My “Eureka” moment. A cure for cancer.

Suggesting a scientific approach and method for the medical treatment of tumorous cancer.

Abstract

A new 2-phase treatment to cure cancer is proposed.

Phase 1 would use a live bio-agent paired with a moderating anti-bio-agent drug to target and kill hypoxic cancer tumour cores.

Phase 2 would employ 2 drug types - firstly a mixture of drugs of the growth factor inhibitor type, some (perhaps most) yet to be developed, would be required to halt selectively all normal cell division but not halt the characteristically aberrant cancer cell division and secondly, conventional chemotherapy drugs would be used to target and kill only the dividing cancer cells.

Summary

A scientific approach and method for the medical treatment and cure for tumorous cancer disease is suggested and described.

The desired performance characteristics of suitable types of biological agents and pharmaceutical drugs and an appropriate method of employing those agents and drugs for the treatment and cure of cancer is described.

Caution

Neither the selection of specific agents and drugs, nor the determination of the optimal treatment regimes are described herein because the details for how best to implement the author’s general approach and method to cure cancer still require further research by the scientific and medical community which it is hoped this scientific paper will inform and inspire.

So the reader should be cautioned that the author does not herein publish detailed suggestions for oncologists to prescribe for their cancer patients which pills to pop when. The author is a scientist who is trying to find a cure for everyone one day, not a doctor who can cure someone today.

Invitation to informed discussion

This is claimed to be a realistic scientific paper, not a snake-oil-style cure-all claim. This may not be obvious to everyone because I am an amateur independent scientist, neither employed as a scientist, nor published in traditional scientific journals.

I have published widely on the internet on mostly non-scientific topics and I am accustomed to debating my ideas on-line and so I’m quite comfortable inviting replies perhaps as helpful comments and criticisms from fellow scientists and I can also take questions from any cancer specialists, doctors or other informed parties who take an educated interest in such matters.

Approach and method

One type of biological agent and 3 types of drugs are utilised in 2 distinct treatment phases, perhaps with an intermission between phase 1 and phase 2 of the treatment to review that the goals of phase 1 treatment have been reached before moving on to phase 2.

Treatment Phase 1

It is proposed that phase 1 use a mild anaerobic biological agent (with the suggestion that this is mostly likely to be a selection of a mild, treatable, non-drug-resistant anaerobic bacteria, sourced from a well-characterised laboratory specimen) with which the cancer patient is purposefully infected and 1 type of drug, matched to be a known effective treatment capable in high doses of eliminating the selected bio-agent from the body or in small doses to moderate the intensity of the infection.

During phase 1 treatment, after purposeful infection with the known mild anaerobic bio-agent, the anti-bio-agent drug is administered but only sufficiently to moderate and limit the intensity and systemic effects of the intended mild infection on the patient yet not overly administered to the point that the bio-agent is destroyed in-vivo before it has it has completed the designed treatment objectives of phase 1 treatment.

In phase 1 of treatment, the expectation would be that the patient’s own immune response will be fighting the bio-agent and so the course of the infection must be monitored and bio-agent and drug doses continuously adjusted to maintain a mild infection.

The objectives of phase 1 treatment

The bio-agent is selected with intention that the infection should establish itself in any anaerobic cores of cancer tumours and be supervised there while the infection attacks and in due course kills those cancerous body cells in any and all anaerobic tumour cores in the patient’s body.

The mild anaerobic bio-agent is selected and managed in-vivo so that it cannot be active, only dormant, in most of the aerobic environments of the body which are routinely supplied with oxygen via the blood, and so an appropriate selection and controlled bio-agent should not harm typical body cells so long as the infection is constrained to be mild with limited systemic effects on the body.

The selected bio-agent is not intended to harm those cancer cells which are growing and dividing in an aerobic environment whether in peripheral parts of all tumours or in aerobic tumour cores which are have grown their own blood supply vessels.

The dangers of a failed phase 1 treatment

Too much bio-agent

Inappropriate selection of a drug-resistant bio-agent, neglecting to moderate the intensity of the infection with sufficient drugs or a patient’s weak immune system failing to eliminate the infection at the conclusion of phase 1 of treatment could lead to a run-away infection causing serious and life-threatening infection or death.

Too little bio-agent

Administering insufficient bio-agent, over-use of drugs or a particularly active immune system could lead to the bio-agent failing to establish itself in all anaerobic tumour cores and a failed attempted phase 1 treatment leaving viable anaerobic tumour cores which would inevitably wreck the hopes for a successful outcome to any attempted phase 2 treatment.

Treatment phase 2

It is proposed that two types of pharmaceutical drug are employed in phase 2 treatment and let’s call them type H drugs ("H" for “Halt cell division!” ) and Type K drugs ("K" for “Kill diving cells”).

Type H drugs - Halt cell division!

Type H drugs are the author's own name for a class of drugs examples of which are used in medicine and biological science and commonly referred to variously as "growth factor blockers", "growth factor receptor blockers", "growth factor inhibitors" or "growth factor receptor inhibitors" and possibly other names as well.

Those drugs are designed to target cell growth factor receptors and interfere with growth factors activating growth factor receptors to prompt growth in cells.

