Month: October 2011
Targeting the bromodomain family? You BET!!!
As I mentioned yesterday, my feet are back on the ground. It has taken me almost two days (well, let’s see, yesterday afternoon, after I got home from work and before I went out; then, this morning/part of this afternoon) to go through the full myeloma-JQ1 study, which was published in the September 16 2011 issue of “Cell.” See http://goo.gl/llsuY
To be honest, the title alone almost made me want to crawl under my covers and take a verrrry long nap: “BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc.” Mamma mia! But really, it’s not that bad. Especially since I’m going to (try to) boil down all this scientific jargon into something more comprehensible…turning it into into a sort of silly action movie 🙂 …So sit back and relax. This is going to take some time…but in the end, I think/hope you will agree that you didn’t waste your time…
Let’s introduce Margaret’s, er, “movie” script:
- The treatment target is called MYC, = one of the padrinos of myeloma progression who keeps instructing the dumbbell myeloma cells surrounding him to grow and divide and go about doing their evil deeds…
- Our superhero is instead called JQ1, a bromodomain inhibitor.
Hmmm, now for a quick digression. Bromodomain. What’s that? For the scientifically-inclined, bromodomains are protein domains that bind and recognize histone acetylation. Yeah, I know, I know. My sentiments, exactly. Let’s see if we can get through the study without getting into all that…skip skip skip.
Oh, quick aside: I’d like to point out that curcumin also inhibits MYC. Yup.
Now let’s continue with the crazy idea, which, however, helped me visualize what might be going on here, more or less:
- Okay, we’ve established (see above list) that JQ1 is the good guy who wants to stop MYC, the bad guy.
- But, oh no!, JQ1 can’t shoot the padrino directly. Why not?
- Because MYC is one of those slippery and slithery evil characters…incredibly efficient at dodging JQ1’s hits. And he has a lot of bodyguards, too.
- No problem. Our superhero is always a step ahead. So he decides instead to identify and hit some members of MYC’s family = the so-called BET bromodomains…
- But JQ1, who’s a really smart (and caring) superhero, doesn’t just want to step inside MYC’s headquarters and waste his bullets by shooting at everything that moves. Besides, he reasons, there might be some folks in there who don’t have anything to do with MM progression (in fact, there are: BRD2 and BRD3, e.g.)…
- So he does his research and manages to single out one BET family member in particular…one of MYC’s most aberrant cousins who happens to be part of the NUTty branch of the family (actually, I’m not kidding, there really is a NUT branch…).
- The aberrant cousin’s name is BRD4. He gets into all sorts of scrapes. But, most importantly, he’s very close to MYC.
- Question: by shooting down the aberrant cousin, will JQ1 be able to stop MYC?
- We’ll reach that part of the story later…But I think you can already figure out what happens… 🙂
We get the first mention of multiple myeloma in the abstract: In experimental models of multiple myeloma, a Myc-dependent hematologic malignancy, JQ1 produces a potent antiproliferative effect associated with cell cycle arrest and cellular senescence. Efficacy of JQ1 in three murine models of multiple myeloma establishes the therapeutic rationale for BET bromodomain inhibition in this disease and other malignancies characterized by pathologic activation of c-Myc. This simply means that JQ1, this fabulous new molecule, works against myeloma. In three different mouse experiments, to boot!
Now for the full study (many thanks to…well, you all know who you are!), and here we’re going to get a bit technical, sorry: c-Myc is a protein that regulates cell proliferation. In cancers such as myeloma, c-Myc becomes a huge problem. Basically, this protein gets all hyperactive and buzzy, going completely wacky and helping cancer/MM cells survive…with very bad consequences. This gene has therefore become a big target in myeloma treatment.
Food for thought: when c-Myc becomes “inactivated,” even if that occurs only temporarily, tumors shrink. Bingo.
Problem is, as I mentioned, inhibiting this gene directly isn’t that simple. And so this group of Harvard researchers chose to use their new discovery, the fabulous “Post-it-eliminating” molecule (remember that part of the video? Loved it…) called JQ1 to target BET bromodomains to inhibit c-Myc-dependent transcription.
