Monthly Archives: June 2008

Two new AML stem cell killers

In my June 11 post I mentioned reading about two compounds that effectively eradicate AML at the bulk, progenitor and stem level: celastrol and 4-hydroxy-2-nonenal or HNE (AML stands for acute myelogenous leukaemia, by the way). Well, thanks to Sherlock Smiley face, I was able to read the whole University of Rochester/University of Pennsylvania study. The abstract can be seen here: http://tinyurl.com/6ltvw5

 

The full study begins with an acknowledgment of the importance of cancer stem cells, or CSCs, for studies of basic tumor biology and the development of improved therapies. Like normal stem cells, CSCs are thought to reside at the apex of a developmental hierarchy and are responsible for the continued growth and expansion of bulk tumor populations. Consequently, the biological activity of CSCs may contribute to initiation, maintenance, and relapse of at least some forms of cancer. Yes, this sounds all too familiar…

 

The researchers further comment that several studies have shown that AML stem cells (AML-SCs) are refractory to commonly used clinical agents such as cytarabine and anthracyclines, thereby further supporting the hypothesis that malignant stem cells represent a probable reservoir from which disease relapse may occur. In vitro studies, they continue, have shown that the combination of the chemotherapeutic drug idarubicin and the proteasome inhibitor MG-132 can effectively eradicate leukemia stem cells via a mechanism involving concomitant inhibition of nuclear factor-kB (NF-kB)–mediated survival signals and induction of oxidative stress.

 

Then they discuss parthenolide (PTL), a substance that can ablate AML-SCs as a single agent. As a single agent, mind you! Impressive. They add that the SC-killing mechanism is similar to the one used by the idarubicin and MG-132 mixture, and that is: combined inhibition of NF-kB and induction of oxidative stress, thus indicating that common biological principles underlie the anti–AML-SC effects of these agents despite their chemical diversity.

 

The researchers decided to explore other AML stem cell killing possibilities using gene expression signatures. They examined the natural antileukemia characteristics of PTL, which has been shown to induce very potent and specific effects, mediating rapid death of AML-SCs, but not normal hematopoietic stem and progenitor cells, looking for other substances that provoke a similar response in cancer stem cells. They then tested those compounds against AML stem cells.

 

For this purpose, they used the GEO or Gene Expression Omnibus, a sort of humongous gene expression warehouse. To their surprise, they found a recurring and chemically diverse group of compounds that mimic the PTL gene expression pattern and, like PTL, are capable of ablating AML cells at the bulk, progenitor, and stem-cell level. The sentence that follows is also important: As with PTL, the mechanism of action for these new compounds involves concomitant inhibition of the NF-kB survival signal and induction of oxidative stress, suggesting their general importance in targeting AML stem cells. Sorry to keep repeating “NF-kB plus oxidative stress,” but this is a crucial point, methinks.

 

The researchers identified and tested four compounds, including the two that I mentioned the other day and that inhibit NF-kB and proteasomes. These two were found to have molecular characteristics comparable to those of PTL. I should note that these compounds, while known for their anticancer activity and for their ability to inhibit NF-kB, had never before been tested for their specific ability to target leukemic stem cells.

 

By the way, the other two compounds, gedunin and hemin, did not target the AML stem cells and were therefore discarded.

 

In conclusion, this study is remarkable not only because of the discovery of two new compounds that exterminate AML stem cells, but also because a gene expression database was used to identify potentially useful compounds. Very very interesting approach…

Myeloma’s Achilles’ heel?

The multiple myeloma patient support list (MMSupport) has been buzzing with a bit of news that you can read about on the National Cancer Institute website: http://tinyurl.com/6rwjx8

 

In a nutshell, our myeloma cells rely on the activity of a single protein, IRF4, for the activation of a wide range of genes responsible for cell survival and spread. Blocking the production of this protein can be strikingly effective in eliminating cancer cells in laboratory models of multiple myeloma. “These findings reveal a hitherto unknown and, for myeloma cells, critical network of gene activity centered on this one protein,” said Louis M. Staudt, M.D., Ph.D., deputy chief of the Metabolism Branch at NCI’s Center for Cancer Research. “What we have now is a new window of opportunity for therapeutic development in multiple myeloma.”  The abstract of the June 22nd “Nature” study can be read here: http://tinyurl.com/47ay24

 

IRF4 is not a mutant form, by the way, but its ability to activate normally inactive genetic programs inappropriately is crucial for the survival of myeloma cells. So, by blocking IRF4, we should be able to kill our myeloma cells. Would this include our myeloma stem cells? Well, that is not clear in the news release. Perhaps there is a mention of this in the full study.