A traditional approach in oncology is to attempt to use those drugs directly against cancer cells to try to modify their aberrant excessive growth behaviour. That is not the new approach explained here which is rather to use those growth factor blocker drugs against the growth behaviour of normal cells.

Type H drugs ("H" stands for for "Halt cell division!") utilise and are intended temporarily to saturate the normal cell-signalling pathways which instruct normal cells not to divide. Normal cells with the exception of cancer cells pay heed to such cell to cell signals and it is one of the defining characteristic of many cancers that cancer cells ignore such signals not to divide and keep on dividing regardless.

The purpose of administering type H drugs is temporarily to overload the normal signals and order an artificial system-wide cessation of all normal cell division in the body. Accordingly, normal cells which frequently divide - skin cells, intestinal wall cells, immune response cells, bone marrow cells, reproductive organ cells etc are tricked into stopping dividing temporarily, so long as the type H drug is administered.

Type H drugs operate in a pharmaceutically reversible way and when the type H drugs clear from the body then the normal body cells which have dutifully followed the artificial signals and temporarily ceased dividing then go back to their normal operation without any permanent damage to the cell.

Clearly, the administration of type H drugs weakens the body systematically which depends on routine cell division and for so long as type H remains in-vivo then harm to the body’s health will accumulate.

Type H drugs don’t do the body any good on their own. Not only that, but for the purpose of treating cancer, type H drugs aren't intended to do anything significant directly to those cancer cells which are pretty much oblivious to the cell signalling pathways which type H drugs are designed to stimulate.

Mechanism of action of type H drugs

Specifically the mechanisms behind the cessation of general cell division which the type H drugs must target are those which usually control cellular division of cells.

The type H drugs work by interfering with the control mechanisms which the body uses to stimulate or start cell division at certain times and under certain conditions and to suppress or stop cell division at other times and that interference would be designed to jam the control mechanism so as to stop cell division so long as the drug is in the body.

Many types of cancer cells divide regardless of the body's control mechanisms - such cancer cell division isn't started selectively so it can't be stopped either naturally by the body's control mechanisms and sometimes even artificially by pharmaceutical drugs

Growth factor mechanisms would be suitable targets for targeting by the type H drugs.

So for example, typical normal cells will wait for the appropriate growth factor to attach itself to the corresponding growth factor receptor on the cell's surface before initiating cell division.

Many types of cancer have cancer cells which will divide regardless of whether there is the appropriate growth factor attached to the cancer cell's corresponding growth factor receptor or not.

One obvious approach the drug developer could take would be to design a type H drug which mimics a growth factor receptor's shape and thus will selectively bind to the corresponding growth factor. If there is a lot more of the type H drug in the extra cellular fluid than there are cell growth factor receptors then the growth factor would be mopped up and leave none free in the extra cellular fluid to be available to bind to the cells' growth factor receptors, thus preventing normal cell growth from being initiated.

A similar approach to date more commonly adopted with blocker-type drugs would be to design a growth factor receptor blocker / inhibitor drug which partially binds to target cell growth factor receptors, not bound accurately enough to activate the cell growth factor receptor function, but sufficiently bound to block growth factor binding to the growth factor receptors.

Whatever the precise mechanism of interference of the type H drug with the growth factor mechanism we can name such type H drugs as "growth factor blockers" or "growth factor inhibitors".

Type K drugs - Kill dividing cells

In order to understand the utility of type H drugs one has to consider their medical use in conjunction with type K (K stands for "Kill dividing cells") drugs.

Type K drugs are the author's name for a class of drugs which are well known to medical science. They are the traditional chemotherapy drugs which have long been used to try to treat cancer by killing dividing cancer cells but the problem with those old drugs is that they tend to kill all dividing cells, not just cancer cells and so have very severe side-effects which can make the patient very ill, very quickly.

OK, well the smarter reader will see by now where we are going with type H drugs. After administration of type H drugs which hopefully succeed in suspending normal cell division without significantly affecting cancer cell division, the administration of the type K drugs is now "a no-brainer"! That is to say, the remaining task for type K drugs becomes a relatively trivial task to accomplish with no undesirable side-effects.

The dividing cancer cells alone should get killed by the type K drugs. The normally dividing cells don’t get killed by the type K drugs because they are no longer dividing thanks to the administration of the type H drugs.

After the dividing cancer cells have died all that remains to be done is to clear the type K drugs from the body while the type H drugs are still in operation. Then later it is safe to discontinue the type H drugs at which point the body will resume normal cell division, free from cancer!

Treatment phase 2 - continued


Limitations of phase 2 treatments

One limitation of the simple approach in phase 2 of shutting down all normal cell division in the body would be with those cancer types which are cancerous not so much because the cancer cells divide abnormally but because the cancer cells don't die or undergo programmed cell death called "apoptosis" normally and are abnormally immortal.

Such normally dividing but abnormally immortal cells would cease dividing if an all-body-tissue type H drugs dose was given and so such cancers wouldn't be killed by the type K drugs and such a broad-brush approach wouldn't achieve the cure in phase 2, only the benefits of the treatment in phase 1.

However, it has recently occurred to me that there is still a prospect for a more customised version of my approach offering an admittedly less-than-ideal phase 2 treatment option even against many such normally-dividing abnormally-immortal cancers where the type H drugs comprise of a mixture of different type H drugs, one such type H drug for each tissue type of cell growth factor which needs to be blocked.

