12 replies to this topic

[s123]

The SENS solution for cancer is eliminating the gene that encodes for telomerase. By doing this we prevent the cell from lengthening its telomeres. By doing so we need to undergo regularly stem cell therapy to replace the cells that die. But because stem cell therapy is not for tomorrow (it will be very difficult to make it suitable for replacing brain cells for instance) we need a faster way for dealing with cancer. I thought but what if you eliminate the telomerase gene and give telomerase to people in pills or injecting it? The telomerase would eliminate the need for stem cell therapy. When you than get cancer you simply stop taking telomerase and because the cancer cells divide faster than normal cells they will feel the lack of telomerase quicker and die before other cells. Then when the cancer cells are dead you simply begin taking telomerase again.

[nihilist]

sounds like a big chance....

[caston]

What if we add a gene that makes cells express flouresence in tandum with expression of telomerese? The cancerous cells can be identified and different expressions of protein analyzed.

[niner]

What if we add a gene that makes cells express flouresence in tandum with expression of telomerese? The cancerous cells can be identified and different expressions of protein analyzed.

Caston, that's a cool idea.

I was going to say that knocking out telomerase was a dumb idea, because all it takes is one bad cell to seed a tumor. However, if you can knock out telomerase in 50% of the cells, and precancerous cells are randomly distributed, that should give you 50% of the cancer risk, and so on, so maybe it's not so crazy. Still pretty far off. Cancer has really been hitting home lately for me. There are three families in my small community where a parent with elementary school aged kids (just like me) has died of cancer, or is about to. Two of them were/are people that I know, and only one of them is older than me. While my first priority is SENS, we still need to knock off cancer and infectious disease.

[HellKaiserRyo]

My personal view on cancer that it is like HIV. It can acquire resistance. (This has been observed with using gefitinib, which is an epidermal growth factor receptor tyrosine kinase inhibitor that unfortunately doesn't demonstrate a survival benefit in humans: http://erc.endocrino...t/full/11/4/793). I do not know if de Grey's idea would work, but I do think we need to assail cancer at multiple fronts, hard and fast. For example, in HAART, reverse transciptase inhibitor monotherapy is never used as it is easy for virus to acquire resistance. However, you have to use multiple drugs to prevent the development of a resistant strain. For example, the best first line threapy for HIV is Atripla ®: this is a combination of the non-nucleoside reverse transcriptase inhibitor efavirenz, a nucleotide reverse transcriptase inhibitor tenofovir, and a nucleoside reverse transcriptase inhibitor emtricitabine.

Unfortunately, cancer isn't HIV. HIV is simple; it has a 9 kb genome and uses the same mechanism to reproduce (e.g. use reverse transcriptase to transcribe its DNA, protease to cleave its gene products such as the pol and gag gene, integrase to incorporate it into host, gp40 and gp120 to inflitrate cells using chemokine receptors) . In contrast. cancer is an extremely diverse disease, can use a diversity of cellular signalling pathways, and will require personalized medicine to properly deal with it.

Gene therapy to replace tumor repressor genes (I am sure you are all familar with p53) might work too, but I don't know much about gene thearpy. Anyone want to give me an abstract on gene therapy being used in human trials? Anywant want to argue why the pharmacological approach with targeted therapies will fail? I think if it is properly done, cancer can be rendered in to a chronic non-fatal disease.

[John Schloendorn]

Good point about multiple approaches HellKaiser -- But it's important to understand what constitutes genuinely different approaches in terms of adaptive resistance. There are ways to resist multiple seemingly unrelated treatments with a single adaptive change. A few I could think of are multidrug transporter overexpression vs any small-molecule; genomic instability vs. any gene therapy; immune defusion against any T-cell vaccine. I think combining interventions from different broad classes of these types should have some potential against adaptive resistance. Unfortunately that's not likely to happen under the current regulatory regime.

[Lazarus Long]

Recently I was reading about the guy that everyone was talking about because he successfully used radio waves for inducing electrolysis and caused the escaping gas to burn. The technique is now being looked into as a novel means of manufacturing H2 but the reason I bring this up in this thread and what is much more important, is what he was doing when he discovered the effect; he was successfully targeting cancer cells within healthy tissue and causing lysis in only the malignant tissue.

You see they were testing the radio transmitter with various frequencies on water when some of the containers of water literally caught fire.

Anyway back to the methodology: he has succeeded in using the tagging technique involving gold nanoparticles and carbon nanorods for malignant tissues to make the cancerous tissues become vulnerable to specific radio frequencies that the surrounding normal tissue is not. He has had remarkably good success in animal trials and the FDA is currently looking at the method.

This is not genetics and it does not go toward the causal aspects of cancer but it may succeed in destroying malignant tissue in the manner that nuclear medicine tries to achieve, with more success and less side effects; IF it works.

I will look for a link if no one has posted this already.