 

Speaking of which, my dear Sherlock sent me the full study, but I haven’t had time to read it yet. I will print it out and read it at some point tomorrow and then post about anything of interest, ah, but not until Sunday at least, since tomorrow my brilliant husband is going to check my computer and almost certainly take it apart in order to change or fix a few components that have been misbehaving recently. This means, by the way, that I will be offline (e-mail included) for most if not the entire weekend.

 

Anyway, I also wanted to mention that the IRF4-myeloma connection does not really appear to be a “new” discovery. There may, of course, be some new findings (I won’t know until I read the full 2008 study), but if you search PubMed you will find an IRF4-myeloma study (see: http://tinyurl.com/5cwqzv) published in “Nature Genetics”…in 1997. More than ten years ago, that is…no comment…

 

Now I just have to do some research to find a natural inhibitor of IRF4. By the way, if anyone finds out something in this sense, please let me know. Thanks! Oh, have a great weekend, everyone! Smiley face

No-guilt chocolate mousse

Last year I found a mouth-watering recipe for chocolate mousse on Debra Fioritto Weber’s Guide to French Cuisine website. I have tried this recipe again and again on friends and family members, and “first-timers” have always been completely taken aback when I inform them that the mousse has no added sugar. I repeat, no added sugar. The only sugar in this recipe is contained in the type of chocolate that you use. Therefore, the darker the chocolate, the better. And by omitting sugar, you can enjoy this mousse without worrying about feeding your myeloma or cancer cells. All you need for the recipe is: fresh whipping/heavy cream, good quality dark chocolate, a bit of salt (a bit of salt enhances the flavour of the chocolate) and a teaspoon of liquid vanilla or a liqueur of your choice.

 

The following will make enough (?) mousse for four people:

 

1. Heat 1/3 cup of whipping/heavy cream over high(ish) heat until it (almost) boils.

 

Finely chop 5 oz. (150 grams) of bittersweet or semi-sweet chocolate. I use very dark chocolate to minimize the sugar content.

 

Now, Debra tells us to pour the hot cream over the chopped chocolate and whisk until the chocolate is completely melted and smooth, and I know this is a common method used by patisserie chefs, but when I am in a hurry I just add the chopped chocolate to the cream heating up on the stove. I haven’t found that it makes a huge difference in terms of taste and consistency. Just make sure that you end up with a smooth and shiny mixture. Important: allow the chocolate cream to cool.

 

2. Once cooled, add 1/8 of a teaspoon of salt  and also a teaspoon of vanilla extract (or a liqueur of your choice, just to give it a nice aftertaste). I make my own vanilla since it’s not a typical Italian sweet flavouring (not in liquid form, anyway).

 

3. Beat one cup of whipping/heavy cream (if you want a less solid mousse, use slightly more cream) until stiff peaks form. Add the cooled chocolate mixture slowly and beat on low speed until the mixture forms soft peaks. This will take a few seconds. Don’t overbeat, or the mousse will be too firm.

 

Pour the mixture into a pretty bowl or whatnot and chill until ready to serve. You can garnish the mousse with shaved chocolate curls, raspberries, mint leaves and so on. I suppose I should have thought of taking a photo of the mousse that I prepared yesterday, but my girlfriends came over to play cards after dinner, and between a laugh and a giggle we managed to polish off most of it. Oops!

 

Anyway, enjoy! And please send me feedback if you try this recipe. Thanks! Smiley face

Curcumin, coffee, diabetes, obesity…

I receive all sorts of daily alerts and newsletters. Frequently I am simply overwhelmed with too much information and don’t have the time, unfortunately, to examine it all. Including, I regret to say, some of my blog readers’ links. Well, I do my best! If only I could teach my cats to use Internet…!

