Lung Adenocarcinoma

P1, N=312, Active, not recruiting, Daiichi Sankyo | Recruiting --> Active, not recruiting

This study proposes a putative prognostic model based on CRGs for LUAD outcome prediction. The hub gene FAM83A may facilitate lung cancer cell growth by regulating glycolysis via PKM2 and LDHA, offering a novel theoretical foundation and a potential target for prognostic assessment and targeted therapy in LUAD patient.

The study highlights a pro-metastatic ELANE + neutrophil subpopulation, with RELB acting as its primary transcriptional regulator. The RELB signature may serve as a biomarker for prognosis and treatment response prediction, indicating a potential target for precision treatment in EGFR wildtype LUAD.

P1/2, N=53, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2025 --> Dec 2026

Our findings provide a comprehensive understanding of the lineage plasticity and the immune landscape in T-SCLC, highlighting the crucial role of the stem-like cell cluster and ISG+ lymphocytes in LUAD-to-SCLC transformation.

Indeed, our de novo somatic indel calling from TCGA RNA-seq increases the TCGA driver indel repertoire by ~ 14%, especially in samples with purity < 0.4, including actionable EGFR indels in lung adenocarcinoma and FLT3 in acute myeloid leukemia. Our study not only reveals confounders in somatic mutant ASE analysis but also demonstrates their utility in RNA-based mutation calling.

Metabolism-related lncRNAs contribute substantially to tumor heterogeneity and prognosis in NSCLC and may serve as valuable biomarkers for patient stratification and personalized therapeutic strategies.

Its expression was rarely observed in other histological types of lung cancer. CLDN18.2 is frequently expressed in IMAs but rarely in other major lung cancer subtypes, suggesting that zolbetuximab may represent a promising targeted therapy for IMA.

The patient was later hospitalized for "recurrent hemoptysis" and received pemetrexed adjuvant chemotherapy combined with cisplatin...Consequently, a targeted therapy regimen combining low to moderate doses of dabrafenib and trametinib was initiated...Moreover, only one low-grade immune-related adverse event was observed during the course of immunotherapy. Patients with advanced NSCLC and BRAF mutations who cannot tolerate targeted therapy are expected to benefit from immunotherapy.

Rescue experiments further confirmed that GPRC5C is required for ARID4B-mediated maintenance of tumor invasiveness and cancer stemness. ARID4B promotes LUAD malignancy by transcriptionally activating GPRC5C, thereby driving EMT and cancer stemness.

The methylation status or expression level of SORD holds promise as a potential biomarker for predicting Osimertinib efficacy, and targeting SORD-related pathways may provide new strategies for overcoming Osimertinib resistance.