An immunogenomic exome landscape of triple positive primary antiphospholipid patients.

Primary antiphospholipid syndrome is characterized by thrombosis and autoantibodies directed against phospholipids or associated proteins. The genetic etiology of PAPS remains unknown. We enrolled 21 patients with thromboembolic events associated to lupus anticoagulant, anticardiolipin and anti β2 glycoprotein1 autoantibodies.

Direct Targeting Mutation in Non-Small Cell Lung Cancer: Focus on Resistance.

KRAS 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.

Molecular Mechanism of EGFR-TKI Resistance in -Mutated Non-Small Cell Lung Cancer: Application to Biological Diagnostic and Monitoring.

Non-small cell lung cancer (NSCLC) is the most common cancer in the world. Activating epidermal growth factor receptor () gene mutations are a positive predictive factor for EGFR tyrosine kinase inhibitors (TKIs). For common mutations (Del19, L858R), the standard first-line treatment is actually third-generation TKI, osimertinib.

KRAS-specific Amino Acid Substitutions are Associated With Different Responses to Chemotherapy in Advanced Non-small-cell Lung Cancer.

Background: Emerging data highlight different clinical behaviors according to KRAS amino acid substitutions (AASs) in patients with non-small-cell lung cancer (NSCLC). We aimed to evaluate whether different KRAS AASs were associated with different responses to chemotherapy.

Patients And Methods: We retrospectively reviewed data from 1190 patients with KRAS mutations who underwent first-line platinum-based chemotherapy for stage IV NSCLC.