I don’t know enough biology to know how feasible these ideas are (how I wish I could find training), but here goes anyway:

I had previously come up with an idea involving selecting out the cells believed to be most sensitive to chemotherapy or other treatments and strategically placing them in the center of existing tumors (in the hopes that the chemosensitive cells would displace the more resistant ones), then delivering a high dose of chemotherapy (or whatever treatment is being used). I have no idea whether this will actually work, but from what little I know of cancer biology, this seems reasonable. Unfortunately, it wouldn’t be completely effective because it depends on infiltration of specific tumors, which could also be removed surgically, for that matter (this is less invasive, however).

I just thought of a particularly nasty extension that we may or may not have the technology for today.

Here’s the basic premise: anything that outright kills cancer cells or prevents them from dividing is going to have a hard time succeeding because it’s fighting evolution (even the most effective treatment, surgical excision, does not outright kill cancer cells; it merely removes them from the body). This is presumably why tumors become resistant to chemotherapy following treatment.

First, the plausible idea: what if we could “tag” the cells we extracted with antigens before placing them? (Is this how traditional immunotherapy works? I was under the impression it relied more on chemical signals such as IL2). We could then insert them into tumors, perhaps in conjunction with IL2 to stimulate the immune system, and let it learn that the cells are not to be tolerated.

Ideally, this could be made genetic and the patient’s immune system could be suppressed for a time, to allow the tagged cell to infiltrate the tumor. Then the immunosuppressants would be withdrawn. Same principle as the first idea, except we’re actually inducing a weakness.

Next, the less plausible but seemingly more promising idea: what if we could infect the specific cells with a lysogenic virus that targets cancer cells? This will cause the cell to silently continue replicating, but with a viral plasmid. Using a lysogenic virus would be helpful here because there would be no chance for the other cells to adapt to counter it; upon initiation of the lytic cycle of the virus, the tumor would be inundated from its own infected cells, “taken by surprise”. Moreover, this need not be left to chance; we can manually initiate lytic cycles when most convenient (say, as a neoadjuvent therapy). This should theoretically cause a substantive die-off of the tumor, while preserving normal cells if the virus were specific enough.

Cold viruses spread through respiratory particles and stimulate the release of these particles (through coughing and sneezing, for example). Gastrointestinal illnesses spread through feces and vomit, both of which they tend to produce as symptoms.

I very much doubt that this is accidental. It seems selected for; viruses that symptomatically increase their own chances of spreading must be more successful than those that do not. Of course, viruses do contain either DNA or RNA, both capable of propagating, and thus are able to evolve in such a manner.

The puzzling thing, then, is why some viral diseases traditionally caused swift death. It would seem that they deprive themselves of living cellular machinery to produce more virus – what would appear to be a losing proposition.

I still think they’re alive.

I’m wondering whether it would be possible to get an organism to “learn” to attack cancer cells. I’m thinking that if we could sensitize a fast-evolving virus (such as an HIV virus that has been stripped of its traditional payload) to tumor antigen, we could create an “evolve or die” environment where the virus would either:

a. Completely die out (then just try it again until it works),
b. Become desensitized to whatever it’s supposed to be sensitive to (likely),
c. Modify its environment to reduce the presence of the target module (could be bad), or
d. Destroy the cells that are emitting it.

Obviously, the fourth choice is what we want. If we could engineer a virus that seeks out and lyses cancer cells like HIV does T-cells, we would have a treatment model whose versatility can match that of the cancer itself.

Obviously, we do not want the immune system interfering in this, so we would perhaps need to tailor the viral capsid to the patient or give the patient immunosuppressants while undergoing treatment.

One day I’ll get the chance to test these hypotheses, but they can only exist as ideas until I have access to biological training and equipment… and I am unbound from other people’s research needs.

Carcinoid tumors are malignant tumors (usually of the neuroendocrine system) that only rarely metastasize. Because they do not readily spread, many patients with them have good prognoses, either with surgical treatment or even in absence of treatment, despite the fact that chemotherapy is not usually effective on these tumors.

The intriguing question is why. Neuroendocrine tumors as a class tend to follow the pattern of poor response to chemotherapy and relative indolence, despite what appears to be going on histologically. If we could figure out the conditions that favor such a pattern, we could perhaps design more effective treatments for other types of malignancies as well.

I hypothesize that sweat acts as a selective disinfectant. This is a relatively easy experiment to conduct (have a bunch of people sweat, put the sweat in one petri dish and water in another, and try to grow some bacteria), but since I don’t have the equipment, I’ll theorize and leave the experimentation to someone who is equipped to, you know, perform science.

There are two theoretical angles that convince me of this: one is physiological behavior (people sweat when they’re sick and when they’re active, and in both cases, an antiseptic effect may be beneficial to the organism. Sweat is also hypothesized to have a sexual function, and indeed a disinfectant may prove especially beneficial in situations where body fluids may be shared) and the other, more compelling reason, is that sweat contains cresols, which happen to be the chemicals found in Lysol.

So someone do the experiment, and please mention me in a footnote or something if you got the idea here 🙂