Publisher’s Note by David Wallace:
The two studies below provide compelling data on the effectiveness of supplementation with curcumin in patients with MPN. Although no recent studies on curcumin have emerged in MPN (since 2019), it would seem prudent to discuss the supplement with your physician. Naturally if you are taking any type of blood thinner medication curcumin would not be an option, as it has inherent blood thinning capabilities. Always discuss any new supplements you are taking or considering with your physician.
A recent search of clinicaltrials.gov shows 51 clinical trials that are recruiting or active, not recruiting. Studies are being conducted for a multitude of conditions, including:
- Acute Lymphoblastic Leukemia (ALL)
- Multiple Myeloma
- Breast cancer
- Prostate cancer
- Tinnitus
- Systemic lupus
- Chronic kidney disease
- Covid-19
- IBS and many other conditions
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.
–> Don’t miss this earlier study below, “Pure curcumin increases the expression of SOCS1 and SOCSS3 in myeloproliferative neoplasms through suppressing the class I histone deacetylases”