You hit something that’s really close to what you really intend to hit, more simply put. Makes sense.
Check out this direct quote: Multiple myeloma (MM) represents an ideal model system for these mechanistic and translational questions, given the known role of MYC in disease pathophysiology. My goodness! For once, I’m almost thankful to have a cancer that turns out to be IDEAL for research of this quality and promise. I mean, if you have to have cancer, it might as well be an IDEAL sort, no? 😉
A bit further on we can read that the Rearrangement or translocation of MYC are among the most common somatic events in early- and late-stage MM. EARLY STAGE? Bloody ‘ell! But I’m not surprised…
And another thing: The MYC pathway turns out to be hyperbonkerscrazy in more than 60% of patient-derived myeloma cells. Yikes.
The “Results” part mentions MGUS and SMM patients specifically. This is important, so I’ll provide the full quote, hoping not to get into any trouble: Among asymptomatic patients with premalignant disease, we observed increasing expression of BRD4 in monoclonal gammopathy of undetermined significance (MGUS) and smoldering MM (SMM) compared to normal bone marrow plasma cells. In a second, independent data set, we observed significantly higher expression of BRD4 in plasma cell leukemia (PCL) compared to MM or MGUS samples. Thus, BRD4 expression correlates positively with disease progression. I don’t think I need to comment on this paragraph…except to underline the fact that the evil cousin BRD4 is involved in progression to active myeloma. 😯
Okay, so BRD4 is like the Voldemort of the BET bromodomain family. His hyperactivity can lead to PROGRESSION…not good!
But holy cats he’s even worse than we thought. Based on tests carried out in the Harvard lab, the nutty cousin was found also to be in tight cahoots with the bone marrow stromal cells or BMSCs (= which provide a very friendly environment for myeloma cells…). No question…the cousin must be stopped…
As you know, I read the entire study. I read exactly how the Harvard researchers identified and hit their target, proving their hypothesis–that, by stopping the cousin in his tracks, they’d block the padrino. I’ll spare you the gory, impossible-to-comprehend details, though. By the time I reached the last few words in the Discussion section, I felt as though I’d just finished reading Proust in ancient Finnish…
But we still have a few things to discuss before calling it a day…We haven’t even reached the part about the mice…Let’s keep going…
Interestingly, while certainly having an effect on the nutty cousin, our superhero JQ1 did not have a significant effect on the traditional pathways that are also targets in MM treatment: NF-kappaB, STAT3 and so on. Hmmm. Don’t know what to make of that, but anyway, let’s keep reading.
The researchers then treated human MM cells with JQ1. And they sat back to observe the consequence of JQ1 treatment on the expression of 230 cancer-related genes in a human MM cell line.
Wait a sec. Did they write 230 GENES??????? Was that a typo? No, it wasn’t! EEEEKKKK!!!!!!
This is what they found: Surprisingly, we observed immediate, progressive, and profound downregulation of MYC transcription itself, a unique finding among all transcripts studied (p < 0.05). Our superhero, in other words, carried out his job perfectly. By hitting the BET family, BRD4 in particular, he hit the evil myeloma-friendly MYC, too…
Important: MM cell proliferation was uniformly inhibited by JQ1 and that included myeloma lines resistant to Dexamethasone and melphalan. Another crucial bit of information is that JQ1 did NOT have the same toxic effect on normal blood cells. Super.
And now we get to the in vivo part of the study: Tumor-bearing mice were treated with JQ1 administered by intraperitoneal injection (50 mg/kg daily) or vehicle control. JQ1 treatment significantly decreased the burden of disease measured by serial, whole-body, noninvasive bioluminescence imaging. SIGNIFICANTLY. By now you must have seen those mice images in the TED Talk video…
The mice treated with JQ1 lived a lot longer than the untreated ones. At the time of writing, two mice with established disease and measurable M-protein have completed 14 days of JQ1 treatment (25 mg/kg daily, adjusted to tolerability). The second mouse was even in complete remission. Now, remember, we’re talking mice with heaps of lesions all over their poor little skeletons. And the poor little critters responded to this molecule…
Now for the Discussion, which begins with this statement: Despite the centrality of Myc in the pathogenesis of cancer, conventional approaches toward direct Myc inhibition have not proven successful. Eh.
