstract: 1. andrographolide blocks the proliferation of myeloma cells; 2. It also KILLS them (“induces apoptosis”). And that’s really all we need to know, although the study offers other important details, too.

Let’s look at one of them, since it is connected to an item of MUCH interest that pops up later in the study: andrographolide reduces the levels of the TLR4 protein and of the NF-kappa B pathway in myeloma cells.

Discussion: andrographolide also inhibits angiogenesis, which is so important for the survival and wellbeing of myeloma cells, so that’s good to know, too.

Now we get to the above-mentioned importance of the TLR4 protein. TLR4 is apparently involved, not in a good way!!!, with a tumor’s microenvironment and has a lot of power over immune cells. So, if its activity can be blocked, that’s very good news. With andrographolide, this can be accomplished…

I mentioned TLR4 in one of my earliest posts, written in 2007: TLRs, or toll-like receptors, play a key role in the immune system. Back then, I was interested in the fact that TLR4 is inhibited by…yes…curcumin. This all makes sense, eh?

Anyway, definitely a very interesting substance. I’ll be looking at more studies on this topic in the next few days. I think it might deserve more than just ONE post. Right now it’s at the top of my list of stuff I intend to test…

“Il gatto non è mica morto!!!”

I dedicate this post to my bestie, to my wonderful life companion…to a normally VERY sensitive guy…  😉 

On Saturday evening Stefano insisted that we watch a 2016 movie called “A street cat named Bob,” based on the true-life story of a homeless man/former heroin addict whose life was completely turned around after he encountered a stray cat named…Bob.

I didn’t know much about this story, so, during a rather difficult part, I turned to Stefano and declared, “that cat had better NOT DIE at the end of this movie!!!”

He reassured me that the cat wasn’t going to die…

Well, of course (if you’ve seen the movie, you will understand…I think!), toward the end I got all emotional and teary-eyed…I mean, who wouldn’t? It’s the story of a wonderful super cat, but: cat gets lost…human companion is desperate…days go by…cat finally finds his way home…happy ending…

I mean, tears were an absolute MUST. From my perspective, at any rate.

As the closing credits were rolling, showing photos of the real Bob and his human companion, Stefano turned to me, saw my tears, and exclaimed, “well, what are you crying for? The cat DIDN’T DIE!!!” (in Italian: “Ma perché piangi? Il gatto non è mica morto!!!”).

Men!!! They just don’t get it… 🙂

Anyway, if you love cats, you will love this movie…highly recommended…

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: http://goo.gl/LHa5Jn

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.

“The bone-marrow niche in MDS and MGUS: implications for AML and MM.” Part 3.

Final post on the Dana-Farber study.

–Another thing mentioned in my 2013 post (see my Jan 31 2018 post for the link) is mentioned in this Dana-Farber study, too: PD-1, which stands for programmed cell death protein 1. Blocking the activity of this protein, which is highly expressed by MM cells, helps our immune system react against the cancerous cells. The Dana-Farber study informs us, however, that the conventional agents used to block PD-1 have been found to be toxic and not very effective, so the patient studies are currently on hold.

But guess what? Curcumin blocks PD-1, without any toxic side effects. Of course, curcumin isn’t a drug, so we cannot expect it to work like one. But it’s one MORE thing that curcumin does.

–There is another target called CXCL12, a chemokine protein (don’t ask!) secreted by stromal cells that helps myeloma cells become drug resistant, among other bad things. If CXCL12 is inhibited in early stages, however, progression to myeloma can be delayed or even prevented.

28 patients with relapsed or refractory MM participated in a relatively recent clinical trial testing bortezomib, dexamethasone, and something called olaptesed pegol whose target is CXCL12. There was a “clinical benefit rate” for 75% of these patients. Not sure what that means, and we are also told nothing about the patients’ quality of life, stuff that I imagine is of HUGE interest to all of us. Oh well.

My comment: curcumin inhibits CXCL12.

I don’t want to go overboard with too many details. So let’s get to the study’s conclusions.

This group of researchers maintains that targeting the myeloma-friendly bone marrow microenvironment is crucial. It might prevent disease progression to myeloma and increase the effectiveness of conventional treatments after progression has taken place.

But the research is in an early stage…more studies are needed.

In the meantime, I say, let’s stick to the “Watch and Wait” strategy (while taking non-toxic stuff and having a normal, splendid life). Until you have CRAB symptoms, it’s the best strategy on the market today.

Incidentally, why don’t we rename “Watch and Wait” with something that sounds more proactive? I mean, most of us aren’t just sitting back and just waiting for a brick to fall on our heads, right? We’re doing something!!!

So, any suggestions?

