Vitamin K2, venetoclax synergy in AMLVitamin K2 sensitizes the efficacy of venetoclax in acute myeloid leukemia by targeting the NOXA-MCL-1 pathway.
We observed how vitamin K2 (VK2) could play a significant role in enhancing the effectiveness of a common treatment for acute myeloid leukemia (AML) called venetoclax (VEN). In our investigation, older patients diagnosed with AML showed promising responses to a treatment combination of VEN and another drug, azacitidine (AZA), alongside daily VK2 intake. Remarkably, we noted a complete response rate of about 79% among patients taking VK2, highlighting the potential of VK2 to improve treatment outcomes.
Our study involved patients who were mostly over 75 years old and considered high-risk. They received a regimen that included AZA and VEN, paired with VK2. We also looked into the mechanisms behind VK2's effects. We found that VK2 significantly increased apoptosis, a process that causes cancer cells to die, particularly through a pathway involving NOXA and MCL-1 proteins. This was driven by an increase in reactive oxygen species (ROS) induced by VK2.
Furthermore, the combination of VK2 and VEN worked synergistically to target two cancer-related proteins, enhancing the treatment's impact. This dual action could be a key factor in the strong clinical outcomes observed in our patient population. Given these exciting findings, further large-scale clinical trials are certainly warranted to explore VK2's role in cancer treatment more broadly.
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PIVKA-II shows promise for HCCPIVKA-II as a surrogate biomarker for therapeutic response in Non-AFP-secreting hepatocellular carcinoma.
We aimed to discover how well PIVKA-II can predict treatment response in patients with non-AFP-secreting hepatocellular carcinoma (HCC) receiving systemic therapy.
By measuring PIVKA-II levels and assessing imaging after 8-12 weeks of treatment, we found a connection between PIVKA-II levels, tumor size, and treatment outcomes.
The study revealed a promising “50-50 rule” that can indicate prognosis based on PIVKA-II changes, making it a valuable marker for HCC treatment success.
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EZJDD improves liver cancer outcomesEfficacy and Safety of Erzhu Jiedu Decoction Granules in Treating Mid-advanced Hepatitis B Virus-Associated Primary Liver Cancer Patients with Pi (Spleen)-Deficiency and Dampness-Heat Syndrome.
We evaluated the effectiveness and safety of Erzhu Jiedu Decoction (EZJDD) Granules in patients with mid-advanced liver cancer linked to hepatitis B.
In a study involving 132 patients, we randomly assigned them into two groups—one receiving standard treatment and the other receiving standard treatment along with EZJDD Granules for three months.
The results showed that EZJDD significantly extended progression-free survival and boosted the six-month survival rate, suggesting it may enhance treatment outcomes for this challenging condition.
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Vitamin K precursor inhibits cancer growthDietary pro-oxidant therapy by a vitamin K precursor targets PI 3-kinase VPS34 function.
We explored how a vitamin K precursor, known as menadione sodium bisulfite (MSB), influences prostate cancer progression in mice. Contrary to concerns surrounding antioxidants like vitamin E, our findings suggest that MSB acts as a pro-oxidant, successfully reducing cancer cell growth via oxidative cell death.
By targeting critical cellular pathways, MSB offers a new route for therapeutic intervention in prostate cancer. These results enhance our understanding of the effects of pro-oxidants and highlight potential opportunities for future treatments.
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Vitamin K implicates glioma progressionAssociation between Fat-Soluble Vitamin Metabolic Process and Glioma Progression.
We examined the connection between fat-soluble vitamins, specifically vitamin K, and the progression of gliomas, which are particularly aggressive brain cancers. Using The Cancer Genome Atlas database, we found that vitamin K-related metabolic processes are closely linked with the severity and poor prognosis of gliomas.
Notably, a key gene, VKORC1, which is vital for vitamin K's function, showed a strong association with glioma aggressiveness. In laboratory settings, silencing this gene reduced glioma cell growth and movement. Although the results are promising, clinical effects in patients remain to be conclusively determined.
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