Somatic mutations frequently disrupt cleavage and polyadenylation signals in tumour suppressor genes in human cancers, likely contributing to tumour progression.
Tissue-resident natural killer cells are important mediators of CD8 T responses in human cancers and these cells can be harnessed to increase immunity against pancreatic ductal adenocarcinoma.
In metastatic NSCLC patients, CHIP showed minimal impact on immunotherapy response but was more prevalent and associated with inflammatory pathways in myeloid cells, particularly in lung squamous cell carcinoma.
CPT1A downregulation enhances radioresistance in colorectal cancer (CRC) via FOXM1-mediated antioxidant response, making it a potential biomarker for radiosensitivity and a novel target for improving CRC radiotherapy.
High mutational load tumors mitigate effects from protein-damaging mutations by up-regulating complexes that buffer against misfolding stress, revealing therapeutic vulnerabilities and suggesting disrupted proteostasis is a hallmark of somatic evolution.
The automated workflow significantly enhances the precision and scalability of cell cycle analysis, enabling high-throughput studies in both non-adherent and adherent cells for advanced cancer research and drug development.