And, further on: An unexpected finding was the pronounced and concordant suppression of multiple E2F-dependent transcriptional signatures. (My own note: curcumin also affects E2F…)
And another thing: BRD4 is an evil cousin also in acute myeloid leukemia. So it seems to me as though JQ1 might well have a glorious future…as a superhero defeater of all sorts of blood cancers…Fingers tightly crossed!
In this study/action movie, all ends well…
As for real life…
What can WE do to help? Blog readers have been excitedly sending me all sorts of links and thoughts and ideas. One suggested that a bunch of us go over to Dr. Bradner’s house and cook and clean for him and his family, so he can focus on his research without any distractions. Great idea! 🙂 Dr. Bradner, if you are reading this, please let us know how we can help you…
Another reader pointed out that JQ1 probably won’t be in human clinical trials for another couple of years. TWO FULL YEARS??? Bloody hell, I don’t know what the cause of such a delay might be, or if that is the case, in fact…but if anyone can find out, please let me know.
So right now I’m trying to come up with tangible things WE can do to help further Dr. Bradner’s research (by the way, I’ve written to him, but he hasn’t answered, not yet, anyway. I imagine he’s super busy, probably overwhelmed with requests and so on…So I don’t expect a reply. Indeed, I hope he focuses on his research, not on replying to enthusiastic supporters such as myself…).
Off the top of my head:
- We can pester our MM foundations, insisting that they do something to hasten the process of getting this BET family inhibitor into Phase 1 and 2 clinical trials AS SOON AS POSSIBLE.
- We can bring up Dr. Bradner’s research at ALL the patient-doctor myeloma meetings. Had I known about this when we met with Dr. Kyle…ah, but I didn’t. (Oh that reminds me…still have to go over my meeting notes…)
- If you have a blog, write about it.
- If you’re on Facebook (Twitter etc.), write about it, making sure you include the link to Dr. Bradner’s extraordinary TED Talk.
- We can also get it circulating in all the cancer support groups. Anyone whose cancer is driven by the MYC gene should be more than happy to help.
- Money, of course. Goes without saying.
- But most of all: LET’S GET THE NEWS OUT!!!
When I first began watching that video two days ago, I’d never have imagined anything this big, potentially. By the way, within a few minutes of my having posted the TED Talk link everywhere I could think of posting it, the Page (where it was located) crashed. No kidding. So Internet can be a powerful tool, and we CAN and SHOULD USE IT! Especially for such a good cause!
And perhaps, some day in the future, we will be able to say that we were THE ones to begin the campaign that ultimately led to THE CURE…Okay, so I’m getting a bit carried away…can you blame me? 😀
And remember the battle cry: OPEN ACCESS FOREVER!!!
Buongiorno a te! :-)
Well, yesterday evening (see yesterday’s post, the second one) was very emotional for me and, when he got home from work, for Stefano, too. As soon as I’d finished telling him about Dr. Bradner’s research, we just hugged. We’re not alone in our joy, either. From the reactions I’ve read on Facebook, private messages I received and the comments left on yesterday’s post, the Jay Bradner video has bowled over other members of the myeloma family…many of us!
My feet are back on the ground now. Well, truth be told, even last night, as happy as I was, I realized that we won’t be slathering our bodies with these molecules any time soon…But, as my friend LPC wrote to me, Dr. Bradner’s research really gives us HOPE. Concrete hope. And we know how important HOPE is in a cancer patient’s life…Just read or re-read Prof. Stephen Jay Gould’s essay (the link is in yesterday’s post, the first post I wrote…). Prof. Gould points out (from memory) this well-known fact, which cannot be explained: patients who never lose hope live longer and do better than those who do (lose hope, that is). That’s why I recommend a belly laugh every day. And that’s why I’ve been seeing my card-playing, game buddies a lot lately. I’m getting picked up in about a half hour, in fact, so I have to hurry. Anyway, we need to have fun and de-stress as much as possible…
I recently heard this pretty song sung by Luciano Pavarotti: http://goo.gl/zr30C I tried to find a proper English translation…but failed. So I translated, more or less, a few of parts I liked the best, including the opening, which sounds better, I must say, in Italian…Still, I found this song/tune so joyful, so hopeful, that I thought it would be appropriate for my state of mind right now:
“Good morning to this day that’s waking up today with you, Good morning to the milk and the coffee, Good morning to those who aren’t here…”
“It’s a new day, and who knows if the world will change…and will dance!”
