I agree with the OP that the search for a broad spectrum anti-cancer drug is still a worthwhile endeavour. But I think it would be wrong to hold back on research into the more specific cancer remedies because the current most effective therapies are very often combination therapies of a type-specific anti-cancer drug co-administered or post-administered alongside a classical broad-spectrum anticancer agent such as cis-platin, or an anti-hormone agent for hormone dependant cancers. It is unlikely that new broad-spectrum treatments be so effective that this situation will change.
Having said that, there is huge research into targets ubiquitous for many cancers but formerly considered undruggable, such as P53 and Myc. We are getting better at finding ways to tackle these problem proteins. One approach,illustrated for example, which has great general promise is proximity induced degradation. A binder for the target is found, which doesn’t need to be at the main active site, if this is unattractive (for example if it is highly polar). This binder is then attached by chemical linker to a molecule that strongly binds to an E3 Ligase. This enzyme then recruits an E2 ubiquitin-conjugating enzyme which then ubiquitinylates the target protein preferentially on account of their proximity. The ubiquitinylated target protein is then recognised by the proteasome for degradation.
AOH1996 has, according to some accounts, been oversold as a cancer cure-all by the media. However, even if that is true, it could still have value as part of a combination therapy.
I’m guessing that the OP’s response would be something like this:
What’s better than a broad-spectrum treatment plus a narrow-spectrum treatment? Two narrow treatments, because the second narrow treatment is more widely applicable.
If developing a broad treatment costs less than developing N treatments that are 1/N as broad, which seems to be a main point of the post, then multiple broad treatments still seems like the better approach.
I agree with the OP that the search for a broad spectrum anti-cancer drug is still a worthwhile endeavour. But I think it would be wrong to hold back on research into the more specific cancer remedies because the current most effective therapies are very often combination therapies of a type-specific anti-cancer drug co-administered or post-administered alongside a classical broad-spectrum anticancer agent such as cis-platin, or an anti-hormone agent for hormone dependant cancers. It is unlikely that new broad-spectrum treatments be so effective that this situation will change.
Having said that, there is huge research into targets ubiquitous for many cancers but formerly considered undruggable, such as P53 and Myc. We are getting better at finding ways to tackle these problem proteins. One approach,illustrated for example, which has great general promise is proximity induced degradation. A binder for the target is found, which doesn’t need to be at the main active site, if this is unattractive (for example if it is highly polar). This binder is then attached by chemical linker to a molecule that strongly binds to an E3 Ligase. This enzyme then recruits an E2 ubiquitin-conjugating enzyme which then ubiquitinylates the target protein preferentially on account of their proximity. The ubiquitinylated target protein is then recognised by the proteasome for degradation.
AOH1996 has, according to some accounts, been oversold as a cancer cure-all by the media. However, even if that is true, it could still have value as part of a combination therapy.
I’m guessing that the OP’s response would be something like this:
If developing a broad treatment costs less than developing N treatments that are 1/N as broad, which seems to be a main point of the post, then multiple broad treatments still seems like the better approach.