To beat the cancer of cells from tissue type X in a normally-dividing abnormally-immortal cell cancers, you'd omit the specific type H drug for the tissue type X growth factor from the type H drugs dose given to that patient and simply intend to kill all dividing cells of tissue type X, which would certainly cause major damage to tissue of type X but maybe in some cases that is a price worth paying to beat the cancer? It's more of a useful treatment option where medicine can offer an artificial or transplant option to replace damaged tissue of type X, or restore the lost function, as required.

For those remaining stubbornly phase-2-insenstive or intractable cancers, a phase 1 only approach can partially treat tumours while never managing permanently to cure the patient and so a series of phase 1 treatments could be used to achieve a series of remissions of the disease.

With a phase-1-only approach it may be observed in some cases that a permanent cure is fortuitously happened upon because the patient's immune system is alerted by a phase 1 treatment to learn to identify the cancer cells and to eliminate them naturally in future.

The dangers of a failed phase 2 treatment

The patient will be rendered vulnerable to infectious disease because of the predictable effect of the Type H drug which will prevent parts of the immune system from responding to infections. Worse case of course is that an opportunist infection may kill the patient.

If the Type H drug is not as effective as intended, if the dose is too low, if it is too quickly cleared from the body then the Type K drug will kill normally dividing body cells as well which cripple multiple body functions which depend on dividing cells and worst case kill the patient.

Without a successful phase 1 treatment which has previously killed anaerobic tumour cores, phase 2 treatment will only kill cancer cells dividing in aerobic environments leaving any and all remaining viable anaerobic tumour cores to provide an inexhaustible supply of cancer cells into the aerobic parts of the body. Phase 2 on its own cannot cure cancer; only after a successful phase 1 can it do that.

Conclusion

Sourcing all the type H drugs required for this approach is the biggest unknown at this point but I'd be hopeful that this approach could treat a very large number of cancers indeed, though I would never claim to be able to cure "all" cancers with this approach.

Conceptually, this would seem to be an excellent scientific approach and method for the cure of tumorous cancers.

Credits

Thank you to all those from whom I have learned so much.

Dedication

This cure for cancer paper is dedicated to my mother who lives still and to the memory of all my friends and relatives who have died from cancer for whom this cure is too little and too late.

This cure for cancer paper is also dedicated to Condoleezza Rice who has inspired me to understand that I may not be able to control my circumstances as a scientist without employment as such but I can control how I react to my circumstances. Condi’s mother also died from cancer and she has participated in Race for the Cure events.



Prizes.

I do not want the Nobel Prize for Medicine or indeed any Nobel prize so long as Sweden remains governed as a kingdom. I want nothing from the Swedish King nor from any King nor Queen.

I am a republican and only wish to receive prizes, awards or recognition while living or posthumously from republics or at least from non “royal” institutions which find themselves in the unfortunate circumstance of operating as I do inside a country currently governed as a kingdom.


Author's glossary

Anti-bio-agent drug - an antibiotic drug selected to be used to moderate or to kill a particular bio-agent as and when desired

Bio-agent - a live micro-organism used as an agent to achieve some useful purpose

Type H drug - a growth factor receptor inhibitor drug used in a dose sufficient only to HALT the growth of normal cells but no more, with the intent of allowing cancer cell growth not to be inhibited preparatory to the use of a type K drug

Type K drug - a cytotoxic antineoplastic chemotherapy drug used to KILL dividing cells especially dividing cancer cells while a type H drug inhibits normal cells from dividing


Some relevant links on Wikipedia

Management of cancer

Clostridium novyi-NT - Potential Therapeutic Uses in Cancers

Obligate anaerobe

Antimicrobial

Hormonal therapy (oncology)

Growth factor receptor inhibitor

Chemotherapy

Hows about a cliffs notes or a tl;dr because wordy things make understanding things complicated when you're trying to get what the idea is.

What is the simple premise.

?

Phase 1 would use a live bio-agent paired with a moderating anti-bio-agent drug to target and kill hypoxic cancer tumour cores.

that means nothing to someone like me. live bio-agent? what is it. Moderating anti-bio-agent? again.. what is it?

Eureka implies you had an insight... not a complex theory.. Oo

-- lol ok third post.

Author's glossary

Anti-bio-agent drug - an antibiotic drug selected to be used to moderate or to kill a particular bio-agent as and when desired

Bio-agent - a live micro-organism used as an agent to achieve some useful purpose


I still have no idea. sticking a bug in someoen to attack a cancer cell, then sticking an anti-bug in to kill the bug.

DOn't they do this already?

I still .. never mind, im not a doctor or a scientist...

winofiend
Hows about a cliffs notes or a tl;dr because wordy things make understanding things complicated when you're trying to get what the idea is.

What is the simple premise.

?

Sure well you got the idea of the phase 1 treatment all worked out yourself.

winofiend

I still have no idea. sticking a bug in someoen to attack a cancer cell, then sticking an anti-bug in to kill the bug.

Correct.

The bugs can only attack those cancer cells which are in the middle of tumours and not growing because they are not getting the oxygen they need to grow there but killing them is worth doing to get a complete cure at the end of the treatment.

winofiend
DOn't they do this already?

