PD-L1 overexpression

The patient received combined dabrafenib, trametinib, and pembrolizumab with close safety monitoring, achieving rapid tumor control and complete remission by six months with manageable toxicity. This case suggests that early integration of PD-1 blockade with BRAF/MEK inhibition treatment may benefit selected patients and underscores the value of comprehensive molecular and immunohistochemical assessment to guide individualized therapy.

Furthermore, linarin treatment significantly inhibited colorectal cancer tumor growth in vivo. In conclusion, linarin could inhibit the proliferative, migratory, and invasive capacity, but enhance the apoptotic ability in colorectal cancer cells through repressing the HIF-1α/PD-L1 axis.

The combination of chemotherapy and immune checkpoint blockade therapy shows great potential in tumor treatment, but their integration remains a great challenge. Meanwhile‌, overexpression of programmed cell death ligand 1 (PD-L1) is suppressed by JQ1, thereby reversing PD-L1-mediated immune resistance to synergistically promote adaptive antitumor immune response. This hypoxia-sensitive versatile nanoplatform provides an elegant paradigm for precise tumor therapy.

Our findings showed relatively high PDL-1 expression in most HNSCC patients. No significant association was found between PD-L1 protein expression and overall survival.

Pulmonary sarcomatoid carcinoma requires immediate and optimal therapeutic intervention because of its aggressive nature and narrow therapeutic window. In health care systems with limited access to immunotherapy, emphasis must be placed on achieving complete surgical resection and intensive postoperative surveillance. This case highlights the need for health care policy discussions regarding expanded access to immunotherapy for patients with favourable biomarker profiles, as current restrictions may significantly impact outcomes in this devastating disease.

Higher levels of YTHDF1 and METTL3 expression in HCC tissues were associated with higher expression of PD-L1. m6A modification participates in regulating immune microenvironment of HCC, and targeting m6A may block the immune escape of HCC cells.

Cemiplimab demonstrated comparable real-world efficacy and safety to pembrolizumab in patients with advanced NSCLC and PD-L1 ≥ 50%. ECOG performance status emerged as the strongest prognostic factor, highlighting the importance of patient selection in routine clinical practice.

Despite low overall expression rates, PD-L1 could serve as a prognostic biomarker and a potential target for immunotherapeutic strategies in liposarcomas. Further studies are necessary to standardize PD-L1 assessment and explore effective immunotherapy approaches for these tumors.

We report a unique case of a 65-year-old man with squamous-cell NSCLC and high PD-L1 expression (80%), who developed a rare complication: radiation recall pneumonitis (RRP), with superimposed Pneumocystis jirovecii pneumonia and severe symptomatic hyponatremia induced by trimethoprim/sulfamethoxazole (TMP-SMX). The coexistence of these three complications-radiotherapy- and immunotherapy-associated lung injury, opportunistic infection, and electrolyte imbalance-represents an exceptional clinical scenario not previously described in the literature. This report highlights the importance of differential diagnosis, early recognition of complications, and close monitoring of electrolytes in NSCLC patients undergoing complex treatment regimens.

Furthermore, TIME-GES-guided screening led to the discovery of NCD, a promising immunomodulatory agent that reprograms the TIME and enhances anti-tumor immunity in TNBC. This study offers both a robust immune gene signature and a candidate therapeutic to improve immunotherapy outcomes in TNBC.

This study revealed the specific compositions of intratumoral microbiota as demonstrating relevance to response to ICI therapy in high PD-L1-TPS lung cancer patients. The intratumoral microbiota components Tetrasphaera and Mesorhizobium may have a key role in determining the response to cancer immunotherapy for lung cancer.

Furthermore, RNA immunoprecipitation and luciferase reporter assays suggest that m6A RNA modification may potentiate LDHA overexpression. Collectively, this work unveils a dual-layered mechanism-metabolic lactate flux and histone lactylation that orchestrates immune evasion in BCa, proposing LDHA and EP300 as actionable targets to restore antitumor immunity.