Tuesday, September 8, 2015

How I'm Planning to Cure Cancer. My Big Idea.

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Okay, so I've been harping on to my friends/family and other connections I have about this big idea I have to "cure cancer". I've been able to explain it to many close friends, and whenever I get time, I explain the idea and process to doctors, researchers, CEOs, med student, as well as laymen friends, but I guess I realised it'd be good to get it down on paper, in a place that many people can access and understand and possibly give feedback or further ideas on. 


So what is it? Is it REALLY a cure? When could it help me or a family member? 

I want to stress that this is just an idea right now. Though many researchers I've talked to are intrigued and say it's very possible that it could be a solution, it's still just in my head for now. There is evidence and proof of concepts for many integral parts of it though. The key is figuring out the gaps and finishing it off. Which I will do soon.

But before I go onto the cure, he's some background on the idea, and the way this disrupts the entire way we're thinking about finding a cure. 


Why The Cure Hasn't Been Found Yet.


The internet is FILLED with conspiracy theories trying to explain this. How can it be that despite BILLIONS of dollars and DECADES of modern research, WE STILL HAVEN'T FOUND IT? 

IT'S THE EVIL PHARMACEUTICAL COMPANIES AND THE GOVERNMENTS! THEY DON'T WANNA FIND A CURE, BECAUSE IT MAKES SOOOO MUCH MOENY!

Well... Yeah... I mean there could be an unknown treaty, or some gang of evil people we don't, and will never know about buried deep beneath every big, small and starting up pharmaceutical/biotech company and government body in the world that stops them from disclosing it... But though there is merit in the idea that pharmaceuticals won't invest in a drug that won't make money (the thing is they have to, it costs billions of dollars to develop 1 drug, takes 10-12 years to do, for an overall 6% chance that it passes trials. Recovering the money alone would require them to charge obscene amounts for drugs. They have to profit on top of that to exist) and though they are bastardly organisations that bribe doctors and misrepresent, or even commit fraud to get drugs approved for sale, this logic fails under the tiniest of scrutiny because if there WAS one single drug out there that could cure it all, or one single target that all cancers are susceptible too, a company would have made tens of BILLIONS of dollars off it by now



A Ted Talk explaining the volatile nature of drug investment; the base reasons behind it that I explained briefly above, and a pretty simple, radical, but very possible solution that can get MORE investment in clinical trials that get drugs to market!

Why Cancers Are So Hard To Treat. How we're doing it Now.


The thing is... there ISN'T a single pathway that you can attack to cure cancer. There isn't some miracle drug or herb that can absolve, or kill off all cancer cells either... Hell, we shouldn't even be talking about curing cancer - because in truth... cancer is not 1 single disease.


We shouldn't even be calling it "cancer." 
We should be calling them "cancers." 

Cancer occurs when a normal cell in our body gets its DNA, the "code" that's behind every function and thing in our body, damaged, which causes it to mutate in such a way that it starts multiplying, uncontrollably, or that it becomes immortal, and doesn't kill itself, as it should, when damaged, or something like that. When multiple mutations occur simulatenously, or when it's combined with other processes that make it evade, or even adapt, almost evoultionarily, to reject the way the body's immune system, which usually polices for, and kills thousands of potential cancers every day, works, it can become bad enough to threaten our very lives. This is a great resource that outlines these methods - be warned though - it is designed to be understood by medical students, so it can be confusing. YouTube gives a lot of this information pretty well though! Ask me anything you want about cancer, I'll try and answer it (if I don't know, I'll learn!)  

There are billions of "base pairs" in a person's DNA, so many pathways a cell could mutate down if damaged (many of which we don't know), so finding the cure for even ONE particular cancer's SUBTYPE is hard. When you consider that every type of cancer has multiple general pathways by which these mutations generally occur, and that EVERY PERSON'S cancer is different (even 2 people with the same, most specific class of cancer will have slightly different mutations), that every person's response to therapy is different and that EVEN IN EVERY PATIENT, THERE'S NOT 1 SINGLE MUTATION PROFILE - pancreatic cancer patients on average have 26 - meaning that every patient has, effectively, MULTIPLE CANCERS at once - which may or may not respond to the same treatments... it seems nearly impossible to find a miracle, silver bullet for even ONE subcategory of cancer. 

