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机译:通过激活PI3K / AKT信号通路,MA 11.07透射微大稻草在NSCLC中促进EGFR-TKIS抗性
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Lung Cancer and Immunity Laboratory Shanghai Pulmonary Hospital Tongji University;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Lung Cancer and Immunity Laboratory Shanghai Pulmonary Hospital Tongji University;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
Shanghai Pulmonary Hospital Tongji University School of Medicine;
Department of Medical Oncology Shanghai Pulmonary Hospital Tongji University School of Medicine;
机译:通过激活PI3K / AKT信号通路,MA 11.07透射微大稻草在NSCLC中促进EGFR-TKIS抗性
机译:MicroRNA-191-5p通过靶向EGR1和激活PI3K / AKT信号通路来促进骨肉瘤的发展
机译:外来通过激活PI3K / AKT信号通路在EGFR-突变体NSCLC中传递T790M突变抗性
机译:PI3K途径在抗IgM(抗IgM(抗-Ig)的作用 - 最终和 - 抗生素B细胞淋巴瘤未脱离PI3K途径信号传导对CH12 B细胞淋巴瘤的I-FI阻力
机译:通过激活PI3K / PDK / Akt信号转导途径,MCF-7乳腺癌细胞对抗癌药物的敏感性降低。
机译:外泌体通过激活PI3K / AKT信号通路在EGFR突变型NSCLC中传递T790M突变诱导的耐药性
机译:通过激活PI3K / AKT信号通路,MA 11.07透射微大稻草在NSCLC中促进EGFR-TKIS抗性