“But it is dancing (through?) life that you will learn that every great purpose is a step you take. It’s a new day for you, too…Celebrate it with me!” 🙂
One last word or two: I have the full study in my possession, and I began going through it as soon as I got home from work today. But I’m only about halfway done. Not enough for a post. And now I have to go get ready for a fun-filled evening. Oops, I’m late! Stay tuned….more tomorrow…Ciao! 🙂
Thank you, Jay Bradner!!!
I know I’ve already published a post today, and I don’t normally “do” two posts in one day, but I’m sitting at my desk, in front of my computer, with my male cat Piccolo draped across my arms (making it difficult for me to type! He’s such a heavy boy!), very excited…and very emotional, too, after having watched one of the most amazing incredible fantastic TED Talks I have EVER seen. It’s less than 13 minutes…You HAVE TO WATCH THIS VIDEO!
I’m too overcome to say more than this: a team of Harvard researchers led by Jay Bradner has discovered a molecule, JQ1, that makes cancer cells become NORMAL cells. And this, my friends and family, INCLUDES MULTIPLE MYELOMA CELLS. Thus far the molecule has been tested in mice (wait until you see this with your own eyes), but human clinical trials are planned (I tried looking for this molecule on the Clinical Trial website, but I couldn’t find it…I will search some more when I get home from work tomorrow).
Tears of joy are running down my face…I’m sobbing, I’m actually sobbing, while my perplexed Piccolo is looking up at me and purring, concerned, Okay, I can hardly see. I’m sooo happy…Oh I just hope that big pharma won’t be able to stop this from happening…
Without further ado, here’s the link to one of the most promising things I’ve heard/read about since I began my journey with myeloma: http://goo.gl/CQiYk
May the information no longer be a secret! Open source FOREVER!!! Thank you, Jay!!!!!!
UPDATE: A friend in the UK notified me just a little while ago (it’s 8:30 PM in Italy now) that the link didn’t work for him. I tried to access the video in different ways, even looking up Jay Bradner on the TED website, but no, nothing worked. I get taken to a “Page Not Found” on the TED website. I hope the problem is only temporary (perhaps too many people linked to the video, and the system crashed?)…Anyway, it is a problem on their end. Bummer! Has anyone else had the same trouble? Well, it’s getting late here in Florence…I have to get off the computer now. Hope it’s up and in proper working order by the time I get up tomorrow morning, before I take off for work. Anyway, I’m on this story like a dog with a steak bone. So exciting…And yes, I’ve already written to Dr. Bradner… 🙂
UPDATE OF THE UPDATE!!! Okay, thanks to Mary, you can view it here: http://goo.gl/p3Qem Until TED gets it up again, this will have to do…
I see the doughnut instead of the hole, too…
This morning, after reading an interesting New York Times article (thanks, DB!), I began writing another one of my yawnzzzzzzzz lengthy boring yawnzzzzzzzz posts, but at one point I decided to stop writing and let the NY Times article speak for itself. I mean, why should I always stick my inquisitive little nose into things…why do I always have an opinion about everything…why can’t I just shut up for once? 😉 So today I’m shutting up. Hey, y’all, this might be a historic moment! 😉 Okay, seriously now…Basically, the article, written by a medical doctor, is about patients who might have been saved by doing…absolutely nothing: http://goo.gl/BDRgk Of course, thoughts of MGUS, SMM and early intervention strategies (AGGGH) came to mind…
When I’d finished reading the article, I scrolled down the page to read some of the comments. I love comments (hint hint).
