osimertinib and Triple-Negative-Breast-Neoplasms

Monotherapy with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) still leads to incomplete responses in most EGFR-mutation positive non-small cell lung cancer (NSCLC) patients, often due to acquired resistance through activation of parallel compensatory pathways. We have previously shown that co-targeting EGFR, signal transducer and activator of transcription 3 (STAT3), and Src-yes-associated protein 1 (YAP1) was highly synergistic in vitro and in vivo. In the present study, we treated EGFR-mutation positive cell lines with the combination of osimertinib plus a natural compound, pterostilbene, which has been reported to abrogate Src and STAT3 activation.

Topics: Acrylamides; Adaptor Proteins, Signal Transducing; Aniline Compounds; Antigens, Neoplasm; Antineoplastic Agents; Carcinoma, Non-Small-Cell Lung; Cell Adhesion Molecules; Cell Line, Tumor; Drug Resistance, Neoplasm; Drug Synergism; ErbB Receptors; Humans; Phosphorylation; STAT3 Transcription Factor; Stilbenes; Transcription Factors; Triple Negative Breast Neoplasms; YAP-Signaling Proteins