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https://www.selleckchem.com/products/pexidartinib-plx3397.html 7 vs. 7.5 months, hazard ratio = 0.33, 95% confidence interval, 0.17-0.63). Higher levels of post-induction mAF and post-induction mean mutant molecules per milliliter (mMMPM), and changes in ctDNA (stratified by a 10-fold or 100-fold reduction in mAF between pre- and post-induction plasma), were associated with shorter PFS. Post-induction mAF and mMMPM generally correlated with each other (r = 0.987, P less then 0.0001). CONCLUSIONS ctDNA quantification in post-induction plasma may serve as a prognostic biomarker for mCRC post-treatment outcomes. Copyright ©2020, American Association for Cancer Research.PURPOSE Esophageal cancer (ESCA) is a deadly malignancy with a 5-year survival rate of only 5-20%, which has remained unchanged for decades. ESCA possesses a high frequency of TP53 mutations leading to dysfunctional G1 cell cycle checkpoint, which likely makes ESCA cells highly reliant upon G2/M checkpoint for adaptation to DNA replication stress and DNA damage after radiation. We aim to explore whether targeting Wee1 kinase to abolish G2/M checkpoint sensitizes ESCA cells to radiotherapy. EXPERIMENTAL DESIGN Cell viability was assessed by cytotoxicity and colony forming assays, cell cycle distribution was analyzed by flow cytometry, and mitotic catastrophe was assessed by immunofluorescence staining. Human ESCA xenografts were generated to explore the radiosensitizing effect of AZD1775 in vivo ResultsThe IC50 concentrations of AZD1775 on ESCA cell lines were between 300 - 600 nM. AZD1775 (100 nM) as monotherapy did not alter the viability of ESCA cells, but significantly radiosensitized ESCA cells. AZD1775 significantly abrogated radiation-induced G2/M phase arrest and attenuation of p-CDK1-Y15. Moreover, AZD1775 increased radiation-induced mitotic catastrophe, which was accompanied by increased gH2AX levels, and subsequently reduced survival after radiation. Importantly, AZD1775 in combination with rad

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