Antibiotics targeting mitochondria kill cancer stem cells of several tumor types(impactjournals.com)
impactjournals.com
Antibiotics targeting mitochondria kill cancer stem cells of several tumor types
http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=3174
8 comments
Is this is the article you're referring to?
https://news.ycombinator.com/item?id=8856043
https://news.ycombinator.com/item?id=8856043
Yeah
General thoughts:
Cancer patients—in particular those with blood cancers—are routinely immunocompromised and put on antibiotics. Any potent effects would almost certainly have been realized by now. There are a lot of people who have made their careers by tracking what therapies work and which don't—and that includes controlling for "confounders" like those given antibiotics, etc.
Oncotarget isn't a bad journal—and this is certainly a good idea which may have applications we can't quite imagine yet. But it's unlikely to be a potent cancer therapy.
Oncotarget isn't a bad journal—and this is certainly a good idea which may have applications we can't quite imagine yet. But it's unlikely to be a potent cancer therapy.
Unless I'm missing something...
Getting rid of the CSC's is great for stopping the formation of new tumor-forming cancer cells, but you still need to kill and/or remove all the existing cancer cells.
So, this could treat the cancer stem cells as if it were an "infection-vector," but you'd still have to stop any current "infection" to save the patient.
This wouldn't really help late stage or aggressive types, but could make treatment efficacy better for cancers in early stages since it may help remove the cells that help a cancer come out of remission.
Maybe people with higher genetic propensity for covered cancer types could rotate on these drugs on a regular basis to reduce their risk? The eternal z-pak... Be interesting to see what the epidemiologists and actuaries come up with to assess the cost-benefit. Consistent anti-biotics would accelerate incidence of anti-biotic-resistant infections. There is no zero-risk since you can't actually take these drugs constantly. A tumor-forming cell could be produced between cycles. The long-term effects at such dosing levels were likely never studied and side-effects could be problems.
More likely, this would become one part of the full-court-press applied to treatment regimens.
Getting rid of the CSC's is great for stopping the formation of new tumor-forming cancer cells, but you still need to kill and/or remove all the existing cancer cells.
So, this could treat the cancer stem cells as if it were an "infection-vector," but you'd still have to stop any current "infection" to save the patient.
This wouldn't really help late stage or aggressive types, but could make treatment efficacy better for cancers in early stages since it may help remove the cells that help a cancer come out of remission.
Maybe people with higher genetic propensity for covered cancer types could rotate on these drugs on a regular basis to reduce their risk? The eternal z-pak... Be interesting to see what the epidemiologists and actuaries come up with to assess the cost-benefit. Consistent anti-biotics would accelerate incidence of anti-biotic-resistant infections. There is no zero-risk since you can't actually take these drugs constantly. A tumor-forming cell could be produced between cycles. The long-term effects at such dosing levels were likely never studied and side-effects could be problems.
More likely, this would become one part of the full-court-press applied to treatment regimens.
At high enough concentrations, you are going to wipe out many eukaryotic cells (cancer or not). I don't really see any good control experiments
There are publications (2002, 2003) publications that reported similar results:
http://www.ncbi.nlm.nih.gov/pubmed/11912125
http://www.ncbi.nlm.nih.gov/pubmed/14597870
I wonder why there were few follow-up studies? or what happened to these lines of research?
http://www.ncbi.nlm.nih.gov/pubmed/11912125
http://www.ncbi.nlm.nih.gov/pubmed/14597870
I wonder why there were few follow-up studies? or what happened to these lines of research?
Here's the quote from the abstract that I found revealing:
Finally, recent clinical trials with doxycycline and azithromycin (intended to target cancer-associated infections, but not cancer cells) have already shown positive therapeutic effects in cancer patients, although their ability to eradicate cancer stem cells was not yet appreciated.
So, the way I read it, "It's a good idea, but we haven't gotten it to work yet, even after some testing, but it's a good idea."
I've been around a few research science labs and understand the pressures on them. Getting published is good...but not sure of the provenance of this outlet.
Finally, recent clinical trials with doxycycline and azithromycin (intended to target cancer-associated infections, but not cancer cells) have already shown positive therapeutic effects in cancer patients, although their ability to eradicate cancer stem cells was not yet appreciated.
So, the way I read it, "It's a good idea, but we haven't gotten it to work yet, even after some testing, but it's a good idea."
I've been around a few research science labs and understand the pressures on them. Getting published is good...but not sure of the provenance of this outlet.
Unfortunately, a lot of negative research results aren't published, so it may be the case that follow-up studies were unsuccessful.
Oddly, they mention azithromycin, but I found this:
http://aac.asm.org/content/50/6/2042.full
which says:
"These results were compared to the inhibitory profiles of other antibiotics that function by inhibiting bacterial protein synthesis. Of these, chloramphenicol and tetracycline were significant inhibitors of mammalian mitochondrial protein synthesis while the macrolides, lincosamides, and aminoglycosides were not."
Seems like "doxycycline" would be more precise than "antibiotics"? After all, I assume this effect can not true of those "antibiotics" that are thought to increase the risk of cancer? (I am thinking in particular of metronidazole, and I put the word antibiotics in quotes because metronidazole is a very strange drug that is difficult to classify, and even though it is sometimes used as an antibiotic, it was not initially thought of as an antibiotic.)
http://aac.asm.org/content/50/6/2042.full
which says:
"These results were compared to the inhibitory profiles of other antibiotics that function by inhibiting bacterial protein synthesis. Of these, chloramphenicol and tetracycline were significant inhibitors of mammalian mitochondrial protein synthesis while the macrolides, lincosamides, and aminoglycosides were not."
Seems like "doxycycline" would be more precise than "antibiotics"? After all, I assume this effect can not true of those "antibiotics" that are thought to increase the risk of cancer? (I am thinking in particular of metronidazole, and I put the word antibiotics in quotes because metronidazole is a very strange drug that is difficult to classify, and even though it is sometimes used as an antibiotic, it was not initially thought of as an antibiotic.)
It sounds like what this means is that after removal of a tumor, a good thing to do would be to undergo a course of antibiotics?
At least doxycycline. Whether the results hold up in phase I/II/III clinical trials is still TBD, https://clinicaltrials.gov/ct2/show/study/NCT01590082.
Oddly enough, I was put on Tetracycline to slow down the progression of my mitochondrial disease, i.e, Tetracycline also offers some protection to the mitochondria.
[1] http://www.neurology.org/content/68/14/1159.short
[1] http://www.neurology.org/content/68/14/1159.short
Who has ever heard of this journal before?
I guess that should be relevant in this case to, since I guess the fasting should decrease the activity of mitochondria in normal cells but not in cancer cells.