But that's not to say there isn't hope. And that there isn't progress. Childhood cancer survival rates for blood cancers (accounting for 40% of all childhood cancers) has improved from less than 10% surviving beyond 10 years in the 1970s, to over 80% today. Survival rates in adult cancers have similarly followed suit, though not all cancers have as high a survival rate as that today. I know mine didn't. But the overall trends are showing improvement due to the fruits of research. And that is good!

Overall survival of cancer for children IS on the up! Data from England from 1990 to now. 
An essay I wrote on how to translate the fruits of basic research into cures faster! I'm writing a book on this topic of improving the pharmaceutical industry soon too. That essay is a "prelude" to it.

More recently though, as we've learned more about cancers, their genetic/tumour profiles and learnt more about how different cancers with different mutated regions of DNA work and respond to treatment, we've been able to start rolling out more personalised treatments. Personalised in the sense that we can now examine a person's cancer cells, look at what mutations have occurred in it, and, through knowledge gained from either our increased knowledge of the molecular pathways of cancer or clinical trials, prescribe treatments that suit the individual patient

This boost in and of itself is remarkable. And as other areas of cancer and of our genome, and body in general become elucidated, we're gonna get overall better outcomes for cancer patients around the globe. Which is bloody awesome! 

The Regulome Explorer - a genome map that highlights to researchers the connections between different mutation regions (often, mutations down one pathway can affect the expression of other proteins in different, but interrelating pathways) and clinical outcomes too. This kind of specificity is becoming a reality! But, as I learned from talking to leading researchers in the Garvan Institute, Sydney, educating doctors, and patients when talking about whole genomes, on how to interpret these things is another issue altogether. 

Immunotherapy is also an emerging, promising field that promises to improve treatments. It essentially describes any effort to engage a patients' own immune system to fight their cancer. This is done by using various mechanisms to allow a patients' immune system to recognise cancers as invaders (eg: dendritic cell cancer vaccines), using specifically designed, cancer targeting immune system components (eg: monoclonal antibodies and adoptive T cell therapies, which are interesting as they take patients' own white cells and redesign them to be cancer killers) or by decrease cancer cells' own immune-evasion mechanisms, to allow patients' immune systems actually stop, recognise and kill cancer cells (eg: checkpoint inhibitors, polsacchraides; aka magic mushrooms). 

A decent summary of the function of the immune cells I'll be talking about most in my solution latet on, that are used most in immunotherapies. CTL = cytotoxic, or toxic to cells, T lymphocyte (lymphocyte = white cell). The B cell pathway, which I'll talk about later, produces antibodies which can go ahead and kill cells without having to go through complex procedures which recruit other cells to come in and help kill them or require cooperation from cells - cancers don't usually cooperate. 
Dendritic cells are professional antigen presenting cells (which are required to activate T helper cells as seen in the diagram above). As seen below, they can activate the immune system against cancers by marking it a foreign substance which T cells can then respond to. Other immunotherapies and their basic ideas are also featured in this great infographic. TCR = T cell reeptor, which allows T cells to go around and examine, or police for bad cells, which their TCRs can regonise. And MHC, seen in both pictures, is, how presenting cells (in MHCIIs case at least) show T cells something bad is about. 





These immunotherapies, if combined with conventional therapy and surgeries, or even on their own, could increase cancer survival rates hugely into the future! Some go so far as to say it's the future of cancer treatment... But hell, my own bone marrow transplant is a crude - hit 'n' miss version of immunotherapy. And it's been around for decades! They gave me someone else's blood stem cells (a common misconecption by many is that they actually need to take your bone marrow. In truth, the procedure on the donor end is similar to a plasma blood donation in over 90% of cases), which make all the blood cells in your body, including your white cells which comprise your immune sysetem. Hence, after the transplant is complete, I've got someone else's immune system in me, and though we're matched, tiny differences between my immune system and my donors are bound to be present, and his immune system will detect and kill those cancer cells, where mine couldn't. 

Adoptive T cell therapy, with a  twist - it's using the HIV virus to manipulate T cells from the patients'  own body to become targeted to cancers. These T cells are then cultured and popped back into the patient's body. But though it's cool this is happening, can this method be used viably on every patient? That's the conundrum my solution seeks to solve.


