TAK1 expression is associated with increased PD-L1 and decreased cancer-specific survival in microsatellite-stable colorectal cancer.

Background: Transforming growth factor β-activated protein kinase-1 (TAK1) plays an important role in MAPK and NFκB pathways and has been associated with colorectal cancer. The aim of this study was to determine how cytoplasmic and juxtanuclear punctate staining of TAK1 relates to immune checkpoint expression and cancer specific survival in colorectal cancer.

Methods: Protein expression was assessed by immunohistochemistry on tissue microarrays from primary curative colorectal cancer resected specimens.

Morphological Evolution of an Intertidal Mudflat in Relation to Mangrove Growth: Implications for Future Erosion Control.

There is limited information regarding the influence of mangrove growth on the morphological evolution of intertidal mudflats. In this study, Tan Phu Dong district, Tien Giang Province, Vietnam, was selected for investigating how mangrove growth influenced the morphological evolution of an intertidal mudflat. The authors analyzed a series of satellite images (from 1995 and 2022), calculated the enhanced vegetation index (EVI), and documented field visits and observations in pursuit of the objective of the study.

Fibroblast activation protein inhibitor-positron emission tomography in aortitis: fibroblast pathology in active inflammation and remission.

Objectives: Epigenetically modified fibroblasts contribute to chronicity in inflammatory diseases. Reasons for the relapsing character of large vessel vasculitis (LVV) remain obscure, including the role of fibroblasts, in part due to limited access to biopsies of involved tissue.68Ga FAPI-46 (FAPI)-PET/CT detects activated fibroblasts in vivo.

Interplay of p62-mTORC1 and EGFR signaling promotes cisplatin resistance in oral cancer.

Cisplatin resistance poses a major challenge in the treatment of oral squamous cell carcinoma (OSCC). Deeper investigations into the mechanisms underlying this drug resistance is of great importance. Here, we used cellular assays and clinical immunohistochemistry to examine molecular pathways involved in both innate and acquired cisplatin resistance.