Well it tends to be an experimental cancer treatment as far as I know.

Maybe its routine clinical practice somewhere but not that I've heard of.

The problem with it, is that it is not a complete cure - it only attacks those cancer cells in the middle of tumours.

The bug treatment needs to be paired up with a 2nd treatment which targets the other cancer cells which are not in the middle of tumours and that's where various bug treatments will differ from each other most in their approach.

So just because some other approach uses bugs that doesn't mean that the approach there is the same as my approach because my secondary treatment will be different from theirs.

winofiend

Phase 1 would use a live bio-agent paired with a moderating anti-bio-agent drug to target and kill hypoxic cancer tumour cores.

that means nothing to someone like me. live bio-agent? what is it. Moderating anti-bio-agent? again.. what is it?

Eureka implies you had an insight... not a complex theory.. Oo

-- lol ok third post.

Author's glossary

Anti-bio-agent drug - an antibiotic drug selected to be used to moderate or to kill a particular bio-agent as and when desired

Bio-agent - a live micro-organism used as an agent to achieve some useful purpose


I still have no idea. sticking a bug in someoen to attack a cancer cell, then sticking an anti-bug in to kill the bug.

DOn't they do this already?

I still .. never mind, im not a doctor or a scientist...

edit on 22-10-2013 by winofiend because: (no reason given)

Well to summarize the phase 2 treatment, it's like conventional chemotherapy but better.

It's better because it doesn't have all the nasty side effects and a long recovery period after the chemotherapy is over.

Yes there are some bad side effects with my phase 2 treatment but those side effects don't last very long after the chemo is over.

My phase 2 treatment spares the long recovery periods by protecting the patient's normal cells from getting killed by the chemotherapy - it makes it more specific against the cancer.

Interesting ideas, I'll give you that, but I'm concerned in a few ways with Phase One (more my area of knowledge, as you can probably guess from my username):

1. Purposefully injecting someone with a bacteria that is capable of causing significant cell death is generally not a good idea. Even many anaerobic bacteria are capable of growing in various parts of the body and limiting the cell-killing effects to just the tumors is likely to be problematic.

2. Establishing infection via induced bacteremia or systemic infection within the tumors may be difficult, especially if there is limited blood supply (which may be the case in the hypoxic regions of the tumor).

3. Even if the process were successful in infecting the tumors (and only the tumors) with a sufficiently virile bacteria to cause cell death in hypoxic environments, the end result would essentially be creating pockets of necrotic tissue in the centers of tumors. Pockets of necrotic tissue are going to cause issues unless removed or debrided, at which point surgical removal of the tumors would probably make more sense.

4. I would imagine there is some possibility of viable bacteria remaining in the tumor cores even once systemic infection has been eliminated. Phase Two would likely cause rupture of these tumors to some degree, potentially releasing extremely large quantities of bacteria into the blood while the immune system is severely weakened from the Phase Two drugs.

I am far less knowledgeable about the biology behind Phase Two, but I do still have a few concerns to raise:

5. The doses and variety of 'Type H' drugs needed to reach the level of inhibition that this phase seems to require is likely to have a significant risk of side effects. Stopping cell division throughout the body is not an easy task and inhibiting certain types of cells is likely to cause significant problems. Many of these problems are may be similar to those currently faced by patients undergoing chemotherapy.

6. Significantly higher doses (or stronger versions/alternatives) of 'Type K' drugs than are currently used are likely to cause major problems if the 'Type H' drugs have not been sufficiently effective. Testing the effectiveness would be difficult at best and may well be impossible without major advances, especially given the short time-frame during which 'Type H' drugs can be given in high doses - too long and severe harm will begin to be caused to various organs.

In Conclusion

Although it may sound like it, by intention is not to discredit or dismiss your idea. I like that you have taken a scientific approach and exhibit clear rational thinking and logic. You've connected many concepts and facts together into a proposal that I have never heard of before.

That said, I am confident that we do not currently have the technology and know-how to make a treatment like this a reality. There is far too much reliance on chance, especially with the bacteria selection and timing and dose for administration of the drugs in Phase Two. A carefully bio-engineered bacterial strain could work well, but would need to be created first. The drug administration would be more complex, mainly because I do not believe we currently have tests to determine proportions of tissues under cell cycle arrest (aka, the effectiveness of the 'Type H' drugs on a body-wide level).

Microbiologist
Interesting ideas, I'll give you that,

Well thank you very much for that.

Microbiologist
but I'm concerned in a few ways with Phase One (more my area of knowledge, as you can probably guess from my username):

I really appreciate you sharing your knowledge here. Let me see if I can address your concerns.

Firstly, I'd recommend this link as a starting point for more knowledge about bacterial treatments in cancer.

Clostridium novyi-NT - Potential Therapeutic Uses in Cancers

Microbiologist
1. Purposefully injecting someone with a bacteria that is capable of causing significant cell death is generally not a good idea.

Yet allowing cancer cells a refuge inside hypoxic tumour cores, where they are quiescent and relatively resilient to traditional chemotherapy, though generally done, is a much worse idea because it allows the cancer to re-emerge.

