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https://www.selleckchem.com/products/4u8c.html The first two highest frequent mutation of genes were the same, but some of mutated genes were inclined to be observed in ctDNA, like AR. And two cases who received personalized therapy achieved better clinical benefit. Conclusion Blood-source ctDNA sequencing could be regarded as a meaningful complement to tissue testing, and might guide clinically therapeutic regimen.Background CDK12 is a potential therapeutic target in papillary thyroid cancer that regulates the c-myc/β-catenin pathway. Objective We aimed to explore the specific mechanism of CDK12 in papillary thyroid cancer and provide a new target of cancer therapy. Methods RT-qPCR was used to determine the CDK12 mRNA expression level. An IHC assay was performed to detect the tissue expression of CDK12. Then, we downregulated CDK12 expression in the thyroid cancer cell lines TPC-1-shCDK12 and KAT-5-shCDK12. CCK8 assays, colony formation assays, and animal xenograft models were used to evaluate the effect of CDK12 on tumorigenesis. Transwell assays and in vivo metastasis models were used to observe whether CDK12 can promote cancer metastasis. Western blotting further confirmed the mechanism of CDK12 in papillary thyroid cancer through the c-myc/β-catenin pathway. Results Upregulated CDK12 expression in papillary thyroid cancer promoted papillary thyroid cancer carcinogenesis in vivo, and in vitro CDK12 strengthened papillary thyroid cancer (PTC) cell migration and tumor metastasis. CDK12 promoted tumor progression by regulating c-myc/β-catenin pathway activation. Conclusions CDK12 affects the c-myc/β-catenin pathway to stimulate papillary thyroid cancer proliferation and metastasis. Inhibiting CDK12 might be a new method in papillary thyroid cancer therapy.Gliomas have been classified into different molecular subtypes based on their molecular features. To explore the prognostic factors of different subtypes of gliomas, we performed a univariate survival analysis bas

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