 

Anyway, yesterday was the birthday of Florence’s patron saint, St. John the Baptist, so I didn’t go to work (in fact, the company was closed on Monday as well, which made this a four-day holiday, hurray). Since Florence is one of the hottest cities in Italy this week (yesterday we had a Stage 3 heat wave alert, and I think we are still in the red zone today…feels like it, at any rate!), I was happy to stay inside under my ceiling fan and do some catching up, reading and writing. So glad I am NOT a tourist in Florence today…

 

Curcumin, obesity and diabetes. One of the items I read was a Eureka alert (http://tinyurl.com/4qzjre) on curcumin and diabetes. A group of Columbia University Medical Center scientists lead by Dr. Drew Tortoriello, an endocrinologist, discovered that turmeric-treated mice were less susceptible to developing Type 2 diabetes, based on their blood glucose levels, and glucose and insulin tolerance tests. They also discovered that turmeric-fed obese mice showed significantly reduced inflammation in fat tissue and liver compared to controls. They speculate that curcumin, the anti-inflammatory, anti-oxidant ingredient in turmeric, lessens insulin resistance and prevents Type 2 diabetes in these mouse models by dampening the inflammatory response provoked by obesity. I am now curious to read their results, to be published soon in “Endocrinology.”

 

Very interesting topic. My glucose levels are perfect, but they have always been within the normal range, so I can’t say that I have noticed a huge difference. Yes, a bit lower compared to before, but I doubt there is much statistical significance.

 

And the link between inflammation and obesity is also interesting: Curcumin administration was also associated with a small but significant decline in body weight and fat content, despite level or higher calorie consumption, suggesting that curcumin beneficially influences body composition.

 

I am going to try to keep an eye on the work of these scientists because they are exploring novel methods of curcumin administration to increase its absorption, and are also interested in identifying novel anti-inflammatory processes invoked by curcumin and in adapting those processes in the development of more potent curcumin analogues. Yeah!

 

Drink coffee! Another item of interest to those of us, especially women!, who drink coffee is that apparently we will live longer. Have a look at this HealthDay article: http://tinyurl.com/3kojwq Okay, you may well object that this holds true probably only for healthy folks since all the Spanish study participants were free of heart disease and cancer, but hey, every little bit counts. And besides, I will never tire of repeating this!, caffeine inhibits angiogenesis, an important tumour-feeding process.

 

Another bit of recent research shows that drinking coffee lowers your risk of developing type 2 diabetes.

 

Okay, so myeloma may kill me in the end, but these studies indicate that thanks to my coffee and curcumin intake I will die without a trace of diabetes and probably with a healthy heart. Small consolation, perhaps…but after all, chi s’accontenta, gode (I found a not-very-good English translation of that Italian saying: there’s no point in complaining…). Eh!

New myeloma stem cell study

Sherlock (grazie!) came across and sent me a study by Carol Ann Huff and William Matsui recently published in the “Journal of Clinical Oncology” (June 10 2008) and titled “Multiple myeloma cancer stem cells.”. The abstract can be viewed here: http://tinyurl.com/4yx38s

 

The full study tells us that most myeloma cells are mature and quiescent and lack the ability to clone themselves. The fact that the majority of plasma cells are quiescent suggests that tumor growth is restricted to a specialized cell population.

 

A bit of history. In the 1970s Salmon and Hamburger showed that more than 86% of tumor samples from patients with multiple myeloma were capable of colony formation, and clonogenic growth occurred at a frequency of 1 in 100 to 100,000 cells. This could be explained by one of the following hypotheses: 1. only a small, functionally unique, subset of cancer cells was able to clone itself or 2. all myeloma cells can clone themselves, but only a few express this property at any point in time.

 

From what I wrote in my second paragraph, we can figure out that Huff and Matsui believe that hypothesis 1 is correct. Based on scientific data, they suggest that myeloma stem cells are clonotypic B cells: The ability of clonotypic B cells to recapitulate multiple myeloma in immunodeficient mice suggests that these cells represent the cancer stem cell in multiple myeloma. This part wasn’t easy to follow, but basically some features of clonotypic B cells are similar to those of healthy adult stem cells, such as resistance to toxic injury, and the continual risk of relapse among patients treated with standard therapies suggest that myeloma stem cells should also be relatively drug resistant. They can also self-renew and give rise to differentiated effectors (ie, plasma cells).