Yes there are risks of injecting someone with bacteria but if the goal of a permanent cure can be had by taking the risks then it's worth it if those risks are manageable.

Microbiologist
Even many anaerobic bacteria are capable of growing in various parts of the body

Most famously in the gut but they can lurk in other places in the healthy body too.

Microbiologist
and limiting the cell-killing effects to just the tumors is likely to be problematic.

Yet limiting the cell-killing effects only to cells likewise in a state of hypoxia should be no problem.

Microbiologist
2. Establishing infection via induced bacteremia or systemic infection within the tumors may be difficult, especially if there is limited blood supply (which may be the case in the hypoxic regions of the tumor).

OK well it ought to be possible to get the infection started by injecting directly into the biggest convenient tumours.

Once there are a number of viable bio-agent colonies thriving my expectation would be that they'd be a source of spores into the lymph-drainage / blood in the same way that those tumours are a source of metastatic cancer cells.

Failing that one could simply keep dripping spores into an intravenous line into the blood supply and sooner or later I would expect those spores are going to get lodged into the growing tumours. Once enveloped by the growing tumour and a hypoxic environment experienced I'd expect spores to germinate and establish a new colony.

How long would that take? Maybe quite a long time. It depends on how fast the tumours are growing as to what the rate of them enveloping a spore might be. Yes it might take quite a long time to get all the tumours you need infected so infected.

It should be noted here that cancer patients sometimes acquire Clostridium infections of their tumours and have been known to die from such infections before they are diagnosed and treated.

The mechanism of spread of obligate anaerobes from tumour to tumour within the body might be easier to achieve than you might think. It may be that the rate of spread and growth of the anaerobe may have to be moderated with anti-bio-agent drugs (antibiotics) rather than encouraged by intravenous drip of bio-agent.

It's difficult to predict at what point the infection would need to be encouraged and at what point the infection would need to be moderated.

All I can do is suggest the methods for encouraging and moderating.

It is like a car designer cannot say in advance at what point the driver will have to use the brake and at what point the driver must use the accelerator.

The car designer simply provides the driver with both brake and accelerator and trusts to the driver's good judgement as to when each should be used.

Microbiologist
3. Even if the process were successful in infecting the tumors (and only the tumors) with a sufficiently virile bacteria to cause cell death in hypoxic environments, the end result would essentially be creating pockets of necrotic tissue in the centers of tumors. Pockets of necrotic tissue are going to cause issues unless removed or debrided, at which point surgical removal of the tumors would probably make more sense.

Well that's a valid point - necrotic tissue, although an acceptable swap for a cancer cell haven within a tumour, is not an ideal end point.

I have read reports of experiments where the tumour so infected by bacteria essentially disappeared and presumably the immune system cells had eaten the bacteria after the bacteria had eaten the tumour?

Whether tumours disappearing typically happens or whether bio-agent colonies would typically maintain some kind of stand off with the immune system I don't know for sure but I'd bet on the immune system cleaning up if it possibly can.

Tumours disappearing altogether in phase 1 is not required in my approach. The oxygenated peripheries or rims of tumours are expected often to survive phase 1 treatment and then be killed in phase 2.

I certainly see a role for surgery but that would typically be to remove the biggest tumours first and that may be done anyway to see if the cancer can be caught before it has metastasized.

Nothing in this approach in any way diminishes surgery as the first best hope of curing cancer. This approach is designed as a systemic treatment for metastatic cancer, the most intractable of cancers to treat and therefore the most interesting challenge for medical science to accept.

Microbiologist
4. I would imagine there is some possibility of viable bacteria remaining in the tumor cores even once systemic infection has been eliminated.

Hence why I have suggested the possibility of an intermission between phases 1 and 2, to assess that the goals of phase 1 have been completed and to be as sure as one can be that no viable bacteria remain in the former tumour cores. So I am thinking it can't be impossible to so saturate the body with anti-bio-agent drug (antibiotic) that it saturates the former tumour cores too?

Microbiologist
Phase Two would likely cause rupture of these tumors to some degree, potentially releasing extremely large quantities of bacteria into the blood while the immune system is severely weakened from the Phase Two drugs.

The phase 2 treatment should include antibiotics to kill off all gut flora and so the bio-agent would be killed off by the circulating antibiotics without requiring the help of the immune system.


Hypoxia-activated prodrugs

Having reviewed the risks and difficulties with using a live bio-agent it is worth mentioning research work which is being done to create new drugs, called Hypoxia-activated prodrugs (HAPs) to target these hypoxic tumour cores.

I would hope that eventually HAPs could prove their potency against hypoxic tumour cores but meanwhile obligate anaerobes have billions of years of a proven record of potency in killing cells in hypoxic environments.

Once HAPs have proved useful they should be much easier and more predictable and need less continuous monitoring than a bio-agent does.




Phase 2 concerns coming up next post ...

Microbiologist
I am far less knowledgeable about the biology behind Phase Two, but I do still have a few concerns to raise:

5. The doses and variety of 'Type H' drugs needed to reach the level of inhibition that this phase seems to require is likely to have a significant risk of side effects.

Well all the intended effects of the type H drugs could fairly be described as "side-effects".

