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My “Eureka” moment. A cure for cancer.

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My “Eureka” moment. A cure for cancer.

Postby PeterDow » Fri Oct 25, 2013 12:14 am

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 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.

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.

Image

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
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Postby PeterDow » Sat Oct 26, 2013 2:33 pm

Synergy

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.
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Postby JackBean » Mon Oct 28, 2013 8:36 am

Is this published in peer-reviewed journal? If so, why don't you post a link? If not, why don't you publish it first if is it so great?
http://www.biolib.cz/en/main/

Cis or trans? That's what matters.
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Re:

Postby PeterDow » Mon Oct 28, 2013 9:56 am

Thanks for replying Jack.
JackBean wrote:Is this published in peer-reviewed journal? If so, why don't you post a link?

No.

JackBean wrote:If not, why don't you publish it first if is it so great?


Like I said in my OP.

PeterDow wrote: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.


So if you'd like to review it yourself here and now Jack then please do.
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Postby JackBean » Mon Oct 28, 2013 10:43 am

I'm hardly (medical) doctor or even cancer specialist.
The phase 1 seems like nonsense. So you infect patient with bacteria and at the same time give him or her treatment against that bacteria? And the bacteria is supposed to kill the tumor cells? BTW all tumours develop blood vessels, because they are dependant on oxygen and nutrient delivery for their huge growth.
How do you imagine you halt all cell divisions? What effect would that have on the patient?
http://www.biolib.cz/en/main/

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Re:

Postby PeterDow » Mon Oct 28, 2013 12:28 pm

JackBean wrote:I'm hardly (medical) doctor or even cancer specialist.

Well neither am I Jack. I've done a little biology, my science degree (many years ago) was in computer science but I have very wide science interests these days.

JackBean wrote:The phase 1 seems like nonsense. So you infect patient with bacteria and at the same time give him or her treatment against that bacteria?

Have you ever driven a car Jack? You use the accelerator and at the same time you use the brake? Does that seem like nonsense to you?

It shouldn't because there's no other way to drive than to use both accelerator and brake. If someone invited you to drive a car that was missing either an accelerator or a brake then you couldn't drive it.

Likewise, with maintaining a mild infection the medical staff would need to accelerate the infection sometimes (adding bio-agent) and brake the infection at other times (adding anti-bio-agent drug).

JackBean wrote: And the bacteria is supposed to kill the tumor cells?

Some of them, the ones which are in hypoxic tumour cores, sure it can kill those ones and that's not my idea alone but has already been proved experimentally to work. Check out this link

Clostridium novyi-NT - Potential Therapeutic Uses in Cancers

JackBean wrote: BTW all tumours develop blood vessels, because they are dependant on oxygen and nutrient delivery for their huge growth.

Correct and phase 1 is not supposed to kill cancer cells in tumours which are well oxygenated. Phase 1 is only supposed to kill cancer cells that are hypoxic because they are in cores of tumours which have outgrown their blood supply.

Of course, some small tumours, some slow growing tumours, don't have such hypoxix cores; their cores have a good blood vessel supply. That's fine. The approach is to kill those tumours in phase 2, not phase 1.

JackBean wrote:How do you imagine you halt all cell divisions?

I imagine that one day big pharma will be able to supply enough growth factor inhibitors for all the tissue types that will do just that.

Growth factor receptor inhibitor

JackBean wrote: What effect would that have on the patient?

Well like I said in my OP.

Peter Dow wrote: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.


The point to note though is that it will be a smaller, less harmful effect on the patient compared to chemotherapy today which kills all dividing cells.

In my approach, the normal cells are not killed so the harm is less and the recovery is quicker compared to chemo today.

Chemotherapy
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Postby Darby » Tue Oct 29, 2013 10:54 pm

Of course, the devil is in the details. A lot of what's being proposed is just a "what if" based on basic properties of cancers - I remember thinking of trying a similar approach when I started my work in parasitology many years ago: what if cancer-aimed parasites could be used? In principle, it works; in reality, it's hard to develop an actual therapy.