Living with two active kittens

This morning, after re-reading the last bit of Dr. Biswas’ EBV-MM thesis, I began looking at another area of research, concerning myeloma, of course. But then I decided to take a break and write a KITTEN POST. The kittens are asleep right now, so I have some time to do that… 

Let’s see. We let the kittens out of their quarantine room on Saturday, December 30, 2017. They had been in that room, full of games and a floor-to-ceiling cat tower, since the beginning of November, when we first brought them home. It took almost two months for them to get their clean bill of health: no more giardia (!), no more ear mites, and their booster shots. They were finally ready to meet the others, the adult cats.

When we opened that door, it was like opening the front door and letting two little kids go outside in the snow for the first time in their lives. Pandora and Pixie were bouncing all over the place, full of enthusiasm, happiness, and fun…A joy to behold.

As for our adult cats, they didn’t quite know what to do at first. In the beginning, they just stayed on our bed (where they’d been napping, as usual), pretending to ignore the ruckus, the thundering noise of small paws rushing about madly on our cotto floors, exploring the house…

When they finally realized the noise (and the noise creators) wasn’t going to go away, most of them simply disappeared. Prezzemolo hid downstairs, in a small room under the kitchen, for two days…

But cats have to eat, right? And the cat bowls are all in our open kitchen/dining room area. That’s when the growling and hissing started. Hiss hiss growl growl hiss growl, whack. Yes, there was an occasional whack, too…

Thus far, the cat who is having the most difficult time dealing with the arrival of the two kittens is Peekaboo (10 years old). She still goes after them every chance she can get and growls at them even when they aren’t even near her. And they are really afraid of her.

She doesn’t hurt them, mind you. No claws out, no scratches, nothing. It’s all just a lot of noise. When Peekaboo manages to chase Pixie into a corner, though, the screeches they emit still make me jump out of my chair and practically hit the ceiling. So LOUD!!!

The noise has been lessening, though…I think it’s simply because the kittens are getting better at avoiding Peekaboo.

The others are behaving much better towards the new girls in town. Pinga, in particular. I’m not saying they are cuddling just yet, but now and again we do have six cats lying on our bed, peacefully (minus Peekaboo, of course). So it’s going to be fine.

And I have to say that Pandora and Pixie are two of the happiest kittens I’ve ever had. They’re amazingly curious, and they do everything together, even when it comes to using the litter box (as they get bigger, though, I imagine that will stop!).

They follow me around like teeny tiny dogs. Everything I do is absolutely fascinating to them. The laundry, making the bed, oh just anything! And they are so helpful (not). It’s mostly okay, except when I’m cooking. They still don’t understand what “NO!,” “Go AWAY!,” or “GET DOWN!” mean. And even when I get them off the counter and put them on the floor, they’re back up within nanoseconds.

So fast!!!  😛 

It was when Stefano was away on a business trip in mid January that I realized the only way I’d be able to eat ANYTHING would be for me to STAND UP IN THE KITCHEN, holding my plate as far from the counters as possible. These two little critters may be small, but they are also strong and athletic. And, as mentioned, QUICK.

And no, it wasn’t because they were hungry. They’re never hungry. They always have dry (kitten) food at their disposal, and I feed them wet food at least twice a day, plus treats on occasion.  No, it’s because they are CURIOUS. They want to know what I’m up to, what I’m eating, they want to know EVERYTHING. 🙂 

And even when it’s the two of us, Stefano and I are no match for those Olympic jumpers, and dinner at the dining room table can become quite challenging. If we get distracted, we end up with a paw smack in the middle of our plate or with a kitten stuffing her silly little face down into our glasses.

There are only two of them, but at mealtimes it’s like having an army of Pandoras and Pixies. Fast and determined, those two!!!

But who’s complaining? I certainly am NOT. Pandora and Pixie are the most adorable creatures on Earth. And they are soooo endearing. Early in the morning Pixie comes up to my face and wraps herself around my neck like a (very warm) scarf, putting one of her paws over my ear (so I won’t hear the alarm go off? How considerate!). I put my arm around her and hug her close, and she begins purring. Irresistible.

They cannot replace Puzzola and Piccolo, the two cats we lost last summer, but they have definitely made their way into our shattered hearts.

And they are helping us heal…For sure! 🙂

P.S. Some of these photos were taken with my cellphone and didn’t come out as well as I’d hoped. And by the way, if you’re wondering why these are mostly shots of the kittens sleeping or at rest, the reason is simple: almost impossible to get a decent photo these two in motion…they’re almost as bad as puffins in flight! 😉 But…I’m trying! 

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 (goo.gl/jPgDtS), the article begins like this: “Researchers have identified two gene regions that contribute to multiple myeloma, an inherited cancer…”

SAY WHAAAAAT??? 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: goo.gl/bTgGmW

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): goo.gl/kr2Fq2

According to another study published in 2016 (see goo.gl/nNqqJh), 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…