Innovative biomaterial accelerates healing of chemotherapy-induced oral ulcers in animal model
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Updates every hour. Last Updated: 12-Jul-2025 04:11 ET (12-Jul-2025 08:11 GMT/UTC)
A new study has revealed that ferulic acid, a natural compound found in various plant-based foods, can significantly inhibit the growth and migration of colon cancer cells at different stages of progression. The research, which offers valuable insights into how ferulic acid induces cell cycle arrest and apoptosis, suggests that this compound could serve as an effective dietary intervention for preventing colon cancer. These findings open new avenues for dietary strategies aimed at reducing the burden of this widespread disease.
Early diagnosis of lung cancer is a critical priority in clinical practice. It may help reduce the rate of lung-cancer-related mortality, extend disease-free survival, and allow patients to live without ongoing medical interventions and complications. Although various diagnostic methods differentiate lung cancer malignancy from benign disease, their low accuracy makes them unfavorable.
A newly published review in Genes & Diseases explores the oncogenic activation of PIK3CA in cancer and highlights emerging targeted therapies designed to improve treatment efficacy while reducing side effects. The research provides a comprehensive analysis of PIK3CA mutations, their role in tumor development, and novel therapeutic approaches currently in development.
Scientists from Finland, USA, UAE, and Thailand find AI responses to cancer-related questions not so reliable particularly in languages other than English.
Researchers at The University of Texas MD Anderson Cancer Center have developed a novel antibody-toxin conjugate (ATC) designed to stimulate immune-mediated eradication of tumors. According to preclinical results published today in Nature Cancer, the new approach combined the benefits of more well-known antibody-drug conjugates (ADCs) with those of immunotherapies.
New findings question assumptions of cancer formation in individuals with the cancer-predisposition syndrome, neurofibromatosis type 1, and offer hope for a personalised approach to early cancer recognition including for those with similar conditions.
One particular challenge in the treatment of cancer is therapy resistance. An international research team has now discovered a mechanism that opens up new treatment strategies for tumours in which conventional chemotherapeutic agents have reached their limits. "Cytotoxic agents from nature lead to an increased incorporation of polyunsaturated fatty acids into the membrane of cancer cells. This makes them more susceptible to ferroptosis, a type of cell death, at a very early stage," reports Andreas Koeberle, a pharmacist at the University of Graz and lead author of the study, which has just been published in the scientific journal Nature Communications.
Background: Over recent decades, findings on the potential correlation between type II diabetes mellitus (T2DM) and the risk of esophageal cancer (EC) have displayed considerable heterogeneity. Furthermore, metformin has emerged as a potentially protective agent against certain site-specific malignancies. This study aims to explore the causal relationship between T2DM, medication treatments (metformin, insulin, gliclazide), and EC risk while addressing the notable variability in previous research findings.
Methods: To elucidate the causal associations between T2DM, medication treatments, and EC, we employed a synergistic methodology that integrates the two-sample Mendelian randomization (MR) approach with meta-analysis. The genome-wide association studies (GWAS) pertaining to each exposure and EC were acquired from a publicly accessible database.
Results: For MR analyses, three out of seven GWAS datasets within the T2DM cohort exhibited statistical significance. Conversely, all MR analyses yielded non-significant results in the medication cohort. Meta-analyses suggested that a genetic predisposition to T2DM correlated with a reduced risk of EC [odds ratio (OR), 0.999612; 95% confidence interval (CI): 0.999468–0.999756; P=0.01; I2=0%]. Moreover, metformin intake was causally linked to a decreased prevalence of EC (OR, 0.988954; 95% CI: 0.979044–0.998963; P=0.03; I2=0%), whereas neither insulin nor gliclazide manifests statistical significance.
Conclusions: Our findings indicate T2DM and metformin are causally associated with diminished risk of EC, while no causal associations exist between insulin, gliclazide, and EC.