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The pituitary tumor-transforming gene 1 (PTTG1), also known as Securin, is considered an oncogene. This study aimed to investigate the role of PTTG1 in clear cell renal cell carcinoma (ccRCC) using in silico bioinformatics approaches. A pan-cancer analysis using The Cancer Genome Atlas (TCGA) data indicated that among all cancer types copy number amplification of PTTG1 gene was most frequently found in ccRCC. However, amplification of PTTG1 gene copy number did not correlate with the increase of mRNA level in ccRCC, and did not predict the patients' overall survival. Instead, ccRCC was correlated with overexpression of PTTG1 mRNA, and its expression level was stage-dependent increased in cancer patients. An outlier analysis using the Oncomine database suggested that PTTG1 mRNA expression served as a good biomarker for ccRCC. Pathway analysis for upregulated genes enriched in PTTG1-high expressing ccRCC patients found that PTTG1 overexpression was associated with mitotic defects. Mining drug sensitivity data using the Cancer Therapeutics Response Portal (CTRP) discovered that PTTG1-high expressing ccRCC cell lines were susceptible to a Rac1 (Ras-related C3 botulinum toxin substrate 1) inhibitor NSC23766. Therefore, this study provides an in silico insight into the role of PTTG1 in ccRCC, and repurposes the Rac1 inhibitor NSC23766 for treating PTTG1-high expressing ccRCC. 相似文献
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Meredith McKean Junna Oba Junsheng Ma Katherine G Roth Wei-Lien Wang Mariana P. Macedo Fernando C.L. Carapeto Lauren E. Haydu Alan E. Siroy Phuong Vo David S. Hong Agda K. Eterovic Keyur Pravinchandra Patel Roland L Bassett Elizabeth A. Grimm Alexander J. Lazar Scott E. Woodman 《The Journal of investigative dermatology》2019,139(3):728-731
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《Journal of thoracic oncology》2019,14(11):1901-1911
IntroductionDespite initial effectiveness of ALK receptor tyrosine kinase inhibitors (TKIs) in patients with ALK+ NSCLC, therapeutic resistance will ultimately develop. Serial tracking of genetic alterations detected in circulating tumor DNA (ctDNA) can be an informative strategy to identify response and resistance. This study evaluated the utility of analyzing ctDNA as a function of response to ensartinib, a potent second-generation ALK TKI.MethodsPre-treatment plasma was collected from 76 patients with ALK+ NSCLC who were ALK TKI–naive or had received prior ALK TKI, and analyzed for specific genetic alterations. Longitudinal plasma samples were analyzed from a subset (n = 11) of patients. Analysis of pre-treatment tumor biopsy specimens from 22 patients was compared with plasma.ResultsDisease-associated genetic alterations were detected in 74% (56 of 76) of patients, the most common being EML4-ALK. Concordance of ALK fusion between plasma and tissue was 91% (20 of 22 blood and tissue samples). Twenty-four ALK kinase domain mutations were detected in 15 patients, all had previously received an ALK TKI; G1269A was the most prevalent (4 of 24). Patients with a detectable EML4-ALK variant 1 (V1) fusion had improved response (9 of 17 patients; 53%) to ensartinib compared to patients with EML4-ALK V3 fusion (one of seven patients; 14%). Serial changes in ALK alterations were observed during therapy.ConclusionsClinical utility of ctDNA was shown, both at pre-treatment by identifying a potential subgroup of ALK+ NSCLC patients who may derive more benefit from ensartinib and longitudinally by tracking resistance. Prospective application of this technology may translate to improved outcomes for NSCLC patients treated with ALK TKIs. 相似文献
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《Journal of microbiology, immunology, and infection》2020,53(6):1030-1034
X-linked agammaglobulinemia (XLA) is a primary immunodeficiency disease. We reported two 7-month-old identical male twins with Pseudomonas aeruginosa sepsis who initially manifested as oral ecthyma gangrenosum and were finally diagnosed to have XLA. In both cases, we confirmed the c.862C > T BTK missense mutation in exon 10 at the SH2 domain. 相似文献
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Elena V. Preobrazhenskaya Aglaya G. Iyevleva Amina M. Suleymanova Vladislav I. Tiurin Natalia V. Mitiushkina Ilya V. Bizin Alexandr O. Ivanstov Olga A. Gorustovich Kseniya V. Shelekhova Denis Y. Kachanov Svetlana R. Varfolomeeva Vitaliy Y. Roschin Anna N. Kazakova Dmitriy V. Litvinov Tatiana V. Shamanskaya Nikita A. Savelov Evgeny N. Suspitsin Evgeny N. Imyanitov 《Pediatric blood & cancer》2020,67(5)
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