Thanks but the approach of that paper is typical of current group-think which intends to use such inhibitors directly against cancer cell growth.
My approach is quite different. I am proposing inhibitors be used temporarily against
normal cell growth.
Now, if you've not got your head around my "Eureka" moment as to why anyone would want to inhibit the growth of normal, non-cancerous cells in a cancer patient then you need to understand my Phase 2 treatment. I've re-written my OP for other forums so here's the latest phase 2 section.
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.
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
with plenty of cites at the bottom.
Yup and google will turn up plenty more links to science paper abstracts, most of which I can't read the full text of without paying a subscription to the publishers but some science papers like the one you linked to are free to read so thanks for that.
Or you could just start with
cancer research in general.
There's loads to read but I've come to teach, to explain my approach.
No this thread, my OP and the updates to it, are not predicated on any one such study.
Interestingly, the site you linked to is called "EurakAlert!" and that's just the right name for a website to promote my paper so I'll try sending them a copy of my latest draft of it next.
Clostridium novyi-NT is an anaerobic bacterium that can infect hypoxic regions within experimental tumors. Because C. novyi-NT lyses red blood cells, we hypothesized that its membrane-disrupting properties could be exploited to enhance the release of liposome-encapsulated drugs within tumors. Here, we show that treatment of mice bearing large, established tumors with C. novyi-NT plus a single dose of liposomal doxorubicin often led to eradication of the tumors. The bacterial factor responsible for the enhanced drug release was identified as a previously unrecognized protein termed liposomase. This protein could potentially be incorporated into diverse experimental approaches for the specific delivery of chemotherapeutic agents to tumors.
https://www.sciencemag.org/content/314/5803/1308.figures-only
Hmm. Well their anti-cancer approach is is an entirely different bacteria-plus-chemo approach to mine.
If you don't mind, I'll concentrate on getting you to understand the main points of my approach before critiquing that approach in this thread.
Their's is at least "an approach" to curing cancer which is more than can be said for your other quote.
Bacteriolytic anti-cancer therapies employ attenuated bacterial strains that selectively proliferate within tumors. Clostridium novyi-NT spores represent one of the most promising of these agents, as they generate potent anti-tumor effects in experimental animals. We have determined the 2.55-Mb genomic sequence of C. novyi-NT, identifying a new type of transposition and 139 genes that do not have homologs in other bacteria. The genomic sequence was used to facilitate the detection of transcripts expressed at various stages of the life cycle of this bacterium in vitro as well as in infections of tumors in vivo. Through this analysis, we found that C. novyi-NT spores contained mRNA and that the spore transcripts were distinct from those in vegetative forms of the bacterium.
http://www.nature.com/nbt/journal/v24/n12/abs/nbt1256.html
This looks to be pure science research pretty far-removed from a focus on curing cancer.
I'm at war with cancer. I have it in my sights and I'm going to take the shot. I don't need any distractions.
I have hope.