 

The scientists tested various novel chemotherapy drugs recently approved for the treatment of myeloma. The myeloma cancer stem cells were relatively resistant to both standard cytotoxic compounds and novel agents in vitro compared with the myeloma plasma cells. This suggests that these drugs work against the bigger population of myeloma cells, the ones that don’t have a cloning ability, but have no effect on the smaller population of stem cells. Nothing new here.

 

For the more scientifically-minded, here are a few comparisons between myeloma stem cells and normal ones: it appears that myeloma stem cells display properties common to normal stem cells, such as expression of membrane-bound drug transporters, intracellular detoxification enzymes, and quiescence. Thus, the chemoresistance of cancer stem cells may be mediated by multiple processes similar to those that protect normal stem cells.

 

The paragraphs that follow deal with therapeutic ways to target myeloma stem cells. For instance, as we know, the aberrant functioning of the Notch, Wnt and Hedgehog pathways is fundamental for the well-being of myeloma stem cells. These pathways therefore represent a good target. Let me add that we have non toxic ways to affect these pathways: curcumin, cyclopamine (by the way, I just read that a new water-soluble form has been developed!), zerumbone, DMAPT…

 

Then we are immersed in a discussion concerning telomerase activity…mamma mia, I confess I had to resort to parts of my brain that I never thought I possessed (!) in order to attempt to understand this section…not easy stuff! But, in essence, telomerase activity is an important process in myeloma, and its inhibition means that myeloma stem cells end up not being able to clone themselves. So, telomerase becomes another target.

 

Another promising target seems to be SOX2 (I wrote a post and page about SOX2 a while ago, by the way), an embryonic transcription factor that is normally turned off after embryonic stem cells differentiate; however, in both MGUS and myeloma patients it becomes reactivated (hah! Figures…).

 

Anyway, even if you don’t understand what this all means (as I don’t, to be honest), the point is this: SOX2 antibodies are present in folks with MGUS but not in those with myeloma. If you are lucky enough to possess those antibodies, you are less likely to develop myeloma. So targeting SOX2 could be another way to injure the myeloma stem cells, since, as Huff and Matsui write, SOX2 is a feature of clonogenic myeloma cells, and stimulation of anti-SOX2 immunity could limit clonogenic tumor growth of primary samples in vitro.

 

The development of new evil-stem-cell-focused treatments won’t happen overnight. That much is clear. New trial designs that incorporate novel end points will be needed to study myeloma stem-cell–targeted therapies. One potential strategy is to incorporate these approaches with existing therapies to determine whether they prevent tumor regrowth and prolong the duration of remissions after cytoreduction with chemotherapeutic or novel agents.

 

The researchers admit that the exact phenotype of the clonogenic cell has not been definitively established and controversy remains. Resolution of the controversy will probably depend on how well patients respond to stem-targeted treatments (read: on long-term outcomes…). Time…time…

 

The study ends as follows: growing knowledge regarding the basic biology of multiple myeloma, such as the identification of prognostic categories based on cytogenetic alterations or transcriptional profiling may allow multiple myeloma to serve as a model system to address general questions regarding cancer stem-cell biology.

 

As a myeloma patient, I confess that I (selfishly) don’t care that much about setting up a model system. I care much more about getting the promising, non toxic, stem-cell-targeting treatments into clinical trials as soon as possible. I’m ready and willing to try them!

 

So, where do I sign?!!!

Diet affects cancer genes

A few days ago a blog reader (thanks!) sent me the link to an interesting Medline Plus story (see: http://tinyurl.com/4j9qku) concerning the effect that dietary/lifestyle changes can have on cancer genes. The effect turns out to be quite startling, to say the least.

 

A study recently published in the “Proceedings of the National Academy of Sciences” (full study: http://tinyurl.com/4abcfo) shows that men with early prostate cancer who changed their diet, decreased stress levels and became more physically active were able to change the expression of hundreds of their cancer genes: Some of the changes positively affect genes that help fight cancer, while others help turn off genes that promote cancer development. How about that?