And, right above that section, my eye (= the left one, to be precise…my right one was a tad distracted…) fell on a link to a Previous Post titled The Doctor’s Remedy: Turmeric for Joint Pain. Here it is: http://goo.gl/eHjzN
Now, even though, ONCE AGAIN SIGH!, no distinction is made between TURMERIC THE SPICE and CURCUMIN THE ACTIVE INGREDIENT (!!!), the “Previous Post” is still quite interesting…especially if you suffer from joint pain, as I used to…not anymore, of course. With all the curcumin I take daily, it’s a wonder I haven’t started sprouting a mass of turmeric roots from every pore…
One last thing. As I was writing my above-mentioned lengthy comments, I was reminded of Prof. Stephen Jay Gould’s excellent essay, “The median isn’t the message,” which everyone, especially patients with cancer, any type of cancer, should read. Verrrrry interesting, especially if you’ve always wondered about that 5-year average (now upgraded to 7 years, I’ve read…) survival statistic for MM patients…I’ve linked to this essay in previous posts, and here it is…again: http://goo.gl/kOgKA He’s soooo right! And I’m with him on those doughnuts… 😉
Enjoy! Oh, wait, let me make at least one comment…
JUST KIDDING! 🙂 (I mean, just kidding about making at least one comment…)
Cancer patients risk picking up infections in outpatient clinics…
Yesterday I read an important post on David’s blog, concerning the issue of infections, even serious ones, that spread from patient to patient, and we’re talking cancer patients undergoing chemo/radio treatments for cryin’ out loud!, in outpatient clinics. Very unsettling, to say the least. No, c’mon, it’s simply bloody O U T R A G E O U S! Well, with no further ado, here’s the link to David’s post: http://goo.gl/vYlhQ. Please also read the Wall Street Journal article on this topic (link provided in David’s post)…
Just one quote: “Cancer patients are especially vulnerable because their immune systems are suppressed from their disease and its treatment. Nearly 60,000 cancer patients a year have to be hospitalized with an infection.” Eh.
And that could be avoided…
We had an important guest over for dinner last night. My boss, actually. So yesterday, around lunch-time (=best time to avoid germy people if you have a low immune system!), I was at the supermarket getting the ingredients I needed for my planned menu. I also had to get some wine. So there I was, in the wine section of the supermarket, reading labels and trying to decide what to buy. At one point a woman passed behind me with her arms full of groceries. Then…suddenly…Crassssssh!
I looked to the right and saw this lady’s groceries scattered all over the floor, right next to my cart. No eggs, luckily! I asked her, in Italian of course!, if she needed any help. Without waiting for an answer, I bent over to pick up something. And then I heard her ask, over my head, in U.S. English: “You’re American, aren’t you?”
I froze in mid air. “Oh craaaap,” I thought to myself, “I must have picked up an accent when I was in the U.S. Bloody hell, why didn’t Stefano or my best buddies tell me???”
Looking up, with my hand on a pack of paper towels, I asked her, a bit chagrined, “How’d you know?”
(Hey, please don’t get me wrong and think that I might be embarrassed to be a U.S. citizen…not at all. Thing is, I’m not just fluent in Italian. I’m compleeeeeetely BILINGUAL, and I’ve always been really proud of the fact that Italians can’t tell I’m NOT Italian, Tuscan in fact…once I open my mouth, that is. Truth be told, I don’t look Italian at all…I mean, I could be German or British or U.S.–tallish, blondish, Anglo features–well, you get the idea…Anyway, point is, I’d be really devastated if I suddenly developed a U.S. accent in Italian…What can I say? It’s one of my pet peeves. I really like being bilingual… 🙂 )
Back to my story. She looked me up and down and remarked, “It’s the way you look…your clothes. Look at me…We could be twins!”