Though there's this trend I talked about above of more personalised therapies coming out, they aren't personalised in the sense that it actually gives a patient their own, unique treatment that's targeted to their own, unique cancer cells (which, as we know now, can vary, and hence react different to treatment, immencely). The same goes for many immunotherapies. Though the method in the video above is using the patient's own immune system, it still is DISEASE SPECIFIC. It isn't using a widely appliable methodology, one that can potentially work for multiple cancers because it FOCUSES ON ONLY 1 TARGET. 

There have been other cool ideas that try and combine the personalised approach with immunotherapies. This is one of them. When I saw this announced, I was almost over the moon that someone had been thinking like me (my solution and how I got to it is right in the next section)! Essentially - these guys look at individual patient's cancer cells and the mutations they have at them through cytogenetics/flow cytometry methods, and then use computer analysis to determine which cancer-specific proteins will appear on the surface, or be excreted by cancer cells and cancer cells alone, because you don't want to attack healthy, needed cells, due to cancer's DNA being scrambled (the damage done to the DNA leads to these "tumour specific antigens" - TSAs or "tumour associated antigens" - TAAs being present on cancers). From there, white cells are drawn from the patient's blood, hypersensitized and then exposed to those "Tumour Specific Antigens" (those cancer-specific proteins they found before). T cells will now find these cancers specifically, and go on to induce death in them.  

Awesome! Genius! But very cost intensive - both time and money wise - as it takes weeks to 6 months to analyse patients' samples and then determine tumour specific proteins, and thousands, even tens of thousands, to perform those tests in highly specified labs.  Time is something not every cancer patient has. And money, well, unforunately, the way our world works, if this method can't make money, or show extraordinary results, that can be worth it (because even if governments decide to take the short straw and fund it when a company won't, they still have to justify its expense. Right now, though it has shown promise in SOME patients, it still may not hit later trials, or the market, for its viability. Unless it cures 100% of people, then I'll be happy I was wrong) it may never reach second or third phase trials. 

My Solution: 

A broader way, a method, rather than a single target, to get patients' own immune systems killing off cancer cells is what I'd been trying to come up with for ages. And unlike others, it has to cheap, and viable for patients too. And for a while now, I've had an amazing idea in my head that I've been developing, reading up on, and, it seems almost too good to be true, it may just work! Here it is: 


Okay, so how did I come up with it? I wanted to find a one-size-fits-all solution for cancer. I'd seen and talked to too many other cancer patients who'd suffered, and who'd died to this disease to just sit around and do nothing. But I understood the challenges that came with this, and I understood the nature of our current way of finding treatment options; the ultimate aim - to get approved for use against one disease, was not going to foster that easily. 

I knew about immunotherapies, and how they worked, and was very excited about them. Particularly about the potential to find, and hence provide targets to attack, tumour specific antigens which could then be used as "cancer vaccines" - (I can hear the collective clenching of butcheeks of the anti-vaccers reading on here...) vaccines that aren't the typical preventative ones we get for the flu or other diseases, but ones that introduce a foreign particle into the body to induce an immune response against camcers. 

I saw the work by this research team, who was using information on cancer genome databases to predict how likely a patient would respond to immunotherapies, and contacted them, suggesting, "Why not use those databases to find tumour specific antigens?" To my glee, they were already doing that. 
I then asked, "Well could you then identify common trends between cancers, once you'd found some, check that the immune response you generate against them won't hurt healthy cells, and design tumour vaccines that could be used for multiple subdivisions of cancers in a way that doesn't require individual patients to be tested, and have specific vaccines designed specifically for them?", essentially asking him if they could scale the operations up and look for common links, and correlate the information they had with clinical knowledge of what healthy cells may express. To that, he said that it was theoretically possible, and his team had published 1 article on 1 disease to that tune, but that it hadn't been done til then. Hopefully I ignited a spark in his mind, and hopefully he's gone out and done a bit more of digging because he seemed excited by the idea...

But I remember agreeing with the words of a Leukaemia Foundation researcher I was speaking to on the night I gave this speech, nearly 2 years ago now. "Though I'm working on, and bringing immunotherapy to Austraila, I wish there was a way we could make it apply more widely." 

I also knew that a lot of them failed because they failed to induct donors' immune cells against their own cancers in the first place, or they were too disease specific. Which is why I thought, "Well, why don't we use a patient's OWN cancer cells, harvest them maybe, and find out what their tumour specific antigens are." I thought of how you could possibly do that, and the idea of using inactivated, or killed off cancer cells came to mind after a while. What better way to create a vaccine against something was there than to use the dead version of itself? And it was actually one of my treatments I was getting for GVHD (graft versus host disease),  the major side effect of my bone marrow transplant, that gave me inspiration for what to do next. 