 

A bit of background (see MedLine for the full story): Previous epidemiological studies have found that the incidence of prostate cancer is significantly lower in areas of the world where people eat a more plant-based, low-fat diet instead of the higher-fat, higher-protein diet often consumed in the United States.

 

So a team of scientists decided to conduct an interesting experiment: In September 2005, they reported that after intensive lifestyle changes — consuming a vegan diet with about 10 percent of calories from fat, walking 30 minutes six times a week, and practicing stress management one hour daily — men with early prostate cancer lowered their PSA scores by 4 percent, while men in the control group saw their PSA score rise by 6 percent. PSA (=prostate-specific antigen), by the way, is a prostate cancer marker.

 

But what were the reasons behind such an improvement?

 

The researchers conducted a second study to answer that question: Thirty men diagnosed with early prostate cancer were enrolled in the study. The men were predominantly white (84 percent), with an average age of 62.3 years, and an average PSA score of 4.8 nanograms per milliliter (ng/ml). Their Gleason scores — another measure of the severity of the cancer — were an average of six. The details can be seen in the MedLine article, but what I found extraordinary is that three months of dietary and lifestyle changes affected more than 500 genes. FIVE HUNDRED!

 

Now, I am not suggesting that we ALL go on plant-based or vegan diets. This may not be a good idea for certain types of cancer. For instance, as I have written before, Dr. Gonzalez has found that his myeloma patients respond better to a high-fat, meat-based diet. So please proceed with caution.

 

But if you are at risk of developing prostate cancer, why not change your diet and see what happens?

 

I must admit that reading these articles gave me a sense of power. Even though I don’t have prostate cancer (!), perhaps I can affect my own type of cancer via certain lifestyle and dietary choices. Yeah! food! 

P.S. Last Thursday’s Cancer Compass newsletter also had an article on this topic: http://tinyurl.com/4xy8uy

Dave Barry’s colonoscopy journal

A myeloma list member (thanks!) sent me this journal, and I almost coughed up a lung laughing, so I thought I would post it. I hope you enjoy it!

 

…I called my friend Andy Sable, a gastroenterologist, to make an appointment for a colonoscopy. A few days later, in his office, Andy showed me a color diagram of the colon, a lengthy organ that appears to go all over the place, at one point passing briefly through Minneapolis. Then Andy explained the colonoscopy procedure to me in a thorough, reassuring and patient manner. I nodded thoughtfully, but I didn’t really hear anything he said, because my brain was shrieking, quote, ‘HE’S GOING TO STICK A TUBE 17,000 FEET UP YOUR BEHIND!’

 

I left Andy’s office with some written instructions, and a prescription for a product called ‘MoviPrep,’ which comes in a box large enough to hold a microwave oven. I will discuss MoviPrep in detail later; for now suffice it to say that we must never allow it to fall into the hands of America’s enemies.

 

I spent the next several days productively sitting around being nervous. Then, on the day before my colonoscopy, I began my preparation. In accordance with my instructions, I didn’t eat any solid food that day; all I had was chicken broth, which is basically water, only with less flavor. Then, in the evening, I took the MoviPrep. You mix two packets of powder

together in a one-liter plastic jug, then you fill it with lukewarm water. (For those unfamiliar with the metric system, a liter is about 32 gallons.) Then you have to drink the whole jug. This takes about an hour, because MoviPrep tastes – and here I am being kind – like a mixture of goat spit and urinal cleanser, with just a hint of lemon.

 

The instructions for MoviPrep, clearly written by somebody with a great sense of humor, state that after you drink it, ‘a loose watery bowel movement may result.’ This is kind of like saying that after you jump off your roof, you may experience contact with the ground.

 

MoviPrep is a nuclear laxative. I don’t want to be too graphic, here, but: Have you ever seen a space-shuttle launch? This is pretty much the MoviPrep experience, with you as the shuttle. There are times when you wish the commode had a seat belt. You spend several hours pretty much confined to the bathroom, spurting violently. You eliminate everything. And then, when you figure you must be totally empty, you have to drink another liter of MoviPrep, at which point, as far as I can tell, your bowels travel into the future and start eliminating food that you have not even eaten yet.