The purpose of type H drugs is to halt all normal cell division for the duration of the chemotherapy in phase 2 and that intended effect, considered in isolation, is a purely bad effect for the body and is only worth it if those bad effects are understood to be side effects of the actions of the combination of type H drugs with the type K drugs.

I am not sure if you are hinting at unintended effects of type H drugs but be assured that the intended effects are bad enough.

Microbiologist
Stopping cell division throughout the body is not an easy task

Particularly now when not all the growth factor inhibitor drugs for all the tissues and cell types that would ideally be halted in their cell division and spared from being killed are yet available for use as type H drugs.

However, once all the growth factor inhibitors are available then administering them to achieve the desired effect should be easy enough.

Microbiologist
and inhibiting certain types of cells is likely to cause significant problems.

Correct, especially with frequently dividing cell types.

Microbiologist
Many of these problems are may be similar to those currently faced by patients undergoing chemotherapy.

Indeed though I'd expect the problems to be less severe than with chemotherapy today when if a normal cell, doing its job, divides and is killed then that is one less cell doing the job.

Whereas with my approach, if a normal cell doing a job is simply inhibited from dividing yet is still able to do its job then that is not one less cell doing the job.

Chemotherapy as practiced today involves a carnage of normal cells and a long period of recovery as those lost normal cell populations are slowly rebuilt (typically from stem cells, as I understand things).

With the phase 2 treatment in my approach as soon as the drugs clear the body then the normal cells can resume dividing and a very quick recovery can be expected.

Microbiologist
6. Significantly higher doses (or stronger versions/alternatives) of 'Type K' drugs than are currently used are likely to cause major problems if the 'Type H' drugs have not been sufficiently effective.

I see no reason why type K drugs require higher doses or stronger versions of typical chemotherapy regimes now in use. They'll be used to kill the same cancer cells that they are currently being used to kill. So the doses and strengths required should be the same.

Equally I see a reason why type H drugs might require to be administered in smaller doses or in lower strength versions compared to how growth factor inhibitor drugs are now used to inhibit the growth of cancer cells which I would expect most often to be less sensitive to growth factor inhibitors than normal cells.

Microbiologist
Testing the effectiveness would be difficult at best and may well be impossible without major advances, especially given the short time-frame during which 'Type H' drugs can be given in high doses - too long and severe harm will begin to be caused to various organs.

Clearly the appropriate doses would require to be established but compared to the bio-agent in phase 1 any drug is easier to dose appropriately.

Microbiologist
In Conclusion

Although it may sound like it, by intention is not to discredit or dismiss your idea. I like that you have taken a scientific approach and exhibit clear rational thinking and logic. You've connected many concepts and facts together into a proposal that I have never heard of before.

Thank you. I trust you will remember me as the author of this original approach when one day it is proven to cure cancer most effectively.

Microbiologist
That said, I am confident that we do not currently have the technology and know-how to make a treatment like this a reality.

Well the main missing part would be those type H drugs, the growth factor inhibitors for all the tissue types one would like to spare from the effects of the chemotherapy.

However, I have confidence in big pharma's ability to create such drugs once they see the commercial opportunity they offer. They've made growth factor inhibitors before and it is simply, for them, a case of "same again" but with other tissue / cell types.

Microbiologist
There is far too much reliance on chance, especially with the bacteria selection and timing

No, one does not leave it up to the doctor to go hunting for either bio-agent or anti-bio-agent drug. Both would be supplied, presumably as a twin-pack fit for purpose from big pharma.

The timing of controlling a bio-agent in vivo is as critical as the timing of brake and accelerator while driving a car. However, drivers do not avoid crashing by chance but by learning how to drive. Likewise, cancer treatment teams, oncologists, doctors, technicians, nurses - could all learn how to "drive a bio-agent in vivo" so to speak.

Microbiologist
and dose for administration of the drugs in Phase Two.

Again dose levels are not determined by chance but usually a quantity per unit patient weight is determined by clinical trials and a treatment dose determined. This is no different from any other drug.

Microbiologist
A carefully bio-engineered bacterial strain could work well, but would need to be created first.

Well we have already seen created a bio-engineered version of Clostridium novyi, the "NT" strain for a similar purpose.

Microbiologist
The drug administration would be more complex, mainly because I do not believe we currently have tests to determine proportions of tissues under cell cycle arrest (aka, the effectiveness of the 'Type H' drugs on a body-wide level).

Well we have experience with growth factor inhibitors targeted directly against cancer cells. See

Hormonal therapy (oncology)

Now I believe smaller doses will be required to inhibit normal cells but precisely what those doses are, which will vary from drug to drug, can be determined in the tried and tested method.

I appreciate you bringing your concerns to this discussion. Your contribution has been most welcome. Thank you very much and please don't hesitate to bring up any further concerns or revisit any of the above as you find the time to do.

reply to post by Mr Peter Dow


I am setting here writing thither with tears streaming down my face. Dad has three cancers and bad heart.
He does not trust doctor's and I need to find something alternative that works.

Can anyone help me save my dad.


The Bot

dlbott
reply to post by Mr Peter Dow

 

I am setting here writing thither with tears streaming down my face. Dad has three cancers and bad heart.
He does not trust doctor's and I need to find something alternative that works.

Can anyone help me save my dad.


