Osimertinib for an Advanced NSCLC Patient with Two Common EGFR Mutations and a Concomitant MET Exon 14 Skipping Mutation: A Case Report.

Background: Lung cancer remains the leading cause of cancer-related mortality. Studies have revealed that a combination of crizotinib and EGFR tyrosine kinase inhibitors (TKIs) could be an effective treatment option for patients with sensitizing EGFR mutations and de novo or acquired MET amplification. Until now, there have been few reports of the response in patients harboring three mutations.

Thyroid hormones as biomarkers of lung cancer: a retrospective study.

Background: Thyroid hormones are key regulators of several physiological processes, including differentiation, embryonic development, proliferation, and metabolism. Several prospective studies have shown a relationship between hyperthyroidism and cancer incidence; however, since the association between thyroid hormone levels and lung cancer remains controversial, this study aimed to determine the correlation between the same.

Methods: We retrospectively analyzed 289 patients, who were diagnosed with lung cancer at the Huzhou Central Hospital between January 2016 and January 2021, and 238 healthy subjects.

Case Report: Heterogeneity of Resistance Mechanisms in Different Lesions Co-Mediate Acquired Resistance to First-Line Icotinib in EGFR Mutant Non-Small Cell Lung Cancer.

Epidermal growth factor receptor (EGFR)-activating mutations are major oncogenic mechanisms in non-small cell lung cancer (NSCLC). Most patients with NSCLC with EGFR mutations benefit from targeted therapy with EGFR- tyrosine kinase inhibitors (TKIs). One of the main limitations of targeted therapy is that the tumor response is not durable, with the inevitable development of drug resistance.

Lipopolysaccharide-induced CCN1 production enhances interleukin-6 secretion in bronchial epithelial cells.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a clinical complication caused by primary or secondary lung injury, as well as by systemic inflammation. Researches regarding molecular pathophysiology of ALI/ARDS are immerging with an ultimate aim towards developing prognostic molecular biomarkers and molecule-based therapy. However, the molecular mechanisms concerning ALI/ARDS are still not completely understood.

STAT1 modification improves therapeutic effects of interferons on lung cancer cells.

Background: Interferons (IFNs) have potent anti-proliferative, pro-apoptotic, and immunomodulatory activities against cancer. However, the clinical utility of IFNs is limited by toxicity and pharmacokinetics making it difficult to achieve sustained therapeutic levels especially in solid tumors.

Methods: Signal Transducer and Activator of Transcription 1 (STAT1) or a modified STAT1 (designated STAT1-CC) that is hyper-responsive to IFN were overexpressed in lung cancer SPC-A-1 and H1299 cells using lentiviral vectors.