PD-1抑制劑與PD-L1抑制劑有何不同? 相信是許多人的疑問 希望這篇能對您有些幫助
建議您先讀 腫瘤是如何抑制抗癌免疫反應的 和 什麼是CTLA4 ? 什麼是PD1? 會比較能夠理解這篇的內容
PD-1抑制劑與PD-L1抑制劑有何不同? 相信是許多人的疑問 希望這篇能對您有些幫助
建議您先讀 腫瘤是如何抑制抗癌免疫反應的 和 什麼是CTLA4 ? 什麼是PD1? 會比較能夠理解這篇的內容
Multiple randomized studies have demonstrated improved response rates, progression-free survival, and quality of life for treatment-naive, advanced-stage adenocarcinoma patients harboring sensitizing EGFR mutations when they are treated with tyrosine kinase inhibitor therapy, as compared with chemotherapy. Despite improved outcomes with these agents, the majority of patients will eventually develop resistance and subsequent clinical progression. Recently, there has been a firmer understanding of the molecular mechanisms of the resistance that develops as a consequence of treatment, most notably the identification of a second-site EGFR mutation, T790M. While this understanding can inform subsequent treatment decisions, disease progression can be heterogeneous, and there are several competing therapeutic options. Treatment decisions must consider this clinical heterogeneity, factoring in the pace of disease growth, lung cancer–related symptoms, and the potential presence of T790M mutations. Herein, we review the available literature addressing these competing strategies and attempt to clarify best treatment practices, including the emerging role of T790M-directed therapies.
During the last few decades, significant efforts of the interaction between immune system and immunotherapy to NSCLC have been acquired. Recent data have indicated that the lack of immunologic control is recognized as a hallmark of cancer currently. Programmed death-1 (PD-1) and its ligand PD-L1 play a key role in tumor immune escape and the formation of tumor microenvironment, closely related with tumor generation and development. Blockading the PD-1/PD-L1 pathway could reverse the tumor microenvironment and enhance the endogenous antitumor immune responses.
重點節錄
Atezolizumab NSCLC第三期臨床實驗收ALK EGFR標靶化療失效的病人
全球共1225名病人 細節將在近期公布