Lung Adenocarcinoma

Overall, our results provided unique perspectives into previously unappreciated molecular dynamics of CSC subpopulations driving LUAD evolution. The stemness signature tailored personalized risk assessment and immunotherapy strategies for individual LUAD patients.

PTPRCAP is downregulated in LUAD and acts as a tumor suppressor by promoting apoptosis and inhibiting proliferation, migration, and invasion. These findings suggest PTPRCAP as a potential therapeutic target for LUAD.

Patients with MET amplified BM had significantly shorter overall survival. These findings highlight MET amplification as a critical driver of LUAD BM, emphasizing its potential as a therapeutic target.

MUC5B facilitates LUAD lymph node metastasis, potentially by regulating the GINS complex and promoting oncogenic signaling. These findings highlight MUC5B as a promising biomarker and therapeutic target for advanced LUAD.

Furthermore, we found a correlation between the expression of SDCBP2 and SLC7A11, and patients with concurrent high expression of both exhibited a poorer prognosis, although the regulatory relationship between the two genes remains to be further investigated. This study demonstrates that SDCBP2 promotes tumor progression and is a novel ferroptosis-related prognostic biomarker for LUAD.

PPP2R1A is overexpressed in LUAD and associated with poor prognosis, potentially serving as an oncogene by regulating key signaling pathways and immune microenvironment. Its knockdown suppresses malignant phenotypes, highlighting its potential as both a prognostic biomarker and therapeutic target in LUAD.

P3, N=339, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Mar 2026 | Trial primary completion date: Dec 2025 --> Mar 2026

P1, N=130, Recruiting, Sairopa B.V. | N=90 --> 130 | Trial completion date: Dec 2025 --> Jul 2027 | Trial primary completion date: Dec 2025 --> May 2027

P1, N=90, Enrolling by invitation, Biogenea Pharmaceuticals Ltd.

ENE represents a pathological prognostic factor characterized by abundant fibrous stroma. It independently predicts distant metastasis and may warrant consideration as a qualitative parameter in N classification for lung adenocarcinoma.

The combination of mebendazole and gefitinib effectively suppresses tumor cell viability and modulates key pathways involved in cancer progression. By targeting cytoskeletal integrity and EGFR signaling, it may disrupt cytokine and tumor-microenvironment interactions, supporting further exploration as a strategy to overcome resistance in lung and breast cancers.

This study identifies the BUB1/E2F1/TMPO-AS1/hsa-let-7b-5p axis as a potential prognostic biomarker and therapeutic target in LUAD. Targeting hsa-let-7b-5p may modulate this network, offering opportunities for both diagnostic and prognostic interventions.