Publications by authors named "F Braye"

Article Synopsis
  • - The MATCH-R trial aimed to analyze the resistance mechanisms to cancer treatments by studying fresh tumor biopsies from metastatic patients, covering data collected from 2015 to 2022.
  • - Out of 1,120 biopsies from patients primarily with lung, digestive, and prostate cancers, 30.9% revealed targetable genomic alterations, with EGFR being the most common altered gene.
  • - Among patients with resistance mechanisms, 45% had treatments tailored based on identified mechanisms, resulting in an average of 11 months of additional clinical benefit.
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Purpose: Understanding resistance to selective FGFR inhibitors is crucial to improve the clinical outcomes of patients with FGFR2-driven malignancies.

Experimental Design: We analyzed sequential ctDNA, ± whole-exome sequencing, or targeted next-generation sequencing on tissue biopsies from patients with tumors harboring activating FGFR2 alterations progressing on pan-FGFR-selective inhibitors, collected in the prospective UNLOCK program. FGFR2::BICC1 Ba/F3 and patient-derived xenograft models were used for functional studies.

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Article Synopsis
  • A study identified 21 patients with FGFR-driven urothelial cancer who were treated with FGFR inhibitors, revealing that 33% had specific mutations in the FGFR tyrosine kinase domain after treatment progression.
  • The research showed that over half (52%) of patients had alterations in the PI3K-mTOR pathway, which may contribute to resistance against FGFR inhibitors.
  • The findings support combining different treatments, such as erdafitinib with pictilisib or gefitinib, to potentially combat resistance in these cancer cases.
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Background: Mucormycosis is a deadly fungal infection that mainly affects severely immunocompromised patients. We report herein the case of a previously immunocompetent adult woman who developed invasive cutaneous mucormycosis after severe burn injuries. Interferon-gamma (IFN-γ) treatment was added after failure of conventional treatment and confirmation of a sustained profound immunodepression.

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Background: The development of targeted agents, such as osimertinib for EGFR-mutated non-small-cell lung cancer (NSCLC), has drastically improved patient outcome, but tumor resistance eventually always occurs. In osimertinib-resistant NSCLC, the emergence of a second molecular driver alteration (such as ALK, RET, FGFR3 fusions or BRAF, KRAS mutations) has been described. Whether those alterations and the activating EGFR mutations occur within a single cancer cell or in distinct cell populations is largely debated.

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