One important detail - I don't think that the hypoxic cores tend to be the sources of metastatic cells, and localized tumors are the most treatable of cancer types...
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Re:

Postby PeterDow » Wed Oct 30, 2013 3:02 am

Darby wrote:Of course, the devil is in the details.

Whilst it is true that there are a lot of details to work out, my view is that the devil is with certain people who don't want to allow new approaches from unknown people even to be heard, even to be allowed to be considered and to be discussed. The devil is in such persons to the extent that they have a strict authority hierarchy in mind and anyone who seems outside of their chain of command ought to be dismissed immediately. Not only do they not want to hear those new ideas, they don't want anyone else to hear them either.

So for example, on some other internet forums, I've not been allowed to post my ideas. Many scientific institutions, even if they have forums at all, they are not open to the public, not open to independent amateur scientists to add their ideas for consideration.

To my way of thinking, closed off places belonging only to the professional establishment, which are not open to me, are where the devil is - hell on earth - because there could be the worry for any good scientist giving their opinion which is they might offend against the hierarchy, been seen to be challenging the authority, so lose favour, be disciplined, lose their jobs.

I think if we could banish this devil and all his works from the worlds of science, medicine and academia generally, we would find working together a much more efficient way of working all those missing details out.

My experience is of here in Scotland so perhaps it is different elsewhere?

Darby wrote: A lot of what's being proposed is just a "what if" based on basic properties of cancers

Well research has already found experimental evidence for all those properties of cancers and the drugs and bio-agents that I am proposing treating cancers with.

I assume you are unfamiliar with many of those findings? I know I wasn't familiar with them all when I had my Eureka moment.

I've been following up some references recently and for example consider this paper on the application of growth factor receptor inhibitors to protect normal cells from the toxic side-effects of chemotherapy.

Exploiting Cancer Cell Cycling for Selective Protection of Normal Cells
Mikhail V. Blagosklonny1, and Arthur B. Pardee

Chemotherapy of cancer is limited by its toxicity to normal cells. On the basis of discoveries in signal transduction and cell cycle regulation, novel mechanism-based therapeutics are being developed. Although these cell cycle modulators were designed to target cancer cells, some of them can also be applied for a different purpose, i.e., to protect normal cells against the lethality of chemotherapy. Loss of sensitivity of cancer cells to cell cycle inhibitors can be exploited for selective protection of normal cells that retain this response. Indeed, inhibition of redundant or overactivated pathways (e.g., growth factor-activated pathways) or stimulation of absent pathways in cancer cells (e.g., p53, Rb, and p16) may not arrest cycling of cancer cells. But growth arrest of normal cells will then permit selective killing of cancer cells by cycle-dependent chemotherapy.


Now I had the idea of my type H drugs originally more as a "what if" Eureka moment but I have since found out that a lot of evidence has been found of the concept being proved in principle a decade and more ago.

I'm happier to be proved right than I am unhappy not to have been the first with this idea. 8)

Darby wrote: - I remember thinking of trying a similar approach when I started my work in parasitology many years ago: what if cancer-aimed parasites could be used? In principle, it works; in reality, it's hard to develop an actual therapy.

How in principle would the parasite attack only the cancer cells?

Darby wrote:One important detail - I don't think that the hypoxic cores tend to be the sources of metastatic cells,

Well the reverse is the case. Metastatic cells can grow into tumours which can in turn outgrow their blood supplies and then the cores can become hypoxic.

Nevertheless, it can work the other way around. For example, after chemotherapy which kills the active rim of a tumour then the rim dies and peels away like the skin of an onion leaving the core exposed and the previously dormant cancer cells get a new lease of life because they are now getting oxygen again and so they come to life, grow and supply new cancer cells to metastasise elsewhere.

That's the limitation with many cancer therapies which only provide a remission but then the cancer comes back again.

Darby wrote: and localized tumors are the most treatable of cancer types...

If the tumours are in a few locations only and can be treated by surgery, yes. That's the first best hope of curing cancer if you can catch it early enough.

