First published in the Science and Engineering forum of the For Freedom Forums

Posted: Wednesday 9th October 2013 05:46 pm

My “Eureka” moment. A cure for cancer.

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


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.


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.


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 more easily manageable undesirable side-effects and a quick recovery after chemotherapy.

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!

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.


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.


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


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.


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 ("as a cancer treatment")

Obligate anaerobe


Hormonal therapy (oncology)

Growth factor receptor inhibitor


Targeted therapy

The restriction point in cancer


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.
Peter Dow,