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My “Eureka” moment. A cure for cancer.


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#1 Peter Dow

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Posted 19 October 2013 - 05:24 PM

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 authors 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 Im 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 patients 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 patients 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 patients 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 lets 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 bodys health will accumulate.

Type H drugs dont 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 dont 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!

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. Condis mother also died from cancer and she has participated in Race for the Cure events.

condiricerace4cure06apkevinwolf.jpg

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

#2 Trof

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Excellent

Posted 20 October 2013 - 04:46 AM

Even though I wouldn't claim to have read it whole I would point out at least one important problem. Not only cancers are hypoxic, but also many stem cell niches are (at least the hematopoietic). Also not all tumors are hypoxic, there are actually many of them that have good vascularization. Cancers want to survive. They find a numerous ways how to do it, if they can. Targeting hypoxic cores with a living organism that also wants to survive is also risky on it's own, not talking about the fact that you will be essencially killing your bone marrow stem cells too.

 

 

Todays targeting of rapidly dividing cells in some cases (not all) cure the the imminent problem, but leave often the primary one. "Screwed" cancer stem cells may (and probably do) exist hidden somewhere within other stem cells, undistinguishable for us, as yet. And by circumstances we didn't really fully understand, they may spawn a new tumor. It is just a play with time, sometimes you just die of something else, sometimes the new tumor will be quicker.

 

 

If there is a future quest for a universal targeted cure I see it more likely in the nanotechnology. Based on the detailed knowledge of the certain cancer type and it's evolution, disposable nanobots could be created to target the specific sites, to either don't disturb the organisms immune system or just the oposite, lure it to the cancer cells, based on the model and individual properties. Afted they're done, distroyed. Machines doesn't have an urge for survival unless you program them to. On the other hand, they can malfunction.

 

But estimated costs? Even when commercially available, both the nanobots and the detailed survey of the biological enviroment of the body and the cancer, tailoring it to an individiual would be a sky high prize. But it would, theoretically, provide a system for universal aplication, given you know the biochemical details. You need to be one step ahead of a cancer.

 

So for now, the more affordible and more "rough" methods, tested to work on certain cancer subtypes has to be used. Cancer is now still one step ahead, but luckily sometimes it takes it some time to do that step if we strike hard.


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#3 Peter Dow

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Posted 20 October 2013 - 07:35 AM

Even though I wouldn't claim to have read it whole

 
For the reading that you have done, I thank you for your interest and your time.

 

I would point out at least one important problem. Not only cancers are hypoxic, but also many stem cell niches are (at least the hematopoietic).

 
So I see.

The hematopoietic stem cell niche: low in oxygen but a nice place to be. J Cell Physiol. 2010 Jan;222(1):17-22. doi: 10.1002/jcp.21908.

Compared to some cancer tumours, some of which can grow hypoxic cores each of which is large enough to sustain a very large population of obligate anaerobic bacteria (and that's why cancer patients can die from unchecked Clostridium infections), is there a disease of hypoxic stem cell niches likewise infected by anaerobes, or would such niches be too small individually or as a tissue type to sustain an infection on their own which was particular to those hypoxic stem cell niches?

I mean I've not heard of hypoxic stem cell niche related anaerobe infections, but maybe you have and if so can you provide a link please?

My doctor has never said to me - "Ah yes, looks like your hypoxic stem cell niches have picked up a little infection there Peter but no worries, here's a prescription for metronidazole, that should clear your hypoxic stem cell niches of any anaerobic infection which has got in there."
 
There's no mention of such infections here - Wikipedia - Anaerobic infections
 
Do you understand my point? Have you heard that hypoxic stem cell niches get such anaerobic infections? Is that something known to happen?

If that's not a known variant of anaerobic infections then maybe nature has evolved some mechanism to protect these hypoxic stem cell niches, perhaps they are too small and isolated to sustain an anaerobic infection, perhaps some immune cells can move in and break those niches up if an infection happens, allowing oxygenated extracellular fluid between the infected stem cell niche so they are no longer hypoxic, meaning that any anaerobes which have got in there are left defenceless and immune cells can function to eat the anaerobes up?

That's not meant to be a careful analysis of hypoxic stem cell niches. I only just heard about them just now in answering this post. I don't really know anything much about the subject. I've not read that article I linked to, just the abstract, but the drift of my point is that maybe nature has a way of ensuring that such hypoxic stem cell niches are not vulnerable to infection from anaerobes?

 

 

Also not all tumors are hypoxic, there are actually many of them that have good vascularization. Cancers want to survive. They find a numerous ways how to do it, if they can.

 

Correct. Cells of the body which feel somewhat hypoxic will, before they are rendered quiescent by severe hypoxia, begin to produce growth factors for new vessel growth and cancer cells are no exception.

My approach doesn't attempt to treat non-hypoxic tumours in phase 1.

Well-oxygenated tumours are treated in phase 2, along with isolated cancer cells which haven't grown much of a tumour around them. I'd refer you to my description of my phase 2 treatment plan in my OP.

 

 

Targeting hypoxic cores with a living organism that also wants to survive is also risky on it's own, not talking about the fact that you will be essencially killing your bone marrow stem cells too.