Explosion of relief in my mind: “PHEW! I DON’T HAVE AN ACCENT!!! YAAAY!” 😀
As for my clothes, it’s certainly true that I don’t get all gussied up when I go to the supermarket. I was wearing jeans that, admittedly, are too big for me, plus a heavy cotton sweater and a lovely Indian scarf that I’d bought in the U.S. a few weeks ago. Yes, I certainly was very casually dressed…Still, I was and am still shocked that she could tell my citizenship just from the way I look…And hey, I was even color-coordinated! 😉 (You know what they say about Americans…)
At any rate, we finished picking up her spilled groceries, chatting all the time. Then she asked: “How come I’ve never seen you around?” A bit taken aback, I almost replied that I don’t really hang out much at the supermarket 😉 , then I realized she meant she had never seen me in the U.S. community in Florence. Well, that was easily cleared up—I simply don’t have any contacts in the American community here. Apart from my blog reader/now friend DB, all my friends are Italian, but that’s a mere coincidence. I grew up and went to school here in Florence. you see, and that is why all of my friends just happen to be Italian. I’d actually love to have more U.S. friends over here, and I’d love to speak more English…
And that may just happen. Perhaps that is why I had this “chance” meeting…that is, to meet more U.S. citizens in Florence. I’d really like that…
In the end, we exchanged phone numbers, e-mail addresses and so on. Ah, that was another weird thing. I mean, I normally would NEVER, not even remotely!, entertain the thought of giving my private contact details to a complete stranger, someone I’d been chatting with for just 15 minutes inside a supermarket. Hellooo? But she was so nice and funny, so I’m really glad I did. We’ll probably get together soon for coffee…and we’re already “friends” on Facebook.
As I was driving home, I considered how odd that encounter had been…I mean, if her groceries hadn’t fallen right next to my cart AND if I hadn’t offered to help pick them up, we wouldn’t have met…The strange things in life, eh…
Smoldering myeloma poll…please go vote!
Hey, all you smoldering hot folks out there! Please go vote in the “Myeloma Beacon”‘s weekly poll! This poll is for those of us who are SMM…not for MGUS or MM folks (the MM poll was the first one…and its results are on the Beacon’s website, in case you’re interested).
I don’t think it’s too late to cast your vote (I got distracted by the Steve Jobs stuff, see yesterday’s post, so I neglected to post this link sooner, sorry about that!), but please HURRY! Here’s the link: http://goo.gl/4ZPBO
I’d like to see at least ONE person in the 15+ years “smoldering” category…I’m currently in the “less than 7 years” category, but my goal is to reach the 15+ one (and much much much higher!), of course! 😉
Good comments, by the way, so have a look at those, too.
Okay, don’t waste any more time…VOTE VOTE VOTE! 🙂
Jobs Tried Exotic Treatments to Combat Cancer, Book Says…
In the past couple of days I’ve read several online newspaper articles announcing the upcoming publication of Steve Jobs’ biography. All these articles roughly claim the same thing, with more or less vehemence…that is, if Steve Jobs had not delayed surgery for nine months after his 2003 diagnosis, he might, even would, still be alive. Over and over I read that by the time he got the operation, it was too late.
Well, that is completely unacceptable. No matter how you spin it.
Before we begin, if the only thing you gather from my post today is that I’m opposed to chemo and radiotherapy and conventional treatments in general, then let me tell you: you missed my point entirely. Okay, now there cannot be any misunderstandings. Or so I hope. So let’s take a quick look at a few of the headlines I read online:
“Steve Jobs died regretting that he had spent so long attempting to treat his cancer with alternative medicine before agreeing to undergo surgery, his biographer has disclosed.” (Telegraph, UK: http://goo.gl/LOns7). Okay, y’all, that’s hearsay. It wouldn’t stand up in court, would it? No. However, that said, I actually don’t doubt that in the end Jobs DID in fact regret not having the surgery in 2003. I can well imagine what pressure he must have been under to start conventional treatment for his cancer. I myself was subjected to some of that pressure back in 2005…
I simply loved this fiery headline: “Jobs Tried Exotic Treatments to Combat Cancer, Book Says.” (The New York Times: http://goo.gl/G4vzr). Hmmm…I’d be very curious to have details on these, er, exotic treatments…I guess they’ll come out sooner or later.