The Bot

All the best for your Dad (and you).
Irrespective of what some of the people will say on here, there is NO alternative "medicine" that will cure cancer.
If there were firstly it wouldn't be alternative and secondly, given the availability and power of the internet, it would be available everywhere. No-one would be dying of cancer.
There are plenty of stories and testimonials to suggest the opposite but not a single one of them can provide irrefutable truth they work.
Not a single one.
I'm sure I'll open a can of worms here with the usual lot screaming that there is but after several years on this site not one of them has been able to show any evidence whatsoever.
That says it all.

Make your Dad see a specialist if nothing else but to discuss the options available.
Get him to explain his feelings and take it from there.
The longer you leave a cancer, the less likely any treatment will be successful.

All the best to the OP for creating a different type of thread.
One question though;
Why are you posting it on this site?

reply to post by Mr Peter Dow


Wow. I'm actually quite impressed with how well you addressed my concerns - huge props on being so well researched. And in all honesty, I had never heard of the work being done with C. novyi, but it sounds fascinating! Too late to read (well, comprehend) any scientific papers tonight, but I'm definitely going to have to look into those studies when I get a chance.

Now that I better understand your intentions with Phase Two - specifically that you aren't proposing new 'Type K' drugs or higher doses - most of my concerns about toxicity are relieved and the need to ensure complete arrest of the cell cycle in non-cancer cells is no longer a need.

That said, unless there's something I'm glazing over or just not understanding, Phase Two seems more like a means of improving quality of life for patients undergoing chemotherapy and/or enabling patients who are currently unable to undergo chemotherapy due to side effects to potentially be able to tolerate it? I don't really see how it becomes a new way of curing when it does not change the varieties or doses of the 'Type K' drugs being used.

Now don't get me wrong, reducing the side effects of chemotherapy is a great goal and well deserving of research, but not the same as a new cure.

drugs aren't as effective as what nature has given us to heal deceases. I think just pray, that's the best cure.

spartacus699
drugs aren't as effective as what nature has given us to heal deceases. I think just pray, that's the best cure.

I'm glad you're not treating me or mine.
Else I wouldn't be typing this.

Pardon?
All the best to the OP for creating a different type of thread.

Thank you.

Pardon?
One question though;
Why are you posting it on this site?

As I said in my OP,

Mr Peter Dow
I am an amateur independent scientist, neither employed as a scientist, nor published in traditional scientific journals.

I have published widely on the internet on mostly non-scientific topics and I am accustomed to debating my ideas on-line and so I’m quite comfortable inviting replies perhaps as helpful comments and criticisms from fellow scientists and I can also take questions from any cancer specialists, doctors or other informed parties who take an educated interest in such matters.

I have 200+ posts on ATS already so posting here is routine for me and this "Medical Issues & Conspiracies" forum seemed the most appropriate.

I suppose the one "conspiracy" I could be blowing wide open or forestalling getting started in the first place by publishing my approach very widely on the internet could be if I didn't so publish but one of the big pharma companies got wind of my approach privately before the others and decided to get ahead of its big pharma competitors by producing new type H drugs and bio-agents in secret, claiming "commercial confidentiality" grounds for not explaining the advantages of my approach with the other big pharma companies until they come to market with a new and better cancer cure, allowing them to inflate their profit margins for a while until the other big pharma companies caught up and offered their own products.

Would stealing a march on its big pharma competitors be a "conspiracy" or simply competitive behaviour by a big pharma company in a lucrative market? I don't mind which view you'd take of that question.

I'd welcome any one of big pharma companies which is first to the market with the cure I have described here but I'd much prefer the competition to be the first to the market to be a fair race, for all of the big pharma companies to be able to read the principles of my approach because I believe a fair race is going to be the quickest way to get this cure saving lives.

Microbiologist
reply to post by Mr Peter Dow

 

Wow. I'm actually quite impressed with how well you addressed my concerns - huge props on being so well researched.

Thank you very much.

Microbiologist
And in all honesty, I had never heard of the work being done with C. novyi, but it sounds fascinating! Too late to read (well, comprehend) any scientific papers tonight, but I'm definitely going to have to look into those studies when I get a chance.

It seems that ATS fascinates parts of the microbiologists community that other forums cannot reach.

Microbiologist
Now that I better understand your intentions with Phase Two - specifically that you aren't proposing new 'Type K' drugs or higher doses - most of my concerns about toxicity are relieved and the need to ensure complete arrest of the cell cycle in non-cancer cells is no longer a need.

For optimal results, the type H drugs should be administered first then wait before the type K drug is administered to allow for sufficient time for those normal cells which had committed to cell division before the type H drugs had been administered, to complete their division.

If you apply the two drugs at the same time, the type K drugs will kill those normal cells which have previously committed to the division part of the cell cycle.

That consideration aside, the aim with using growth factor inhibitors as type H drugs is to ensure to arrest the normal cells from entering the cell division phase of the cell cycle.

If one wishes to spare a normal cell from being killed by the type K drug then you do need to ensure it is arrested from entering the division part of the cell cycle, and that's what growth factor blockers do.

Dividing for a cell is sort of like being pregnant for a woman - she can't be a little bit pregnant, either she is or she isn't. Likewise a cell is either dividing or it isn't.