Here is one link to the guy and his method.

http://www.cbsnews.c...in3206892.shtml

and another

http://www.scienceda...71101132853.htm

BTW another study I read about recently that may offer insight into why this simple technique may turn ot to be effective is related to another characteristic of cancer cells, they have been found to have softer and more vulnerable cell membranes.


Nanotech researchers discover cancer cells 'feel' much softer than normal cells

http://www.scienceda...71202155301.htm

http://www.eurekaler...--unu112907.php

http://www.reuters.c...Name=healthNews

http://www.physorg.c...s115823674.html

[caston]

Lazarus:

Instead of using radiowaves to "heat" or increase the molecular motion of cancers, intending to result in their destruction, it may be a better idea to use radiowaves to "cool" the cancers to the point where their molecular motion is much slower than healthy cells.

http://www.physorg.c...s108988434.html

[Lazarus Long]

Whichever way works Castor. My point in bringing it up is to highlight a reasonably novel, yet simple method being examined that is showing some practical success on this subject.

I have also heard of using the nanoparticles to carry minute quantities of binary compound toxins (a MOPP mimicry) that by themselves are encapsulated in fullerenes and unable to effect body chemistry but once absorbed by the cancer cell exclusively are activated by the radio wave signal or even ultrasound to release the binary toxin and kill the cell, destroying even the nuclear DNA of it to further prevent metastasis.

The dosage is only enough to kill a single cell and there is minimal residue.

Freezing is good too as well as using nanoparticles to deliver gene switching compounds that make the cancer cells unable to access blood supply or block its reproductive cycle.

The other point is that awe are seeing new approaches to combinative methods that are less destructive to surrounding tissue even as they are more effective at specifically targeting cancer cells.

Another possible activation frequency being examined ma use fMRI to focus extremely powerful magnetic radiation on specific sites that are also tagged with nanoparticles that are able to be targeted without surgery or microwaves as activation signals.

In each case the use of tagging molecules with very specific characteristics is the crucial common factor and how this overlaps nanotech.

It is my understand some of this is also being considered for being able to carry gene switching compounds to targeted tissues for other medical conditions like genetic disease. I wonder if the approach could also be used to insert a gene switch all the way into the mtDNA since it is in the cytoplasm and more accessible. This would allow treatment of the mutagenic phase of mtDNA and might increase cell reproduction ability.

Could this combinative approach also be used to manipulate telomeres?

What if telomeres could be lengthened artificially with a kind of nanotech prosthesis?

Telomeres are only really critical during mitotic division. Imagine if we could deliver a nanoparticle actually onto the telomere that artificially extends it and may even recycle to the next generation of at least some of the daughter cells that is basically an expendable molecular appendage?

In other words we would be inhibiting the shortening process with a routine treatment (like a supplement) that is distributed throughout the body attaching itself to every telomere. Even if teh sustance didn't recycle from generation to generation of mitotic divisions it woud itself be expendable and prevent damaging shortening.

The earlier post puberty and physical development that one began such a treatment the more it would freeze the subject's age at that point. Old fa*rts like me would have only the rest of the aging cycle slowed but this is not yet a reversal strategy unless we could tag a molecule on that effectively lengthens the telomere to a earlier cell reproductive age point.

These are actually two different methods involving nanoparticles, one simply substitutes an expendable particle that is destroyed during mitosis but simply allows the remaining telomere to sustain a constant size.

The second is to design a truly artificial telomere that is built as a nanoparticle and carried into the nucleus by a series of yet to be established conveyor methods but is reasonable to propose because these all mimic the tagging methodologies currently under development.

Remember in terms of nanotechnology a telomere can be described as a sort of micro molecular machine. Designing a synthetic telomere is not really beyond our capability it is just that nobody has looked at the problem in such a bio-mechanistic manner before.

[caston]

Lazarus: something like the patients own sperm could perhaps be re-purposed for the delivery of fresh autologus genetic materials including telemeres and telomarese (perhaps even some tumor supressor genes) into the cell.

Edited by caston, 11 December 2007 - 04:11 PM.

[Lazarus Long]

Caston not all cancer patients are male, not all are fertile, and not all women will have ovarian tissue available but still it is an interesting approach. I suggest a better method might be built around using stem cells cultivated from fat, skin, or bone.

[Athanasios]

Recently I was reading about the guy...

Yeah, I have been following this type of research too. I tend to think that brute force techniques on cancer is the way to go. There seems to be quite a few new tricks in town that show to have potential. I give cancer about 20 years before its threat of striking down someone in early life is very limited.

[caston]

Caston not all cancer patients are male, not all are fertile, and not all women will have ovarian tissue available but still it is an interesting approach. I suggest a better method might be built around using stem cells cultivated from fat, skin, or bone.

Yes, I believe there has already been research into making sperm from other cells in the body for reproductive purposes. Some men though still continue to produce sperm well into an advanced age. There are lots of places you can get genetic material. I like the idea of using sperm or SPCs because they are amongst the few cells in the body that still express telomerase. IMO for a non-cancerous cell this is a good sign of genetic integrity.

Edited by caston, 12 December 2007 - 12:01 AM.