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Zhang Z Lee JC Lin L Olivas V Au V LaFramboise T Abdel-Rahman M Wang X Levine AD Rho JK Choi YJ Choi CM Kim SW Jang SJ Park YS Kim WS Lee DH Lee JS Miller VA Arcila M Ladanyi M Moonsamy P Sawyers C Boggon TJ Ma PC Costa C Taron M Rosell R Halmos B Bivona TG 《Nature genetics》2012,44(8):852-860
Human non-small cell lung cancers (NSCLCs) with activating mutations in EGFR frequently respond to treatment with EGFR-targeted tyrosine kinase inhibitors (TKIs), such as erlotinib, but responses are not durable, as tumors acquire resistance. Secondary mutations in EGFR (such as T790M) or upregulation of the MET kinase are found in over 50% of resistant tumors. Here, we report increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation. Genetic or pharmacological inhibition of AXL restored sensitivity to erlotinib in these tumor models. Increased expression of AXL and, in some cases, of its ligand GAS6 was found in EGFR-mutant lung cancers obtained from individuals with acquired resistance to TKIs. These data identify AXL as a promising therapeutic target whose inhibition could prevent or overcome acquired resistance to EGFR TKIs in individuals with EGFR-mutant lung cancer. 相似文献
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M. Alavaikko A. Rinne M. Järvinen V. K. Hopsu-Havu P. R. Meyer A. M. Levine R. J. Lukes 《Cellular and molecular life sciences : CMLS》1985,41(9):1173-1175
Summary One of two cases of acquired immune deficiency syndrome-related persistent generalized lymphadenopathy revealed a profoundly altered pattern of dendritic reticulum cells as demonstrated by immunoreactive acid cysteine proteinase inhibitor. The alterations could be related to totally or partially destructed lymphoid secondary follicles.Acknowledgments. This work has been partially supported by the grant from the Sigrid Juselius Foundation, Finland. 相似文献
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The p53 tumour suppressor gene 总被引:266,自引:0,他引:266
The cell cycle is composed of a series of steps which can be negatively or positively regulated by various factors. Chief among the negative regulators is the p53 protein. Alteration or inactivation of p53 by mutation, or by its interactions with oncogene products of DNA tumour viruses, can lead to cancer. These mutations seem to be the most common genetic change in human cancers. 相似文献
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Growth regulatory effects of cellular interaction 总被引:8,自引:0,他引:8
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Adjuvant principle of pertussis vaccine in the mouse 总被引:7,自引:0,他引:7
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Intestinal absorption of pralidoxime and other aldoximes 总被引:1,自引:0,他引:1
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R. Pieroni Amina E. Bundeally L. Levine 《Cellular and molecular life sciences : CMLS》1971,27(3):332-333
Résumé Un constituant deBordetella pertussis, et la drogue antagoniste, le propranolol-adrénergique, peuvent causer un renforcement semblable similaire de la sensibilité des souris à l'anémie hémolytique immune expérimentale. Il est connu que l'insuline se comporte de la même façon.
This work was supported in part by Public Health Service Research Grant No. CC00223 from the National Communicable Disease Center through the Massachusetts Health Research Institute. 相似文献
This work was supported in part by Public Health Service Research Grant No. CC00223 from the National Communicable Disease Center through the Massachusetts Health Research Institute. 相似文献