My approach is only intended for treating those cancers which are already metastatic, where surgery cannot offer a cure.

These metastatic cancers are the hardest to treat and therefore the most interesting challenge for medical science in my opinion.
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Postby Darby » Fri Nov 01, 2013 1:27 pm

In some ways, science is a closed-off group, since it takes a lot of training to assess most ideas. Cancer research, from looking at the avenues that people are exploring, is one of the more open-to-anything groups, but I'm not surprised that they don't entertain many ideas from "amateurs."

Oncology is not a major area that I keep up with, but I didn't find too much in your general suggestions that I haven't seen discussed before. I think that, if you were more in the "inner circle," you'd find that at least a few of your ideas have been checked out unsuccessfully. Unfortunately, research results of the "well, THIS doesn't work in any useful way" variety don't get published, but that doesn't mean than folks in the field don't know about them.

If you feel REALLY strongly about this, find people doing research in the area closest to your suggestions and contact them directly (I acknowledge that this might be a VERY BAD IDEA). Distill your idea down, though - what you've written here is too long (and too pedantic if you're sending this to someone working in that field). They might totally ignore you, but you might get someone to tell you why your idea probably won't work based on research that just never made it into the literature.

One possible place to start is here:

http://scienceblogs.com/insolence/

He is an oncological surgeon, but he definitely keeps up with the broader literature.
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Science versus a job as a "scientist"

Postby PeterDow » Fri Nov 01, 2013 11:52 pm

Darby wrote:In some ways, science is a closed-off group, since it takes a lot of training to assess most ideas.

I don't think that is the way the best teachers look at science teaching with respect.

The best science teachers are empowering individuals to able to do science because they have the facts or know where to find the facts, understand the principles and can take science forward to new frontiers.

What you describe is more the way that the worst teachers tell students to conform, reply by rote, never question authority, keep their heads down, get a job and merge into the profession seamlessly - like good children are supposed to be, seen but not heard.

A real scientist can shatter an orthodoxy but a groupie of the mainstream dare never try.

Darby wrote:Cancer research, from looking at the avenues that people are exploring, is one of the more open-to-anything groups, but I'm not surprised that they don't entertain many ideas from "amateurs."

I've noticed a lot of home-remedy type cancer cures out there - unscrupulous confidence tricksters taking advantage of sick people. I hope you can see that is not me.

I trust you can understand the difference between an amateur scientist like me and a professional conman, offering his snake-oil cure-all?

Darby wrote:Oncology is not a major area that I keep up with, but I didn't find too much in your general suggestions that I haven't seen discussed before.

Where and when before did you see discussed growth factor receptor inhibitors used to protect normal cells from the toxic side-effects of chemotherapy?

Before my article and my links and reference?

Darby wrote:I think that, if you were more in the "inner circle," you'd find that at least a few of your ideas have been checked out unsuccessfully.

Are you comfortable with the word "prejudiced" applied to your thinking there? You think that but you've no actual evidence or argument to support that thought, so if it is not "prejudice" what is it?

Darby wrote: Unfortunately, research results of the "well, THIS doesn't work in any useful way" variety don't get published, but that doesn't mean than folks in the field don't know about them.

Well there is so much to know, so many papers to read, I don't think one can assume that oncologists and cancer research scientists know everything which has been written in their own specialist literature, never mind assume that somehow they have superpowers also to know what has never been written down in their literature.

Darby wrote:If you feel REALLY strongly about this, find people doing research in the area closest to your suggestions and contact them directly (I acknowledge that this might be a VERY BAD IDEA). Distill your idea down, though - what you've written here is too long (and too pedantic if you're sending this to someone working in that field). They might totally ignore you, but you might get someone to tell you why your idea probably won't work based on research that just never made it into the literature.

Well who knows, I may run into such persons in forum such as this?

Darby wrote:One possible place to start is here:

http://scienceblogs.com/insolence/

He is an oncological surgeon, but he definitely keeps up with the broader literature.

Now why don't you drop him a note inviting him to post in this topic?
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