Lung Adenocarcinoma

Those treated with PD-1/PD-L1 inhibitors (Pembrolizumab) had limited benefit, with a median overall survival of 4.1 ± 2.8 months...Comprehensive genomic profiling may help refine understanding of tumour biology and potentially inform treatment decisions. Larger studies are needed to validate these findings, but integrating genomic, pathologic, and clinical data may advance personalized therapy for these patients.

Human T lymphocytes were engineered with a lentiviral vector to express anti-FRα-CAR5, which incorporates a fourth-generation CAR backbone (CD28, 4-1BB, CD27, and CD3 zeta) augmented by a secreted anti-PD-L1 scFv derived from atezolizumab...This fifth-generation CAR offers a promising strategy to enhance CAR T cell therapy efficacy in PD-L1-mediated immunosuppressive TMEs. These findings suggest that anti-FRα-CAR5 T cells therapy warrants further preclinical validation as a potential treatment strategy for NSCLC patients.

This dual action establishes a feedforward loop that exacerbates metastatic progression. Our findings identify ATP6V1C1 as a dual regulator of LUAD metastasis and suggest a potential stroma-targeted therapeutic approach.

This study offers causal evidence supporting the protective effects of exercise against lung cancer, potentially through pathways dependent on SULT1A1.

The in vivo experiments showed that CA significantly inhibited tumor growth and enhanced NK cell infiltration in mice, accompanied by decreased Ki67+ proliferating cells, increased cleaved caspase-3+ apoptotic cells, and upregulated FBXO38 expression. Collectively, our findings demonstrate that CA may be exert anti-LUAD effects through FBXO38/CCL5-mediated NK cell recruitment.

Furthermore, CKMT1B overexpression facilitated lipid accumulation and stemness, effects that were reversible by the lipase inhibitor Orlistat...In functional rescue experiments, PITX2 knockdown significantly reduced lipid accumulation and stemness, while these effects were partially restored by CKMT1B overexpression. PITX2 promotes lipid accumulation and enhances stemness in LUAD cells by transcriptionally activating CKMT1B, suggesting the PITX2/CKMT1B axis as a potential therapeutic target for LUAD treatment.

P1/2, N=37, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027

Given the high mutation frequency of PDLIM4 recorded in the TCGA cancer database, our findings reveal a critical regulatory signaling pathway that suppresses LUAD progression and augments chemotherapy efficacy.

We describe the clinical course of a 65-year-old woman who developed a violaceous cutaneous metastatic lesion beneath the left breast during treatment for metastatic lung adenocarcinoma. This case highlights the importance of recognizing cutaneous signs as indicators of disease progression and emphasizes the diagnostic challenges and prognostic implications of cutaneous metastases in lung cancer.

These findings were further validated by in vivo experiments, where TMT1A expression was found to promote CD8+ T cell infiltration in LUAD. These findings demonstrated tumor-suppressive functions coupled with its immunomodulatory capacity position TMT1A as a promising therapeutic target for LUAD treatment.

The predicted regulatory network of FOXM1 shows significant discrepancies with experimental validation data. Therefore, FOXM1's regulatory role in the cell cycle requires further experimental verification.