 

Quite. Well Hypoxia-activated prodrugs haven't quite made it into standard oncology clinical practice as yet, as far as I know.

Wikipedia: Hypoxia-activated prodrugs

If and when HAPs do prove themselves then certainly a drug treatment against hypoxic tumours should be easier to control and to predict than a live organism, so at that stage, I'd probably recommend replacing the bio-agent in phase 1 with a good hypoxia-actived prodrug for phase 1 instead, yes.
 
I'm hopeful about HAPs eventually but obligate anerobes have been proving for billions of years they can kill other cells in a hypoxic environment so to my mind they are a sure thing for potency, whilst admitting bio-agents will need careful control.

 

Todays targeting of rapidly dividing cells in some cases (not all) cure the the imminent problem, but leave often the primary one. "Screwed" cancer stem cells may (and probably do) exist hidden somewhere within other stem cells, undistinguishable for us, as yet. And by circumstances we didn't really fully understand, they may spawn a new tumor. It is just a play with time, sometimes you just die of something else, sometimes the new tumor will be quicker.

 

Well to my mind the main problem to solve with cytotoxic antineoplastic chemotherapy is that those drugs kill all kinds of dividing normal cells, not just the dividing cancer cells. That's what phase 2 of my approach offers a solution to, or at least a solution in some, perhaps many, kinds of cancer.

 

It is the killing of normal dividing cells which is what makes patients undergoing chemotherapy for cancer, bone marrow transplants etc very ill, sometimes intolerably or fatally ill and if they do survive the chemo a long recovery period can be required. It's not an easy cure but it is often the only hope.

 

I'm suggesting an alternative approach which doesn't involve killing normal cells for cancers which respond as described in my phase 2 treatment (see my OP).

 

 

If there is a future quest for a universal targeted cure I see it more likely in the nanotechnology. Based on the detailed knowledge of the certain cancer type and it's evolution, disposable nanobots could be created to target the specific sites, to either don't disturb the organisms immune system or just the oposite, lure it to the cancer cells, based on the model and individual properties. Afted they're done, distroyed. Machines doesn't have an urge for survival unless you program them to. On the other hand, they can malfunction.
 
But estimated costs? Even when commercially available, both the nanobots and the detailed survey of the biological enviroment of the body and the cancer, tailoring it to an individiual would be a sky high prize. But it would, theoretically, provide a system for universal aplication, given you know the biochemical details. You need to be one step ahead of a cancer.

 

Certainly it is much cheaper and realistic to produce a sci-fi TV episode which features nanobots - the Borg in Star Trek for example have nanobot technology deployed in strength.

 

 

So for now, the more affordible and more "rough" methods, tested to work on certain cancer subtypes has to be used. Cancer is now still one step ahead, but luckily sometimes it takes it some time to do that step if we strike hard.

 

Excuse my lack of modesty if I suggest that I've just taken one giant leap for mankind ahead of many cancers with the publication of my OP above. cool.png


Edited by Peter Dow, 20 October 2013 - 07:49 AM.


#4 Ameya P

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Excellent

Posted 25 October 2013 - 05:12 AM

I think its a fair hypothesis. It may or may not work. But what is the harm in trying. Until  we try and prove their efficacy, all drugs and methods of treatments have some drawback or the other. Just because Pfizer makes a drug does not make it wonderful. It is all about how effective it is and at a latter point in time, how economically feasible it is. Nanobots will be great, but they are still far away. We need to work with what we have or will soon have at our disposal. 


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#5 Peter Dow

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Posted 25 October 2013 - 05:56 AM

I think its a fair hypothesis. It may or may not work. But what is the harm in trying. Until  we try and prove their efficacy, all drugs and methods of treatments have some drawback or the other. Just because Pfizer makes a drug does not make it wonderful. It is all about how effective it is and at a latter point in time, how economically feasible it is. Nanobots will be great, but they are still far away. We need to work with what we have or will soon have at our disposal.

 
Thanks Ameya.
 
On the general subject of drawbacks and side-effects of the various drugs and methods in relation to my approach, I'd like to start by updating from my OP here to the latest draft of my paper.
 
I've changed this
 

That is to say, the remaining task for type K drugs becomes a relatively trivial task to accomplish with no undesirable side-effects.

into this

That is to say, the remaining task for type K drugs becomes a relatively trivial task to accomplish with more easily manageable undesirable side-effects and a quick recovery after chemotherapy.

This is a better description of the overall effect of the phase 2 drugs, both type H and type K drugs considered together as they effect the patient.

Whereas in my approach the action of type K drugs considered in isolation have no side-effects - all they do is kill cancer cells and that's a pure good - the type K drugs are only able to do that in my approach (even though those same cytotoxic antineoplastic drugs when used in conventional chemotherapy today have massive undesirable side-effects) thanks to the protective effect of the type H drugs which do have some, more easily managed side-effects.

Whereas traditional chemo kills normal cells which attempt to divide, those same drugs in my approach don't kill normal cells which have been inhibited from dividing by the type H drugs and whilst that inhibition from dividing does cause side effects, those are modest and easily manageable and quickly recovered from, compared to traditional chemo side-effects.