Another headline (different newspapers used the same one): “Steve Jobs Refused Potentially Life-Saving Surgery, Says Biographer.” For crying out loud, didn’t he have the right to choose what to do with his own bloody body? Oh, and please don’t fail to spot that adverb, “Potentially.” Potentially, not “Definitely.” So surgery MIGHT or MIGHT NOT have saved his life. Most people (myself included, at first), however, will interpret this headline as determining that Jobs refused THE surgery that WOULD have saved his life. But hey, nothing is certain, is it? There are so many variables in cancer treatment. I mean, Jobs might have died during surgery (I’ll return to this particular point later)…or right after…or he might have done just fine and still be alive today. Who knows? Who possesses that all-revealing crystal ball?
Now I would like to digress for a few moments and tell a personal story: a few years ago one of Stefano’s cousins, a man in his mid 30s, seemingly strong and healthy, went to the doctor with what he believed was a minor stomach complaint. After various tests, he was diagnosed with pancreatic cancer. Not the slow-growing type, either. Well, long story short: he consulted the best pancreatic cancer specialists thatItalyhas to offer…and he began chemotherapy immediately. Unfortunately, he declined rapidly and died within a few weeks, leaving behind a wife and baby son. Let me tell you, it was absolutely horrible…
I would NEVER maintain, of course, that the cousin might still be alive or might have lived longer and in less pain IF he had NOT gone to the doctor in the first place or had NOT done any chemotherapy. And I’m certainly NOT saying that he’d still be alive or would have lived longer if he’d INSTEAD chosen to do any alternative treatments. To be honest, I think he would have died no matter what…And in the end he was suffering so much (from the chemo or the cancer, who knows?) that we were almost relieved when we got the final phone call…
So let’s go back to that “potentially” life-saving surgery that Jobs refused in 2003…And, just for the heck of it, let’s argue the following: what would have happened if Jobs had agreed to the surgery but then had died during the operation? Would the headlines have shrieked “Steve Jobs killed by surgery”? Or, even more preposterously, “Steve Jobs refused potentially life-saving alternative treatments”? Of course not. No, the headlines would most likely have been: “Steve Jobs died during surgery. His doctors did their best to save him.” And I don’t doubt his doctors did whatever they could to save him, mind you. Again, please don’t miss my main point…
…which is: you do not question conventional medicine…
…but you can question alternative medicine…
Of course there’s some REALLY bad stuff out there, some very toxic stuff that could REALLY, not just potentially!, make you worse, much worse. I’m referring now to those purported “miraculous cancer cures” that you should NOT touch with a ten-foot pole. Beware! There are a lot of snake oil merchants who feed greedily and callously on a cancer patient’s fear and desperation. They’ll assure you that they can cure your cancer. Ah, you have no idea what I would do to those ruthless bastards…And it is certainly possible that Steve Jobs fell prey to some of them. Who knows?
It takes quite a bit of experience to filter the potentially good from the unmistakably bad stuff. If you read about a substance that has no scientific backing whatsoever, stay away from it. And even when it IS properly scientifically-backed, do your research thoroughly, peruse PubMed, ask the experts, consult with your healthcare providers. Check it out carefully, as it could have unwanted side effects or toxicities (cyclopamine comes to mind). And we have to be super careful with dosing, too. Too much of a good thing is probably NOT such a good thing in the end, y’know!
But please remember: there are also some solid alternative treatments out there, which won’t cure you but might really help keep you stable or even bring down some of your markers. And, with integrative oncology, who knows what the future may bring? I have high hopes.
You know, sometimes I wonder how well I would be doing today if, back in 2005-6, in the absence of any CRAB symptoms, I’d chosen to take my hematologist’s advice and go ahead and do chemo + a stem cell transplant. I might be just fine. But I suspect that I’d probably be worse off, to some degree. Back then, you see, I didn’t know about the negative impact of early intervention. Back then, I didn’t know about CRAB symptoms. Again, though, where’s that crystal ball?
At any rate, whenever you read newspaper headlines screeching and squealing that Steve Jobs made a mistake in not choosing surgery, please stop to consider that we just cannot know everything, and that it’s pointless to speculate.
And also…who are we to judge?