This corner of the board is what I'm talking about.

Extracorporeal photopheresis is the name of that traetment. More detail on it is here (a blog post I did on it). And while I was reading up on it, weighing up whether I should do it or not (though it was non toxic, I find this ironic, because it potentially caused my blindness in my left, and near-miss with blindness in my right eye, it was intrusive), as I always do for any of my treatments, I inevitably came across how they thought it worked. Though they weren't sure yet, the proposed mechanism of action for it was essentially that by taking out the white cells of the body, siphoning them away (which required the insertion of a permanent central line into my jugular vein. You can see how that'd be intrusive) from the blood, and irradiating them under UV light, activated T cells, the ones that were currently attacking me from inside and causing my GVHD (graft versus host disease, the side effect of having someone else's blood stem cells - which produces THEIR white cells, aka immune system, in my body), would "apoptose", or self destruct. As they apoptosed, their membranes, or outside, would "bleb" away, or break apart and wrap around the insides of the cells, allowing for them to be taken up by antigen-presenting cells, mainly dendritic cells, that prime the immune system to recognise from those blebs (which would contain protein particles specific to those T cells attacking me - you coudl almost call them T-cell specific antigens) by gobbling up the T cells that were attacking me from within, and presenting their marker proteins for killing by other T cells in lymph nodes, When memory T cells are also recruited, this kills off T cells attacking me indefinitely.

"This same process could be used for cancer!" I thought. So I rushed away and did my research and found that not too many people were actually thinking down this line. See, prior to this, the idea of using your own, dead cancer cells as vaccines had been tried. Others had gotten as excited as I was by the idea, but they had always failed to do significantly better because it had failed to induce a strong enough immune response, if one at all. But this method, which broke those cells down and allowed antigen presentation of tumour markers to T cells, could! And so I went on to learn more about apoptosis, how it worked, the latest we knew about it (because we don't know everything yet), antigen presentation and the methodology of cancer vaccines before one day I stumbled onto this article. 

People were already doing, essentially my idea! Havesting a mouse's own own tumour cells, killing them off, outside the body, with radiation (which I also was thinking of using, as its cheap, easy and most importantly, it induces apoptosis in cells) and then injecting those apoptosing, blebbing away products back into the body to see if an immune response was generated. And it was. That article focused on the idea that it needed to be BLEBS, not the rest of the dying cell material that inevitably comes with them, that needed to be injected in, and is urging that the results from this warrant further investigation of this in actual leukaemia patients - my very own disease. One phase 1 clinical trial had actually used leukaemic blast cells to do that and 2/4 patients with AML - the most aggressive leukaemia, had responded!!  Only last year too had those papers been published. They probably weren't as I'd thought up my ideas, I realised.  Hell - while writing this, I found that one company was already looking to try these in large scale studies for melanoma and had even produced a video explaining the process! Check it out!


Great, right? My work was done! My idea was coming true!!

But not yet... 

Though it is exciting my idea is already out there, being investigated and being done, the fact is, it's still not helping all patients. Meaning it wasn't the cure, as I thought it could be. There were various things blocking the way. I've made a pact to send the researchers, who may not be aware of the work of others in the field, information about other techniques others were using, or more insights into immunology and dendritic cell vaccines that they hadn't looked at, that they may want to add into methods in the future to increase efficacy. Things such as those I wrote up in this corner of that board. 

One of a few extra things they could do to increase the efficacy of this method. And below - more of this, and the fact that this methodology will work best with other standard, and other newer cancer therapies. Sorry about the bad quality pics. Click for close ups. I'll get a better one when I'm home.




There are many reasons why this method could be failing. I plan on sending these to those researchers soon. Perhaps the cancer cells harvested weren't being apoptosed properly in the first place? Radiation is the methodology used in both of these studies, as well as others that have looked into this idea, but there are other agents around that could induce apoptosis more effectively in cells ex vivo (out of the body). Maybe apoptotic blebs and dendritic cell/antigen presenting cell complexes (antigen-MHCII  complex formed at least) weren't reaching lymph nodes? Ensuring dendritic cell loading of vaccines happened in areas of inflammation or areas where immune system signalling molecules, chemokines, of the right type were being released was vital.  Maybe the wrong version of CD4+, or T helper cells, the ones that respond to antigen presentation, were being produced. TH17 cells have been shown to be several times more immunogenic than TH2 cells and there are different signalling molecules that induce their activation. Maybe these need to be given to patients simultaneously?  

