Stanzione, Marcello; Zhong, Jun; Wong, Edmond; LaSalle, Thomas J.; Wise, Jillian F.; Simoneau, Antoine; Myers, David T.; Phat, Sarah; Sade-Feldman, Moshe; Lawrence, Michael S.; Hadden, M. Kyle; Zou, Lee; Farago, Anna F.; Dyson, Nicholas J.; Drapkin, Benjamin J. published the artcile< Translesion DNA synthesis mediates acquired resistance to olaparib plus temozolomide in small cell lung cancer>, Application of C19H34O2, the main research area is small cell lung cancer olaparib temozolomide deoxyribonucleic acid synthesis.
In small cell lung cancer (SCLC), acquired resistance to DNA-damaging therapy is challenging to study because rebiopsy is rarely performed. We used patient-derived xenograft models, established before therapy and after progression, to dissect acquired resistance to olaparib plus temozolomide (OT), a promising exptl. therapy for relapsed SCLC. These pairs of serial models reveal alterations in both cell cycle kinetics and DNA replication and demonstrate both inter- and intratumoral heterogeneity in mechanisms of resistance. In one model pair, up-regulation of translesion DNA synthesis (TLS) enabled tolerance of OT-induced damage during DNA replication. TLS inhibitors restored sensitivity to OT both in vitro and in vivo, and similar synergistic effects were seen in addnl. SCLC cell lines. This represents the first described mechanism of acquired resistance to DNA damage in a patient with SCLC and highlights the potential of the serial model approach to investigate and overcome resistance to therapy in SCLC.
Science Advances published new progress about Cell cycle (kinetics). 112-63-0 belongs to class esters-buliding-blocks, and the molecular formula is C19H34O2, Application of C19H34O2.
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