Publications by authors named "M Beau-Faller"
Background: BRAF V600E mutations occur in 2-5 % of advanced non-small cell lung cancer (NSCLC) patients. The dabrafenib-trametinib (D-T) combination was associated with improved and durable OS in patients in phase II. This study (IFCT-2004 BLaDE study) reported the efficacy of D-T combination in a large retrospective French real-world multicenter cohort of patients with advanced BRAF V600E-mutated NSCLC.
View Article and Find Full Text PDFBackground: Factors to accurately stratify patients with early-stage non-small cell lung cancer (NSCLC) in different prognostic groups are still needed. This study aims to investigate 1) the prognostic potential of circulating cell-free (CF) and extracellular vesicles (EVs)-derived microRNA (miRNAs), and 2) their added value with respect to known prognostic factors (PFs).
Methods: The RESTING study is a multicentre prospective observational cohort study on resected stage IA-IIIA patients with NSCLC.
Article Synopsis
- Radiation therapy and platinum-based chemotherapy are standard treatments for lung cancer, but low survival rates are influenced by factors like the patient's health and tumor complexity.
- Current treatments often fail due to tumor resistance, highlighting the need for precision medicine to enhance patient survival and quality of life.
- A new patient-derived tumoroid model shows promise in predicting the effectiveness of radiation therapy and cisplatin-based chemotherapy in non-small-cell lung cancer, correlating with actual patient outcomes.
The therapeutic algorithm of lung cancer has recently been revolutionized by the emergence of immune checkpoint inhibitors. However, an objective and durable response rate remains low with those recent therapies and some patients even experience severe adverse events. Prognostic and predictive biomarkers are therefore needed in order to select patients who will respond.
View Article and Find Full Text PDFKRAS is the most frequently mutated oncogene in non-small cell lung cancers (NSCLC), with a frequency of around 30%, and encoding a GTPAse that cycles between active form (GTP-bound) to inactive form (GDP-bound). The mutations favor the active form with inhibition of GTPAse activity. mutations are often with poor response of EGFR targeted therapies.
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