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Cinnamomum zelanicum is one of the popular medicinal plants. The plant has many pharmaceutical uses in traditional medicine. In this study, copper nanoparticles were synthesized using the aqueous extract of Cinnamomum zelanicum. The CuNPs were characterized using different techniques such as EDX, FE-SEM, XRD, and FT-IR. The FE-SEM results confirm spherical morphology for the nanoparticles with size of 19.55 to 69.70 nm. For investigating the antioxidant property of CuNPs, the DPPH test was used in the presence of butylated hydroxytoluene as the positive control. To survey the cytotoxicity and anti-human lung carcinoma effects of CuNPs, MTT assay was used on the NCI-H2126, NCI-H1437, NCI-H1573, and NCI-H661 cell lines. DPPH test revealed similar antioxidant potentials for Cinnamomum zelanicum aqueous extract, CuNPs, and butylated hydroxytoluene. Copper nanoparticles had very low cell viability and anti-lung carcinoma properties dose-dependently against NCI-H2126, NCI-H1437, NCI-H1573, and NCI-H66 cell lines without any cytotoxicity on the normal cell line. The best result of anti-lung carcinoma properties of CuNPs against the above cell lines was seen in the case of the NCI-H2126 cell line. According to the above findings, the copper nanoparticles containing Cinnamomum zelanicum can be administrated in humans for the treatment of several types of lung carcinoma. [ABSTRACT FROM AUTHOR]

Background: Anaplastic lymphoma kinase (ALK) is a validated molecular target in non-small-cell lung cancer (NSCLC). However, the clinical benefits of ALK inhibitors are almost universally limited by the emergence of drug resistance. Methods: We monitored the plasma circulating tumor DNA (ctDNA) using captured-based ultra-deep sequencing analysis of one patient with metastatic ALK-positive NSCLC who had received therapies including first-, second- and third-generation ALK inhibitors. Functional in vitro studies were further undertaken to elucidate the mechanism of resistance. Results: ALK T1151Sins mutation was detected when the patient developed resistance to ceritinib, and undetectable when she responded to lorlatinib. MET amplification was present when the tumor developed resistance to lorlatinib, and reduced when the patient received combination therapy of lorlatinib with crizotinib, which corresponded to clinical radiologic responses. In addition, further functional in vitro studies demonstrated that ALK harboring the T1151Sins mutation, while conferring resistance to ceritinib, was inhibited by lorlatinib. Conclusions: Clinical evidence and in vitro validation revealed the clinical usefulness of captured-base ultra-deep sequencing on longitudinal plasma ctDNA in revealing the underlying resistance mechanism and guiding the precise administration of ALK inhibitors in patients with advanced ALK-positive NSCLC. [ABSTRACT FROM AUTHOR]