Okay. I guess I’d better stop here. This post is getting to be way too long. I don’t want to beat a dead horse, as the horrible saying goes!
Luckily, there is at least ONE reporter with some sense out there (she also gives the reason why all those stupid headlines came out in the first place). And so I choose to end my post with her words: http://goo.gl/MbRYr
Last but not least, I’d like to dedicate this post to Lucie, wonderful writer of the “Green Bananas” blog, who had pancreatic cancer and died last year. She and I corresponded privately for quite some time…She attributed her “longevity” to her curcumin intake. Anyway, a very funny, lovely, talented woman. I miss her quirky sense of humor, just as I miss Nancy’s (La Cootina). You can still check out her blog if you want (see link on the right, under “Other cancer blogs”). There’s some really funny stuff there…
Sensitizing human multiple myeloma cells to the proteasome inhibitor bortezomib by novel curcumin analogs…
Yesterday, Stefano, my smoldering blog reader now real-life friend DB and I attended the meeting with Dr. Robert Kyle (see day before yesterday’s post). I was finally able to shake his hand and thank him for his kindness and for telling me, back in 2005, that I was in the “watch and wait” category and should NOT be treated. He remembered me and was clearly very happy that I am still stable and smoldering. I think I might even have convinced him that curcumin could have had a hand in that. 😉 But that’s for my meeting post, not for this one.
Ah, at the meeting I also met, in the flesh!, a member of the Italian MGUS group of which I am co-administrator on Facebook. It’s so much fun meeting people that you chat or correspond with, I must say. And MF turned out to be a real hoot! Stefano, DB and I also met a couple of other people who were interested in my curcumin regimen. One, another “smolderer,” has already contacted me via the blog…and in fact, I just found out that, following the e-mail exchange we had earlier today, he has already ordered enough curcumin for the initial two-month protocol…wow, that was FAST! 🙂
Anyway, I took copious notes, and Stefano even taped the entire meeting with his iPhone (ahhhh, technology…!), so it will take me a few days to get my thoughts organized enough to write a post.
In the meantime, it just so happens that I received a Google Alert on a new curcumin myeloma study just now. Hah! Timely! So I decided to write a quick note about that today. Here’s the link: http://goo.gl/tYa2u
Okay, so what is this? It’s another proteasome study, an in vitro AND in vivo one. Now, the big proteasome inhibitor in conventional myeloma treatment is, of course, bortezomib or Velcade. But we now know that some natural thingies also inhibit those pesky proteasomes, including curcumin (goes without saying! 🙂 ) and quercetin (see my quercetin post, which I wrote last week)…Therefore, I’m always super pleased when I come across a study integrating conventional with “alternative” (I use quote marks, because I take into consideration ONLY scientifically-backed stuff, not crazy wacky cancer “cures” that have no scientific validity whatsoever…). I mean, c’mon, it doesn’t take a genius to point out that we should stop ignoring the fact that conventional and scientifically-backed natural extracts could really work together to punch our myeloma right where it hurts!!! So let’s team them up! Yeah!
Anyway, these are the bits of the abstract that I found interesting:
- speaking about the use of Velcade for refractory myeloma, about 60% of patients do not respond to bortezomib due to the emergence of resistance. Sixty percent??? I had no idea.
- Here we show that the water-soluble analog of curcumin #12, but not curcumin, in combination with bortezomib could enhance the proteasome-inhibitory effect in multiple myeloma cells. Yeah! Incidentally, until I read the full study, I cannot obviously comment on the finding that “curcumin” (unlike its water-soluble analog, that is) apparently did NOT enhance the proteasome-inhibitory effect of bortezomib. Which type of “curcumin” was used as a control in this study? The abstract doesn’t tell us that. For now, we’ll leave it at that…
- when the myeloma cells were first incubated together with this curcumin analog, they ended up being more susceptible to the bortezomib, even at almost-but-not-quite-lethal doses. I’d say that is really something.
- in conclusion, the researchers state that These findings justify further investigation into those combinations that may yield potential therapeutic benefit.
I’d say so, too! Hear hear!