Primary liver cancer is the third leading cause of cancer-related deaths, of which hepatocellular carcinoma (HCC) accounts for approximately 90% of all liver cancer cases. Given that the development of HCC is a multifactorial and multistage process, its increasing incidence underscores the need to understand its molecular mechanisms and identify potential biomarkers and therapeutic targets.

Prostate cancer (PCa) is one of the most common malignant tumors in men worldwide. While early detection has improved patient outcomes, effective therapies for advanced disease remain limited. Identifying the molecular drivers of PCa growth and metastasis is therefore essential to developing new treatment strategies that can overcome resistance to standard therapies.

Polycyclic aromatic hydrocarbons (PAHs) are carcinogenic compounds introduced in food due to cooking methods such as smoking, grilling, and frying. Recently, researchers from Seoul National University of Science and Technology have leveraged a new method called QuEChERS-GC-MS to extract and detect PAHs in common food items, finding the highest levels in soybean oil, followed by duck meat and canola oil.

An international research group led by The University of Osaka has developed scODIN, a novel computational tool to classify cell types from single-cell RNA sequencing (scRNA-seq) data. Existing methods struggle to balance speed and accuracy, often misclassifying rare or transitional cells. scODIN overcomes this limitation by combining a hierarchical classification system (Tier system) with k-nearest neighbor inference. This approach allows for the rapid and accurate classification of large datasets, processing 650,000 cells in just six minutes. The tool's improved accuracy stems from its ability to identify cells at varying levels of detail, recognize intermediate phenotypes through double labeling, and recover cells affected by dropout events. scODIN promises to accelerate biomedical discoveries by enabling more precise and efficient analysis of complex biological processes and disease mechanisms.

Scientists at St. Jude Children’s Research Hospital explored how mutations in mitochondrial DNA contribute to cancer, the extent of their impact, and when and how they become a factor.

New research published in Immunity by researchers at the University of Pittsburgh found that, in mice, the toxic tumor environment causes mitochondria to generate reactive oxygen species (ROS) that travel to the nucleus and damage telomeres, driving T cells to a dysfunctional state. By preventing damage to telomeres via a targeted antioxidant, scientists hope to rescue T cell function, opening the door to novel therapies to improve the effectiveness of cancer immunotherapies.