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

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Anti PD1藥品 對多數人而言 附作用比化療輕許多
Anti PD1藥品雖然毒性低 但是卻有可能會造成嚴重問題 威脅生命甚至導致死亡

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癌症擴散與腫瘤能夠抑制抗癌免疫反應息息相關
一旦腫瘤能抑制抗癌免疫反應從此身體裡再也沒有可以阻止它擴散的力量

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FDA核准上市全球首支anti PDL1藥品Tecentriq (atezolizumab)治療4期肺腺癌

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毒殺型T細胞 是抗病毒與癌症的主力
T細胞被激活的過程上面有談到

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DC Dendritic cells 是人體主要的抗原承現細胞
DC 吞噬病原體 將消化後的病原體碎片(抗原)承現於細胞膜表面

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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.
https://www.cancernetwork.com/oncology-journal/attacking-moving-target-understanding-resistance-and-managing-progression-egfr-positive-lung-cancer/page/0/1

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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

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鄭醫師的部落格
https://delightdetox1268.pixnet.net/blog/post/280267793-%E8%A6%8F%E5%BE%8B%E9%81%8B%E5%8B%95%E5%8F%AF%E4%BB%A5%E5%B9%AB%E5%8A%A9%E9%9B%8C%E6%BF%80%E7%B4%A0%E5%81%A5%E5%BA%B7%E4%BB%A3%E8%AC%9D%EF%BC%8C%E9%99%8D%E4%BD%8E%E4%B9%B3%E7%99%8C

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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
https://www.roche.com/media/store/releases/med-cor-2016-09-01.htm
Atezolizumab NSCLC第三期臨床實驗顯示

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羅氏藥廠公佈PDL1抑制劑atezolizumab與奈米太平洋紫杉醇併用治療三陰性乳癌數據
約三分之二的病人有反應 無論腫瘤是否有PD-L1表象

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文 / 胡涵婷醫師 (血液與腫瘤內科)
筆者在美國重新接受住院醫師訓練時,親眼見證了癌症如何以野火燎原的攻勢,掠奪免疫機制被壓抑的病人的生命。我的訓練醫院內科副主任十多年前診斷早期大腸癌,開刀治癒了。後來,他因為一種罕見的膽道疾病造成肝衰竭,接受肝臟移植。雖然移植成功,他沉寂了超過十年的大腸癌,卻因為預防肝移植排斥所必須服用的免疫抑制劑,來勢洶洶地復發了。大腸癌細胞侵佔他的肺、骨頭以及甫移植的肝臟;短短三個月內,他就離開人世。這個活生生的例子告訴我們,人體有高度有效的控制癌細胞的免疫機制。當免疫機制崩潰或削弱時,癌症往往就一發不可收拾。
類似的故事實例與科學證據,比比皆是,一再說明了癌症與免疫機制的重要相關性。

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