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.

Edited by Peter Dow, 25 October 2013 - 06:44 AM.


#6 bob1

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Posted 25 October 2013 - 11:22 AM

One problem is that many cancer patients are immunosupressed in some manner, so giving them a bug (even an anaerobe) that will cause an active infection is likely to cause a fair bit of harm (check out Clostridium sepsis for example).  One of the key precepts of medicine is "first do no harm", in other words don't do something that will cause harm to the patient.  Now, it can be easily argued that treating with anything biologically relevant is going to cause some harm, as all chemotherapy drugs do, so the idea is debatable.  However, there is one difference between giving an actively living organism and a chemical - the living organism has the potential to multiply, whereas the drug won't...

 

People also have many many different anaerobic environments in their bodies - all of these would be infected and damaged.  Cellular damage in large amounts causes a lot of problems for the body - mostly related to removal of decay products (check out crush related injury) which leads to multi-organ failure.



#7 Peter Dow

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Posted 25 October 2013 - 01:40 PM

One problem is that many cancer patients are immunosupressed in some manner, so giving them a bug (even an anaerobe) that will cause an active infection is likely to cause a fair bit of harm (check out Clostridium sepsis for example).  One of the key precepts of medicine is "first do no harm", in other words don't do something that will cause harm to the patient.  Now, it can be easily argued that treating with anything biologically relevant is going to cause some harm, as all chemotherapy drugs do, so the idea is debatable.


The manner of that immunosupression being the chemotherapy drugs which, as used today, kill all dividing immune system cells.

My approach differs in that

  1. the bio-agent treatment is phased first, achieving phase 1 goals before killing the bio-agent at the end of phase 1.
  2. not until phase 2 of my approach would chemotherapy drugs be used and even then immuno-suppression would be less devastating than that of traditional chemotherapy because thanks to the type H drugs the immune cells would only be inhibited from dividing while kept alive instead as happens now, killed-as-they-divide by the chemo.

 

However, there is one difference between giving an actively living organism and a chemical - the living organism has the potential to multiply, whereas the drug won't...


That is the one the disadvantage that the bio-agent will always have if there were ever to be the alternative available of potent Hypoxia-activated prodrugs (HAPs) to target and to kill those cancer cells in hypoxic tumour cores.

Meanwhile, before HAPs have proved their potency, the only good option for my phase 1 that I am sure today of the potency of, is the admittedly difficult to control bio-agent option.

In future I would envision HAPs being the agent of choice for phase 1 treatment because of the difficulty of controlling a bio-agent in vivo.

 

People also have many many different anaerobic environments in their bodies - all of these would be infected and damaged.  Cellular damage in large amounts causes a lot of problems for the body - mostly related to removal of decay products (check out crush related injury) which leads to multi-organ failure.


Well the selection of bio-agent should be such that it is only active at the very low levels of oxygen found in the very hypoxic tumour cores, where it is so hypoxic that the cancer cells are quiescent, unable to divide because of lack of oxygen. Such a suitable bio-agent represents no threat in parts of the body which maybe slightly more hypoxic than other better oxygenated parts but where the somewhat lower oxygen level is still sufficient to support the activity of body cells and sufficient to inactivate the particular obligate anaerobe selected as the bio-agent.

Also the selection of bio-agent should be such that it has no, or at most a limited, potential to cause any harm to cells other than those in its immediate very hypoxic environment, where the bio-agent as an obligate anerobe can function but its victim cancer cells lacking the oxygen they need, cannot.

For ideas on the selection of an appropriate bio-agent here's a suitable starting reference regarding a bio-engineered strain of Clostridium novyi, the "NT" strain which has been engineered without a major toxin for precisely this purpose.

Clostridium novyi-NT - Potential Therapeutic Uses in Cancers

By infecting those hypoxic tumour cores with a mild and easily controllable bio-agent which, so to speak, "eats up" that food source, it deprives other much more dangerous infections of the opportunity to infect those hypoxic tumour cores and thereby endanger the life of the patient.

Cancer patients have been killed by uncontrolled opportunistic Clostridium infections but the bacterial treatment approach by confronting and eliminating the problem of dangerous hypoxic tumour cores in a controlled and methodical way, makes an uncontrolled, damaging infection much less likely.

Therefore not only does the bacterial treatment approach remove the threat of a cancer come back after chemo, it also removes the threat of a dangerous infection of hypoxic tumour cores.


Edited by Peter Dow, 25 October 2013 - 02:03 PM.


#8 bob1

bob1

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Posted 18 November 2013 - 12:36 AM

Interestingly, I was just at a seminar today using the idea that you postulated - to some extent at least.  Apparently the idea has been around for about 20 years, mostly using drugs that can only be activated in hypoxic environments (prodrugs), mostly activated through the use of viruses to produce enzymes that will only function in hypoxic environments.

 

According to the presenter, the large hypoxic environments in the gut are not a problem, as these are not really accessible to organisms circulating in the blood.  The presenter also acknowledged the difficulty of clearing an infection in someone who is already compromised in some manner.






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