Publications by authors named "Luc Stoven"

Background: The KBP studies are real-life nationwide, prospective, multicenter cohort studies of patients diagnosed with primary lung cancer that have been conducted in French non-academic public hospitals each decade since 2000.

Methods: Patients were analyzed in three prospective cohorts using the same methodology. In this study, we describe and compare the characteristics and outcomes of patients with small cell lung cancer (SCLC), with a focus on treatments in the 2020 cohort.

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Background: The optimal duration of immune checkpoint inhibitor (ICI) treatment for patients with advanced non-small cell lung cancer (NSCLC) remains to be determined. Treatment durations in cornerstone phase 3 clinical trials vary between a fixed 2-year duration and pursuit until disease progression. Clinical practices may thus differ according to the attending physician.

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Introduction: It is not known whether patients with NSCLC who are hospitalized because of cancer-related complications are liable to benefit from salvage immunotherapy.

Methods: This is a multicenter observational study including five centers, which involve all patients with advanced-stage NSCLC exhibiting a level of programmed death-ligand 1 (PD-L1) greater than or equal to 1%, having been hospitalized because of complications attributed to the evolution of the NSCLC, and having started pembrolizumab treatment during their hospitalization because of a risk of clinical deterioration in the short term. The analysis measured overall survival (OS) and the rate of discharge to home at 3 months.

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Background: Five to 20% of metastatic EGFR-mutated non-small cell lung cancers (NSCLC) develop acquired resistance to EGFR tyrosine kinase inhibitors (EGFR-TKI) through MET amplification. The effects of MET amplification on tumor and patient phenotype remain unknown.

Methods: We investigated,in vitro and in vivo, the impact of MET amplification on the biological properties of the HCC827 cell line, derived from an EGFR-mutated NSCLC.

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Various solid tumors including lung or gastric carcinomas display aberrant activation of the Met receptor which correlates with aggressive phenotypes and poor prognosis. Although downstream signaling of Met is well described, its integration at the transcriptional level is poorly understood. We demonstrate here that in cancer cells harboring met gene amplification, inhibition of Met activity with tyrosine kinase inhibitors or specific siRNA drastically decreased expression of ETV1, ETV4 and ETV5, three transcription factors constituting the PEA3 subgroup of the ETS family, while expression of the other members of the family were less or not affected.

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The concept of cancer stem cell (CSC) was established from models of leukemogenesis explaining tumor repopulation by the clonogenic properties of this specific population of tumoral cells. Among solid tumors, glioblastoma are currently the most documented models. Cancer stem cells reside in specific locations within tumors called niches.

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