Brain radiotherapy and dorsal vagal complex irradiation: A new organ at risk to decrease radiation-induced nausea and vomiting?

Purpose: Nausea is a common symptom in patients irradiated for benign brain tumors. The dorsal vagal complex (DVC) located in the brainstem (BS) has been identified as the center of nausea and vomiting. The objective of our study was to determine an association between mean dose to the DVC and nausea.

A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression.

The uniqueness in each person's cancer cells and variation in immune infiltrates means that each tumor represents a unique problem, but therapeutic targets can be found among their shared features. Radiation therapy alters the interaction between the cancer cells and the stroma through release of innate adjuvants. The extranuclear DNA that can result from radiation damage of cells can result in production of the second messenger cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) by cyclic GMP-AMP synthase (cGAS).

Investigating the Significances of Thiol Functionalities in SARS-CoV-2 Using Carbon Dots for Viral Inhibition.

While the World Health Organization has declared the end of the SARS-CoV-2 public health emergency, studies related to corona viruses are still under course. As of 2024, the severity of COVID-19 has diminished with current treatments and vaccinations. However, individuals can still face severe complications, highlighting the importance of ongoing research into innovative treatments for current and future coronavirus-related diseases.

Smyd3-mediated immuno-modulation in HPV-negative head and neck squamous cell carcinoma mouse models.

SET and MYND-domain containing protein 3 (SMYD3) mediates epigenetic repression of type I IFN response genes in human papillomavirus (HPV)-negative HNSCC cells, and Smyd3 depletion using anti-sense oligonucleotides (ASOs) increases the sensitivity of syngeneic mouse oral carcinoma (MOC1) models to anti-PD-1 therapy. In this study, we utilized single-cell RNA-seq of MOC1 tumors treated with Smyd3 ASOs and found enrichment of type I IFN response pathways in cancer cells, a shift of CD8 T-cells toward an activated/memory phenotype, and a shift of neutrophils toward an anti-tumorigenic phenotype. Mechanisms of resistance to the Smyd3 ASO and anti-PD-1 combination were derived from cancer cells, macrophages, and CD8 T-cells, including neutrophil enrichment through the upregulation of , repression of and defective antigen presentation.