Lung Cancer

It shows high specificity in the differentiation of mesothelioma from lung or breast carcinoma but is of little value in differentiating mesothelioma from tubo-ovarian carcinoma. The potential role of HEG1 as vascular marker merits further research.

It inhibits integrin α8β6-mediated PI3K/AKT and MAPK/ERK signaling to suppress tumor growth, promotes CD8+ T-cell infiltration, and augments cisplatin sensitivity via the JNK/c-Jun pathway. These findings nominate MUC14 as a prognostic biomarker and therapeutic target, suggesting combinatorial strategies integrating immunotherapy and chemotherapy.

In selected settings, nano-enabled pyroptosis promotes immune cell infiltration and restores responsiveness to PD-1/PD-L1-based immunotherapy, particularly when combined with chemotherapy or radiotherapy. Despite these advances, clinical translation remains constrained by tumor heterogeneity, delivery inefficiency, and the need for stringent control of inflammatory spillover in lung tissue.

RAS or MEK inhibition co-targeting is effective against this resistance mechanism. This study provides preclinical rationale for clinical testing of exarafenib in BRAF Class II/III cancers and unveils RAS-mediated ARAF-KSR1 complex formation as a resistance mechanism and rational co-therapy strategies.

RWE confirms the effectiveness and safety of multiple recently approved oncology drugs reinforcing the external validity of RCTs.

xCell2 analysis indicated reduced plasma cells and increased smooth muscle, muscle, adipocyte, and endothelial cells, suggesting normalization of tissue remodeling. Nintedanib appears to exert anti-inflammatory effects and promote tissue repair in non-tumor lung, while facilitating tissue remodeling in fibrotic areas, indicating potential benefits in patients with interstitial pneumonia and lung cancer.

Importantly, this work moves beyond static baseline markers by emphasizing dynamic, pathway-level changes and provides a hypothesis-generating framework for longitudinal therapeutic monitoring. Candidate proteins such as tetranectin and coagulation factor XIII A chain are proposed as molecular features associated with treatment response, warranting further validation in larger, prospective cohorts before translational application.

These findings uncover a previously unrecognized EP300-H2BK5ac-HSPA1A regulatory pathway that links environmental exposure to biomechanical and epigenetic remodeling in lung cancer. Targeting this axis may offer new strategies to mitigate B(a)P-driven metastasis.

Therefore, it might be indicated that BT improved Dox retention and increased the Dox responsiveness in A549 cells. BT-mediated selective suppression of the NRF2, re-stabilized the KEAP-1-independent NRF2 regulators and made the non-responsive A549 cells partially sensitive to Dox.