But I also knew one thing. Perhaps this methodology alone was doomed to fail in some people, because of the fact that cancers have many methods of escaping the immune system. Some patients may have cancers with these mutations or adaptations in them. Meaning that with this alone... they'd be doomed. 

How cancer cells evade the immune system. 4 major ways they do. 4 ways for this method to fail.

But. 

I've recently come up with a solution to the next part of the problem. One to help even those patients whose cancers could evade the immune system! Because so far we've been talking solely about inducing a T cell response against cancer. What about the B cells? The other major leukocyte? Why not get them involved? 

I can't believe, looking back, that it took me so long of thinking of this idea. But then again... many great solutions, great businesses, and great cures have come from simple, elegant solutions, from a new way of looking at a problem. The fourth and final corner of my whiteboard goes into what that idea is.


Essentially - it's a way to get patients to get their own, autologous, tumour-specific antibodies to be produced to attack cancers! I'd call it "autologous tumour specific antibody production". Or an "autologous /b cell vaccine". Antibodies, unlike T cells, don't require co-stimulation that can be blocked by cancers, through methods such as those in the video above. They don't have limits on where they can go (at least not as much) due to poor tumour microenvironments adapted to shooing away regular immune cells (antibodies are just glorified proteins in comparison to cells). They can be produced by the body in almost endless amounts, and though B cells do often require T cell costimulation, or T cell independent costimulation to start producing antibodies, these can be stimulated in other ways simultaneously to  allow B cells to produce those vital antibodies. 

How this works? Well to explain it better - when we harvest cells for use for use to induce apoptosis in them and bare the cancer's secret treasure - the Tumor Specific Antigens or Tumour Associated Antigens - that mark them as different, we keep a portion (I say half on the whiteboard, but the real proportion will vary) to use as testers to determine what T cells bind to them. 

There is a chance we could skip the whole apoptosis inducing, tumour cell harvest process altogether and skip to this B cell part if there were a way we could create and mature naive T cells, which haven't been taken out if they're autoreactive (I say naive ones, because they'd be more likely they'd adhere to tumour cells, though thinking about it, it could produce false positives, or 'B cell vaccines' that produce self reactive antibodies which is unsafe - a procedure would be needed to eliminate these in that case. I get ahead of myself, this part of the idea is under formulation as you can see haha), and activate them. But preferentially, the other method will be used, as it produces tumour specific T cells which is vital for the next part. 

The tumour specific T cells that are determined from the responses to tumour cells themselves can also be cloned (T cells can be cloned right now, and the major thing which stops them from being cloned, the lack of stimulation by target cells, isn't an issue in this environment, where we're using the target cells - cancer cells) to isolate clones anyway and reinjected back into a patient, to create a larger adoptive T cell response. Perhaps a reason why the first step fails in many patients is that a large enough response isn't generated. And this may be enough to kill cancers on their own.

What needs to be done then is we run the patients' entire (or a large portion of their entire) T cell/white cell population, after having had the patients' cancer cells being apoptosed, introduced into the body with Dendritic cell adjuvants and allowed time to create ample amounts of tumour-specific T cells, against isolated tumour cells, and see which ones adhere. An apheresis machine, or a "donation" of patient T cells and sending it to a lab capable of doin his, will be required. That bit, seeing if/which T cells adhere, can potentially be monitored robotically, independent of people (as is done in the video below, in what is an amazingly cool project), or it can be done in a more scientific manner which I'm sure I, or one of you, will think up soon (as I'm writing this, I'm realising that we could simply monitor for release of Il5, IL9 or other cytokines they release - depending on what kind of THelper cell attaches, as they release different ones, once they've attached to a target cell. OMG I'VE FOUND IT, a much easier way to do this!), but once it is, the T cell will then have its T cell receptor examined, which will elucidate the antigen that the cancer has as its tumour associated antigen!



