Vitamin K2 has been studied for its effects on various oncogenic pathways. Studies have shown that Vitamin K2 activates the tumor suppressor p53, which is known to be involved in the regulation of cell cycle, apoptosis, and DNA repair. Vitamin K2 also inhibits the activity of oncogenic proteins such as Bcl-2 and c-Myc, both of which are known to be involved in the promotion of tumor growth and metastasis. Vitamin K2 has also been shown to modulate the activity of the Wnt/Ξ²-catenin pathway, a major oncogenic pathway involved in cell proliferation and survival.
Impact of vitamin K dosing during sorafenib treatment for hepatocellular carcinoma
https://ascopubs.org/doi/10.1200/JCO.2016.34.15_suppl.e15585
Median PFS was 7.0 months vs. 2.0 months in vitamin K dosing group and sorafenib alone one (P < 0.001), respectively. Vitamin K dosing also prolonged OS significantly (median survival: 12.5 months vs. 10.0 months, P = 0.016). Subgroup analysis revealed that vitamin K dosing prolonged OS especially in patients without vascular invasion or extrahepatic spread. In such patients, median OS was 29.0 months in vitamin K dosing group, whereas that of sorafenib alone group was 15.5 months (P = 0.014). On the other hand, a unique difference in DCP changes (pre vs. 8 weeks after) were observed in patients with partial response or stable disease. Serum DCP levels was increased in sorafenib alone group despite suppressed tumor growth (2.28±0.91 → 2.64±1.03 Log mAU/mL, P = 0.048). In contrast, vitamin K dosing group showed decreased DCP levels (2.01±0.58→1.30±0.29 Log mAU/mL, P = 0.003).
(45mg MK-4)
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