 

After an action-packed evening, I finally got to sleep. The next morning my wife drove me to the clinic. I was very nervous. Not only was I worried about the procedure, but I had been experiencing occasional return bouts of MoviPrep spurtage. I was thinking, ‘What if I spurt on Andy?’ How do you apologize to a friend for something like that? Flowers would not be enough.At the clinic I had to sign many forms acknowledging that I understood and totally agreed with whatever the heck the forms said. Then they led me to a room full of other colonoscopy people, where I went inside a little curtained space and took off my clothes and put on one of those hospital garments designed by sadist perverts, the kind that, when you put it on, makes you feel even more naked than when you are actually naked.

 

Then a nurse named Eddie put a little needle in a vein in my left hand. Ordinarily I would have fainted, but Eddie was very good, and I was already lying down. Eddie also told me that some people put vodka in their MoviPrep. At first I was ticked off that I hadn’t thought of this, but then I pondered what would happen if you got yourself too tipsy to make it to the bathroom, so you were staggering around in full Fire Hose Mode. You would have no choice but to burn your house.

 

When everything was ready, Eddie wheeled me into the procedure room, where Andy was waiting with a nurse and an anesthesiologist. I did not see the 17,000-foot tube, but I knew Andy had it hidden around there somewhere. I was seriously nervous at this point. Andy had me roll over on my left side, and the anesthesiologist began hooking something up to the needle in my hand. There was music playing in the room, and I realized that the song was ‘Dancing Queen’ by Abba. I remarked to Andy that, of all the songs that could be playing during this particular procedure, ‘Dancing Queen’ has to be the least appropriate.

 

‘You want me to turn it up?’ said Andy, from somewhere behind me. ‘Ha ha,’ I said. And then it was time, the moment I had been dreading for more than a decade. If you are squeamish, prepare yourself, because I am going to tell you, in explicit detail, exactly what it was like.

 

I have no idea. Really. I slept through it. One moment, Abba was shrieking ‘Dancing Queen! Feel the beat from the tambourine …’

 

…and the next moment, I was back in the other room, waking up in a very mellow mood. Andy was looking down at me and asking me how I felt. I felt excellent. I felt even more excellent when Andy told me that it was all over, and that my colon had passed with flying colors. I have never been prouder of an internal organ.

 

Dave Barry is a Pulitzer Prize-winning humor columnist for the Miami Herald. The whole story can be read here: http://tinyurl.com/yt8xd8

Evidence-based medicine…the Vioxx story

When Stefano got home from work last night, I told him about the FDA’s “avoid non toxic” warning, and he commented “that implies that everything that the FDA approves is toxic!” Eh!

Well, today I thought I would provide a sort of segue to yesterday’s tirade by discussing the Vioxx story and other related matters. Let me start off with an overview of evidence-based medicine…

 

1. The May 11 2008 Moss Report (see: http://tinyurl.com/3q8x2y) has an essay on the issue of so-called “evidence-based medicine.” This expression, Moss tells us, implies that medicine comes in two varieties – the kind that is based on a solid foundation of objective evidence, and the kind that is not. Because of the apparently stark good-versus-bad division it suggests, the phrase lends itself well to being used as a pejorative by those who are outspokenly opposed to complementary and alternative medicine (CAM). To such people, anything other than standard conventional medicine is by definition unproven, speculative, founded on dubious premises and inherently inferior.

 

Okay, so “evidence-based medicine” is generally equated only with conventional treatments. But, and I found this very interesting!, Moss informs us that this was not at all the intended meaning of the term as it was originally conceived. The Evidence-Based Medicine Working Group (EBMWG), a research collaborative of clinicians and epidemiologists from Ontario’s McMaster University, who first coined the phrase in 1992, were not attempting to draw a contrast between orthodox and unconventional medicine; far from it. They were in fact trying to change the medical profession’s entrenched tendency to cling, mainly out of habit, to procedures and treatments for which there was little if any solid evidence of effectiveness (EBMWG 1992). Aha!