Microbiologist
That said, unless there's something I'm glazing over or just not understanding, Phase Two seems more like a means of improving quality of life for patients undergoing chemotherapy and/or enabling patients who are currently unable to undergo chemotherapy due to side effects to potentially be able to tolerate it? I don't really see how it becomes a new way of curing when it does not change the varieties or doses of the 'Type K' drugs being used.

Now don't get me wrong, reducing the side effects of chemotherapy is a great goal and well deserving of research, but not the same as a new cure.

I am actually much happier that you seem to be understanding the role of type H drugs than I am unhappy that you are not declaring my approach to curing cancer "new".

I admit, it is not all new. It brings together existing techniques in a synergistic way to provide a better cure. Nothing I have posted here would be possible if it were not for the previous work of medical science.

If I see further today, it is because I stand on the shoulders of giants.

Mr Peter Dow

Pardon?
All the best to the OP for creating a different type of thread.

Thank you.

Pardon?
One question though;
Why are you posting it on this site?

As I said in my OP,

Mr Peter Dow
I am an amateur independent scientist, neither employed as a scientist, nor published in traditional scientific journals.

I have published widely on the internet on mostly non-scientific topics and I am accustomed to debating my ideas on-line and so I’m quite comfortable inviting replies perhaps as helpful comments and criticisms from fellow scientists and I can also take questions from any cancer specialists, doctors or other informed parties who take an educated interest in such matters.

I have 200+ posts on ATS already so posting here is routine for me and this "Medical Issues & Conspiracies" forum seemed the most appropriate.

I suppose the one "conspiracy" I could be blowing wide open or forestalling getting started in the first place by publishing my approach very widely on the internet could be if I didn't so publish but one of the big pharma companies got wind of my approach privately before the others and decided to get ahead of its big pharma competitors by producing new type H drugs and bio-agents in secret, claiming "commercial confidentiality" grounds for not explaining the advantages of my approach with the other big pharma companies until they come to market with a new and better cancer cure, allowing them to inflate their profit margins for a while until the other big pharma companies caught up and offered their own products.

Would stealing a march on its big pharma competitors be a "conspiracy" or simply competitive behaviour by a big pharma company in a lucrative market? I don't mind which view you'd take of that question.

I'd welcome any one of big pharma companies which is first to the market with the cure I have described here but I'd much prefer the competition to be the first to the market to be a fair race, for all of the big pharma companies to be able to read the principles of my approach because I believe a fair race is going to be the quickest way to get this cure saving lives.

edit on 24-10-2013 by Mr Peter Dow because: (no reason given)

Apologies if you took my post the wrong way.
Nothing negative was implied.

I've never worked for pharma but I've extensive experience working in the health service in various guises, notably in several research projects initiated by the hospitals themselves (as opposed to industry led research).

Certainly what happens time after time is that a development is made independently. The research/results are published (and if possible publicised) then the full rights to this research is sold to industry who then run with it, usually a single company.

Alternatively, the method is patented then the patent is licenced to industry with the owner keeping full rights.
Quite often individual companies will push to have sole rights but I've witnessed a couple of cases where the owners of said patents have refused this and licenced their methods to several companies at once.
So it can happen.

Mr Peter Dow
I admit, it is not all new. It brings together existing techniques in a synergistic way to provide a better cure.

My approach offers a better cure by using various drugs and methods in a synergistic way, each making up for the short-fall of the other.

I'd like to review the drawbacks of existing anti-cancer methods and drugs in a simple way and identify how my approach gets around that drawback


Bacterial treatments

Drawback when used in isolation - bacterial treatments cannot be relied upon to kill oxygenated, active cancer cells

Solution in my approach - the phase 2 treatment kills those oxygenated active cancer cells



Traditional chemotherapy using cytotoxic antineoplastic drugs

Drawback when used in isolation - chemo doesn't kill hypoxic tumour cores meaning that the cancer can come back later & they have serious side-effects and a long recovery period

Solution in my approach - phase 1 kills hypoxic tumour cores so the cancer cannot come back & the side-effects of these drugs used as type K drugs are diminished and the recovery period shorter thanks to the type H drugs



Growth factor inhibitors

Drawback when used in isolation - they only work on some cancers and even then, they don't kill the cancer cells so the patient has to live life on that medication to stop the cancer growing

Solution in my approach - used as type H drugs, they can protect a tissue or cell type from being killed by chemotherapy; the more type H drugs we can source, the more tissue or cell types can be protected and the patient only needs to take them during the chemo session never after.

If you really think it's all that good of an idea, then take it to a University and see if they'll run with it. You never know. Put together a good presentation and show their chemistry dept head. They'll need money to run with it but if they like what they see, they might be able to get the funds.

FlyersFan
If you really think it's all that good of an idea, then take it to a University and see if they'll run with it. You never know. Put together a good presentation and show their chemistry dept head. They'll need money to run with it but if they like what they see, they might be able to get the funds.

I think the Universities of the world have internet and the people there can read my stuff same as anyone else can.

If they want to run with it, or some variation of it, there's nothing stopping them, same as there is nothing stopping them discussing it with me here on ATS or in other forums.

Also it's not just chemistry but also biology and medical departments that might be interested.