Once we know what that tomour specific antigen, or that protein complex that marks them, we can simply inject it into the blood, in an environment where T cells are simultaneously active (which it will be if tumour-specific THelper cells are floating around) or in other circumstances, where other co-stimulators of B cells are present, and get B cells that'll produce antibodies specific to a cancer acting against cancer. From there - you could essentially have a T and B cell, autologous antibody production unit that is specific to one person's cancer!

Holy shit. I may have done it. I may have fucking done it. 

Why this will Work. Why this could Fail. 
The pros and cons and the assumptions I've made.


Pros:

  • This works on A LOT of levels, simulatenously. 
  • This method can be combined with other therapies right now. 
  • It is one that can be applied to a whole bunch of cancers, and initiate immune responses to them. 
  • It is one that can work in poor areas too, if the methodology can be reduced to something easy, and replicable, which I believe it can. 
  • Even if it can't, the costs of this will be minimal in contrast to the cost it takes to treat people with the top of the line, latest cancer drugs right now. 
  • And the fact that part 2 of this will require a machine, which can be commercialised, means it can still make money, and hence, it won't be lost in the latrines of the pharmaceuticals and the patents they've made. 
  • If this doesn't work to cure cancer, the very technique, at least the "second half" involving the removal and immunostimulation of patients' tumour cells, could be used to find targets for cancer drugs in a new manner. 

I can potentially patent this idea. But I don't really care if someone else gets it. If it's someone who doesn't want to do anything with it - I've got all these documents of work stored up in Peddal - an electronic public dating list for files which can prove I got to these conclusions before anyone else did. 

The reason this has kept me up at nights... thinking... are the friends I've lost to this disease. The people I know still suffering because of it. The heartbreak I've seen others go through, and the pain I've gone through myself. 

That's what I want to end. 

For Good. And I hope this can actually do this. But. As my wise old dad says - if you have an idea, put it out there and don't be ashamed, afraid, or scaerd if it gets shot down, because in the end, that will allow you to stand back up next time with a better, more bulletproof idea. So let's do that!

The cons/The Assumptions:

  • It will require specialised labs/equipment to do some of these procedures. Apheresis machines aren't cheap. To run or purchase. (You only need apheresis for part 2 - the B cells - though.) 
  • I'm assuming that analysing T cell receptors as they attach to cancer cells will lead to antigens being found. T cell receptors are slightly different to antigens (proteins/antigens don't necessarily act as ligands to them) so it may take a few shots to find the right antigen. I've read up on it briefly. I'll be looking into it in more detail later.   
  • I'm assuming a lot about the potential for antigens, once they're found, to be converted into antibodies inside the patient. I may be going too many steps ahead, and realise later that it's an easy process that a dumb ol' medical student could've reseaerched. Don't worry, I'll be looking into it. But how a protein or peptide (the patient's own antigen), if found, can be replicated and reinjected back into the patient at levels to initiate a B cell response is, right now, beyond me. Don't worry, I'm looking into it though. 
  • I'm assuming all cancers will have external Tumour Specific Antigens or Tumour Associated Antigens (the difference, TAAs usually refer to antigens secreted by the cancer) that can be targeted by antigens if the entire process works. Of course, combination with other therapies to make tumour microenvironments, for instance, more permeable to the immune system which'll be key to this treatment, will be advocated for; probably required to be honest. 
  • The latter brings about another idea. This assumes a patient's immune system is still intact. That isn't always the case, especially with blood cancer patients. However, with current treatment, in many instances, patients can be brought to a stage where their immune systems are competent. If not, perhaps extracorporeal (outside the body) applications will need to be looked into in more detail too. 
  • There are a lot of steps in this process, where each part could fail. Maybe I need a direct route/plan. 


But if this works... goddamnit... it could be amazing. And I really hope it does.

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    medication came to our door step through the delivery agent and

    deliver it to us. immediately we emailed him that we have gotten the
    medication, and the usage instruction manual was also delivered to us.

    my friend Jane started the medication immediately just after a month of using RSO, Jane is now free from cancer problem, she is

    living a healthy life my utmost priority of sharing this short
    testimony is for those that are suffering from this kind of cancer

    diseases or if your friend or family members are suffering from this
    deadly disease, please don't die in silence there is a cure
    for your cancer today don't waste anytime further you have to email Rick Simpson directly and save your live and the lives of
    others email (ricksimpsoncannabisoil97@gmail.com) please spread the goodness of Rick Simpson and his miraculous cannabis oil.

    ReplyDelete

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