 

In this utopian context, the medical experience of an individual (that of yours truly and of many blog readers and list members/friends) would not be dismissed as unproven or anecdotal…how many times have I been told that I am merely an interesting anecdote? Too many times to be counted…makes me smile, actually. On the contrary, in such a context, our results would be studied and compared to the best available external clinical evidence from systematic research. Ah, were that the case…!

 

The “British Medical Journal,” Moss continues, had experts review 2500 commonly used treatments: of these, only 13 % were found to be definitely beneficial, 23 % likely to be beneficial, 8 % equally beneficial and harmful (!), but 46 % were rated as being of unknown effectiveness.

 

Almost half these treatments were of UNKNOWN EFFECTIVENESS? A mere 13% were BENEFICIAL? And this is “evidence-based medicine”!!! EEK! Since at first I wondered if the above-mentioned “treatments” referred to conventional CANCER treatments, I went to the “BMJ Clinical Evidence” website where I found out that no, the term refers to conventional treatments in general; ones, that is, tested in clinical trials for a variety of ailments, not just cancer.

 

The final part of the Moss essay is also interesting, so if you have a snippet of time please go check it out. It has to do with plugging individual cancer patients into so-called standard protocols that are designed mainly to make things easier for our doctors. But what about us, what about the cancer patients?

 

Just a quick comment. I remember my first haematologist (a very nice, gentle man who meant well) telling me that my chemotherapy regime would be “personalized”…I believed him then. But really, what he was suggesting was a standard myeloma drug, Velcade. There is nothing personal about Velcade, whose only variable could be dosage. Back then, though, I believed him (I have not had any chemotherapy thus far, by the way).

 

So let’s define these protocols by what they really are: standard treatments. Period.

 

2. Let’s go to item number two—the Vioxx story that I mentioned yesterday. The April 16 2008 edition of the British “Guardian” has an article about Merck, the well-known multinational drug company, that had hidden death rates caused by Vioxx, also known as rofecoxib, a painkiller of its manufacture. For many years. Merck provided the FDA only with selected data on deaths in its clinical trials, and failed to include people who had a fatal heart attack soon after coming off the drug. Oh, but the story gets “better”…

 

[…] papers published in journals on the results of Vioxx trials were ghostwritten by employees or contracted medical writers, and […] leading doctors were later invited to be named as authors. Financial links were sometimes but not always declared. So, basically you (=drug company) hire a medical writer to write a favourable clinical trial report extolling your newest bestest drug and then ask a couple of doctors to put their names on the report. Nice, huh?

 

The revelations about Merck’s scandalous, indeed criminal!, conduct were published in the “Journal of the American Medical Association” in April (see: http://tinyurl.com/4z6jch and http://tinyurl.com/4pga4h). Vioxx, by the way, was pulled from the market in September of 2004, the biggest market pull in history!, after reports of deaths, heart attacks and/or strokes. Merck officials knew of the risks, apparently as early as 1997, but did nothing until a clinical trial in 2004 showed an increased risk of heart attacks and strokes. Merck knew. Did nothing…

 

This drug, like (I am sure!) many others, had no business being put on the market in the first place. Ah, but you see, it was a bestseller during the five years or so that it was on the market. Must have made Merck a bit more than a pretty penny, don’t you think? Speaking of pennies. Last November Merck settled with $ 4.85 billion the thousands of Vioxx lawsuits that involved 47,000 people. Take a look at the New York Times article on the settlement: http://tinyurl.com/4ajxrc. Appalling.

 

And, by the way, the practice of hiring folks to write up fake clinical trial results (etc.)—ghostwriting—is apparently widespread, as we can read in this April 16 2008 New York Times article: http://tinyurl.com/5ydl2u.

 

Evidence-based medicine. I’d say this is evidence that some or most or all drug companies are about as trustworthy as little kids caught with their hands inside the cookie jar…

 

P.S. According to a long 2006 report (see link below), Merck’s top management lost no sleep whatsoever over the Vioxx disaster, and in fact would be happy to see Vioxx put back on the market (!). Oh, and the FDA apparently knew about the problems caused by this drug as early as 1999 (the proof is in a 1999 memo). Shameful. See: http://tinyurl.com/4lsv5j 

Medicine is no longer about health, it’s about market share and profits.

