"Some" Aggressive Cancers May Be Treatable By NSAID

[haidut]

I find it odd that the article says "some" cancers even though JAK is upregulated in virtually all cancers. Also, instead of listing some common non-prescription drugs (NSAID) that are known JAK inhibitors they talk about proprietary drugs used for rheumatoid arthritis.

http://www.sciencedaily.com/releases/20 ... ceDaily%29

Now, guess what is well-known NSAID, that is also a JAK inhibitor, available everywhere and without prescription? You guessed it - aspirin. Another point for Peat and his claims that aspirin is good not only for cancer prevention but also cancer treatment.

http://www.ncbi.nlm.nih.gov/pubmed/11801685

"...Although salicylates inhibited the in vivo activation of Janus kinases, their kinase activity was not affected in vitro by salicylates, suggesting that other kinases were involved in IL-4-induced STAT6 activation."

 

[Suikerbuik]

Aspirin is indeed being found to be beneficial in many tumors. If it can be used as the primary treatment remains to be seen. Likely it can "improve" the tumor micro-environtment which is a key factor driving a tumor ((could even possibly be the key factor driving a tumor)). And aspirin might also help reduce induced resistance by established treatments. So aspirin can certainly be useful in the treatment of tumors and we are are definitely not exploiting this cheap drug. Let that be clear.

However there's several jak proteins and several stat proteins which cannot be regarded as the same. I don't think it is easy nor I think we can blame the authors. And actually you are giving the answer yourself, which also at the same time admits the complexity:

their kinase activity was not affected in vitro by salicylates

and

suggesting that other kinases were involved in IL-4-induced STAT6 activation.

also from the same article

Src kinase was involved in STAT6 activation ... Src kinase activity, but not Janus kinase, was inhibited by salicylates in vitro

So aspirin isn't a JAK inhibitor by directly targetting JAK. Which I think is what the authors targeted I guess. NSAIDs can certainly reduce JAk activation by reducing cytokines, but that's still not a direct JAK inhibitor. It's like the example you quote above. Check out what this study said..:

We found that aspirin not only significantly enhanced IFN-α-induced antiproliferation and apoptosis of HCC in vitro study but also enhanced tumor growth inhibition in nude mice. Although IFN-α alone resulted in significant phosphorylation of both STAT1 and STAT3, aspirin only prompted the IFN-α-induced phosphorylation of STAT1. Further study revealed that aspirin-prompted phosphorylation of STAT1 was activated through phosphorylation of JAK1.

http://www.ncbi.nlm.nih.gov/pubmed/23703473

 

[haidut]

Aspirin is indeed being found to be beneficial in many tumors. If it can be used as the primary treatment remains to be seen. Likely it can "improve" the tumor micro-environtment which is a key factor driving a tumor ((could even possibly be the key factor driving a tumor)). And aspirin might also help reduce induced resistance by established treatments. So aspirin can certainly be useful in the treatment of tumors and we are are definitely not exploiting this cheap drug. Let that be clear.

However there's several jak proteins and several stat proteins which cannot be regarded as the same. I don't think it is easy nor I think we can blame the authors. And actually you are giving the answer yourself, which also at the same time admits the complexity:

their kinase activity was not affected in vitro by salicylates

and

suggesting that other kinases were involved in IL-4-induced STAT6 activation.

also from the same article

Src kinase was involved in STAT6 activation ... Src kinase activity, but not Janus kinase, was inhibited by salicylates in vitro

So aspirin isn't a JAK inhibitor by directly targetting JAK. Which I think is what the authors targeted I guess. NSAIDs can certainly reduce JAk activation by reducing cytokines, but that's still not a direct JAK inhibitor. It's like the example you quote above. Check out what this study said..:

We found that aspirin not only significantly enhanced IFN-α-induced antiproliferation and apoptosis of HCC in vitro study but also enhanced tumor growth inhibition in nude mice. Although IFN-α alone resulted in significant phosphorylation of both STAT1 and STAT3, aspirin only prompted the IFN-α-induced phosphorylation of STAT1. Further study revealed that aspirin-prompted phosphorylation of STAT1 was activated through phosphorylation of JAK1.

http://www.ncbi.nlm.nih.gov/pubmed/23703473

Thanks, good catches. I should have said that aspirin is an indirect JAK inhibitor (just like it is an indirect aromatase inhibitor) - i.e. it inhibits stat proteins that activate JAK.
I wonder if some of the others like paracetamol or ibuprofen do the same. Both of them were listed in the caffeine life extension study I posted a while ago. Both of them extended lifespan so I am thinking some of reason for those results may be anti-cancer activity.