CURCUMIN? – IS IT THE NEXT BEST THING...?
Posted: Wed Sep 25, 2019 8:29 pm
Hey all my MPN colleagues & friends...
Thought that you might all enjoy a quick scan of this article on Curcumin, that seems to suggest that its powers might be just what the Pharmacist decided not to order... because it is possibly much less expensive than its well publicised rivals: i.e.: HU, Interferon & Jakafi... to name a few...
While all of this article's testing is granted a "small cohort of participants w/ the JAK2+ mutation"
It does hold promise based upon its early results.
Hopefully, we might see further testing and larger cohorts into the Not To Distant Future? "Watch this space!"
Best
Steve
Article:
Curcumin induces apoptosis in JAK2‐mutated cells by the inhibition of JAK2/STAT and mTORC1 pathways
Abstract
Myeloproliferative neoplasms are chronic myeloid cancers divided in Philadelphia positive and negative. The JAK2 V617F is the most common mutation in Philadelphia negative patients and results in a constitutive activation of the JAK/STAT pathway, conferring a proliferative advantage and apoptosis inhibition. Recent studies identified a functional crosstalk between the JAK/STAT and mTOR pathways. The identification of an effective therapy is often difficult, so the availability of new therapeutic approaches might be attractive. Previous studies showed that curcumin, the active principle of the Curcuma longa, can suppress JAK2/STAT pathways in different type of cancer and injuries. In this study, we investigated the anti‐proliferative and pro‐apoptotic effects of curcumin in JAK2 V617F‐mutated cells. HEL cell line and cells from patients JAK2 V617F mutated have been incubated with increasing concentrations of curcumin for different time. Apoptosis and proliferation were evaluated. Subsequently, JAK2/STAT and AKT/mTOR pathways were investigated at both RNA and protein levels. We found that curcumin induces apoptosis and inhibition of proliferation in HEL cells. Furthermore, we showed that curcumin inhibits JAK2/STAT and mTORC1 pathways in JAK2 V617F‐mutated cells. This inhibition suggests that curcumin could represent an alternative strategy to be explored for the treatment of patients with myeloproliferative neoplasms.
CONCLUSION
J essica Petiti_et al_2019. "Curcumin induces apoptosis in JAK2‐mutated cells by the inhibition of JAK2/STAT and mTORC1 pathways"
Department of Clinical and Biological Sciences, University of Turin, Turin, Italy; Department of Oncology, University of Turin, Turin, Italy;
SSD Transfusional Center, San Luigi Gonzaga Hospital, Turin, Italy:(Mar. 06, 2019). DOI: 10.1111/jcmm.14326
https://onlinelibrary.wiley.com/doi/epd ... jcmm.14326 (Direct Link)
Thought that you might all enjoy a quick scan of this article on Curcumin, that seems to suggest that its powers might be just what the Pharmacist decided not to order... because it is possibly much less expensive than its well publicised rivals: i.e.: HU, Interferon & Jakafi... to name a few...
While all of this article's testing is granted a "small cohort of participants w/ the JAK2+ mutation"
It does hold promise based upon its early results.
Hopefully, we might see further testing and larger cohorts into the Not To Distant Future? "Watch this space!"
Best
Steve
Article:
Curcumin induces apoptosis in JAK2‐mutated cells by the inhibition of JAK2/STAT and mTORC1 pathways
Abstract
Myeloproliferative neoplasms are chronic myeloid cancers divided in Philadelphia positive and negative. The JAK2 V617F is the most common mutation in Philadelphia negative patients and results in a constitutive activation of the JAK/STAT pathway, conferring a proliferative advantage and apoptosis inhibition. Recent studies identified a functional crosstalk between the JAK/STAT and mTOR pathways. The identification of an effective therapy is often difficult, so the availability of new therapeutic approaches might be attractive. Previous studies showed that curcumin, the active principle of the Curcuma longa, can suppress JAK2/STAT pathways in different type of cancer and injuries. In this study, we investigated the anti‐proliferative and pro‐apoptotic effects of curcumin in JAK2 V617F‐mutated cells. HEL cell line and cells from patients JAK2 V617F mutated have been incubated with increasing concentrations of curcumin for different time. Apoptosis and proliferation were evaluated. Subsequently, JAK2/STAT and AKT/mTOR pathways were investigated at both RNA and protein levels. We found that curcumin induces apoptosis and inhibition of proliferation in HEL cells. Furthermore, we showed that curcumin inhibits JAK2/STAT and mTORC1 pathways in JAK2 V617F‐mutated cells. This inhibition suggests that curcumin could represent an alternative strategy to be explored for the treatment of patients with myeloproliferative neoplasms.
CONCLUSION
REFERENCE"In conclusion, this study showed that curcumin exerts an antitumor effect on human JAK2‐mutated cells by inducing apoptosis and inhibition of proliferation, through the regulation of both JAK2/STAT and mTORC1 pathways.These findings suggest that curcumin seems to be a promising nutraceutical compound that should be further evaluated in different pharmaceutical formulation for the treatment of MPNs."
J essica Petiti_et al_2019. "Curcumin induces apoptosis in JAK2‐mutated cells by the inhibition of JAK2/STAT and mTORC1 pathways"
Department of Clinical and Biological Sciences, University of Turin, Turin, Italy; Department of Oncology, University of Turin, Turin, Italy;
SSD Transfusional Center, San Luigi Gonzaga Hospital, Turin, Italy:(Mar. 06, 2019). DOI: 10.1111/jcmm.14326
https://onlinelibrary.wiley.com/doi/epd ... jcmm.14326 (Direct Link)