Big Brother

A blog reader (thank you!) sent me some interesting info and links about warnings issued recently by the FDA (= Food and Drug Administration) to 23 companies and 2 individuals promoting various unproven cancer treatments that falsely claim to cure, treat or prevent cancer (see: http://tinyurl.com/3o89hf). I found this all so interesting and maddening at the same time that I wrote about ten pages of comments and denunciations…then did some drastic editing so I wouldn’t bore you all to tears.wink smiley What follows is what is left over from my drastic bit of chopping (so I hope it makes sense!).

 

The following link takes you to an FDA page titled “125 fake cancer cures consumers should avoid”: http://tinyurl.com/5hfj6e. I became exceedingly concerned when I saw that curcumin is listed here, too.

 

Now, I agree that, even though curcumin inhibits Notch signalling (important for the well-being of cancer stem cells) etc., it will not “cure” cancer, not by itself at any rate. As far as myeloma is concerned, we have to eradicate the myeloma stem cells to achieve a cure, and that, I am afraid, is not in the immediate future.

 

So curcumin may not be a cure, but in my particular case (I could also cite dozens of other curcumin-taking cancer patients whose results have been even better than mine!) it has kept my myeloma inactive and stable for more than two years…not to speak of how much I have benefited from more than a few unexpected side effects: cholesterol decrease, no more infections, aches or pains, etc. etc. etc.!

 

No, I was not at all pleased to find curcumin mentioned on this page in the same breath as “fake.”

 

http://tinyurl.com/67fz7n: this FDA page is titled “Beware of Online Cancer Fraud” and contains some valid suggestions, for instance how to protect ourselves from fraudulent cancer-curing online claims. Run in the opposite direction if you read sentences such as “treats all forms of cancer,” “skin cancers disappear” and so on. I too have come across some blatantly false, even absurd, cures for cancer online…and I for one would be very glad to see these types of websites disappear into the huge cyberspace rubbish bin.

 

However, scrolling down this particular FDA page to “Red flags,” I had a bone to pick with the warning against anything that claims to be “non-toxic.” Now, why should “non-toxic” be considered to be a “red flag” as a general rule if, and I repeat IF!, there are scientific studies to support such a claim for a certain substance?

 

Let’s take curcumin, for instance. Every single scientific study that I have read so far classifies curcumin as “non-toxic.” Therefore, based on the FDA red flag warning, I should avoid taking it… right? Does that make any sense? No, thought not. This business totally irritated me, and even the fact that Italy won against France last night didn’t mollify me.

 

A June 17 Bloomberg article (see http://tinyurl.com/6c24mu) provides an overview of the recent FDA activity. A few sentences in particular struck me: Regulators are concerned that patients could suffer side effects or forgo treatments that work, said Michael Levy, director of the FDA’s division of new drugs and labeling compliance. And, he continues, the FDA is very concerned that consumers will purchase these products from the Internet and use them instead of products that have been proven safe and effective. “Proven safe and effective”? Wait a sec. What the heck does that mean?

 

Hmmm, let’s see…if I got it right, according to the FDA it’s okay to take something that might harm or poison or even kill us if we fall within the small percentage of folks who have a reaction to an approved and allegedly “safe” FDA drug (shall I tell you the FDA-approved Vioxx story?), but it’s not okay to take something that has been used by folks for centuries and that has zero toxic side effects? I see…

 

In sum, I would like to state that I agree with the FDA that there are a lot of bogus online claims peddling miraculous cures for cancer. I have read some of ‘em myself. So if you come across a substance that sounds intriguing, please make sure it is backed up by scientific studies (the NCBI website can be very helpful in that sense: http://www.ncbi.nlm.nih.gov/).

 

At the same time, I am concerned that curcumin is mentioned on an FDA no-no list. I am afraid that that might scare people off, people who instead might benefit from taking curcumin. I hope that won’t happen.

 

It’s easy enough to sift through and separate the good information on Internet from the bad. If there is no scientific support for a product/substance, I don’t even take a second look at it. Period.