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Background: To evaluate the cost-effectiveness of first-line sintilimab plus chemotherapy versus chemotherapy for advanced esophageal squamous cell carcinoma (ESCC) from the perspective of the Chinese health service system., Methods: A partitioned survival model was constructed to simulate quality-adjusted life years and incremental cost-effectiveness ratios over a patient's lifetime based on a phase III clinical trial., Results: Sintilimab plus chemotherapy increased by 0.316 QALY and 0.285 QALY with the additional cost of $5692 and $5269, which led to the ICER of $18000/QALY and $18519/QALY gained in the overall population and the patients with CPS ≥ 10, respectively., Conclusions: Compared with chemotherapy alone, sintilimab may be a cost-effective first-line treatment choice for locally advanced or metastatic ESCC.

Current research has shown that inhibiting deoxythymidylate kinase (DTYMK) can significantly reduce development of lung cancer without liver kinase B1. However, its underlying regulatory mechanism is still unclear. We therefore aimed to investigate whether DTYMK inhibitors could suppress lung adenocarcinoma (LUAD) progression. In this study, human tissues, A549 cells, and xenograft tumors were used to explore the regulation and mechanism of DTYMK on LUAD cell proliferation and migration. Meanwhile, YMU1 (a DTYMK inhibitor) was applied to A549 cells and xenograft tumors to investigate its potential as a drug for LUAD. DTYMK was overexpressed in LUAD tissues and correlated with tumor stage. Knockdown of DTYMK suppressed cell viability, migration, and invasion. In addition, the activation of signal transducers and activators of transcription 3 (STAT3) was repressed upon DTYMK inhibition. YMU1 showed the same effect as DTYMK knockdown in vivo and in vitro. DTYMK plays an important role in progression of LUAD through the STAT3 signaling pathway. YMU1 may have the potential to inhibit the development of LUAD. NEW & NOTEWORTHY DTYMK plays an important role in progression of LUAD through the STAT3 signaling pathway. YMU1 may serve as a novel drug to suppress the development of LUAD.