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開發雙重阻斷HSP90/HDAC6 之策略以有效破壞免疫抑制性腫瘤微環境

為了解決ap-1220b ptt的問題，作者吳彤芸 這樣論述：

目錄目錄 i圖目錄 iv表目錄 v縮寫表 vi中文摘要 vii英文摘要 viii第一章 前言 1第二章 文獻回顧 4(一) T細胞之作用 4(二) 癌細胞逃脫免疫細胞之攻擊 4(三) 免疫療法於實體腫瘤治療所面臨之挑戰 5(四) 免疫曾敏藥物:HSP90抑制劑 6(五) 免疫增敏藥物:HDAC抑制劑 7第三章 實驗材料與方法 8第一節 實驗材料 8藥品 8抗體 8細胞株 9動物 10第二節 實驗方法 11(1) HDAC活性分析 11(2) HSP90活性測定 11(3) 細胞存活率分析(3-(4,5-Dimethylthiazol-2-

yl)-2,5-diphenyltetrazolium bromide;MTT assay) 11(4) 西方墨點法 (Western blot) 12(5) 流式細胞儀偵測細胞表面PD-L1之表達 12(6) 體內抑制鼠源老鼠大腸癌之生長 13(7) 流式細胞儀分析腫瘤區域免疫細胞浸潤 13(8) 免疫組織染色 14(9) 流式細胞儀分析血液之T細胞族群變化 15(10) 體內試驗-細胞因子TGF-β或IL-2之含量測定 15(11) 體外試驗-細胞因子TGF-β含量測定 16(12) 體內抑制鼠源大腸癌之再復發 16(13) 分離腫瘤細胞進行體外培養 16

(14) 流式細胞儀分析脾臟記憶型T細胞表現量 17(15) 統計分析 17第四章 結果 19評估一系列HSP90/HDAC6雙重抑制劑(compound 4-18)對HDAC和HSP90抑制效果分析 19HSP90/HDAC雙重抑制劑(compound 4-18) 抑制人類大腸癌細胞(HCT116)之增生 19Compound 17 促進大腸癌細胞之α-tubulin 和Histone H3 乙醯化 20Compound 17促進大腸癌之HSP90 客戶蛋白(client protein)降解 20Compound 17降低IFN-γ誘導大腸癌細胞之PD-L1和IDO之表達

21Compound 17在體內有效抑制老鼠大腸癌(CT26)之腫瘤生長 22Compound 17破壞腫瘤微環境，促進毒殺型T細胞浸潤至腫瘤區域 23Compound 17 降低全身性之Treg細胞 23Compound 17 提升記憶型T細胞比例，抑制腫瘤細胞之復發 24Compound 17 併用Anti-PD-1療法增強抗腫瘤之功效 25圖表 26第五章 討論 48參考文獻 50發表論文 61圖目錄Figure 1. 開發HSP90/HDAC6雙重抑制劑之治療策略 27Figure 2. 化合物設計原理 28Figure 3. Compound 17對不同癌細胞株

之抗增生能力 29Figure 4. Compound 17對正常細胞株細胞毒性之影響 30Figure 5. Compound 17對大腸癌細胞中α-微管蛋白和組蛋白H3乙酰化以及多種HSP90客戶蛋白降解之影響 31Figure 6. Compound 17阻斷IFN-γ誘導大腸癌細胞株之PD-L1和IDO表達 32Figure 7. Compound 17在不同癌細胞中阻斷IFN-γ誘導之PD-L1表達 33Figure 8. HSP90/HDAC6衍生物阻斷IFN-γ誘導大腸癌細胞株之PD-L1表達 34Figure 9. Compound 17抑制活體老鼠大腸癌腫瘤之生長

35Figure 10. Compound 17 對老鼠臟器重量之變化 36Figure 11. Compound 17 對老鼠各臟器之組織影響 37Figure 12. Compound 17對白血球以及淋巴球之數量影響 38Figure 13. Compound 17 之血球毒性分析 39Figure 14. Compound 17於免疫健全小鼠體內對鼠源大腸癌(CT26)之腫瘤微環境/免疫細胞之調節能力 40Figure 15. Compound 17對周邊血液之免疫細胞調控 42Figure 16. Compound 17對周邊血液之細胞激素之影響 43Figure

17. Compound 17抑制正常細胞分泌TGF-ß1 44Figure 18. Compound 17抑制腫瘤再度之生長 45Figure 19. Compound 17誘導記憶型T細胞之表現 46Figure 20. Compound 17與PD-1抗體合併治療對體內腫瘤生長之抑制作用 47表目錄Table 1. Compounds 4-18對HDAC異構體之抑制能力、HSP90 抑制活性和抗增殖活性 26

Oral aspirin for preventing colorectal adenoma recurrence: a systematic review and network meta-analysis of randomized controlled trials

為了解決ap-1220b ptt的問題，作者HOANG DINH KHANH 這樣論述：

Objective To evaluate the preventive effect of aspirin on polypoid lesions in the colorectum and recommend the optimal dose for clinical useDesign Systematic review and network meta-analysisData sources A multilingual, comprehensive source of aspirin clinical trials for colorectal adenoma preventio

n updated to December 31st, 2021Study selection Only randomized controlled trial studies, consisting of participants randomly assigned to receive aspirin (high dose or low dose) or placebo, were included.Methods Pairwise meta-analysis, meta-regression, trial sequential analysis, and network meta-ana

lysis were done after all eligible studies inclusion. ROB 2.0 tool was used for assess risk of bias assessments in included studies, and confidence in the results of network meta-analysis was evaluated by using CINeMA approach.Results The network meta-analysis included eight randomized controlled tr

ials (nine reports) – four of aspirin (low dose or high dose) alone (n = 1,820 participants), four of aspirin in combination with one another medication including folic acid (n = 421), resistant starch (n = 342), eicosapentaenoic acid (n = 326) and mesalazine (n = 102), all compared to placebo. For

pairwise meta-analysis, based on data from seven trials aspirin (any dose) substantially reduced the colorectal adenoma recurrence in participants with or without adenoma-related genetic syndromes (risk ratio 0.86, 95% confidence interval: 0.75 to 0.99). Meta-regression indicated that there was no

correlation between aspirin dose and colorectal adenoma recurrence (p-value = 0.58 for linear model, p-value = 0.76 for non-linear model). For network meta-analysis, low-dose aspirin was still more protective than both high-dose aspirin and placebo, with risk ratio and 95% confidence interval being

0.76 (95% confidence interval 0.58 – 0.99), 0.7 (95% confidence interval 0.54 – 0.91), respectively. Synchronously, low-dose aspirin was ranked the best treatment among the network of low-dose, high-dose aspirin, and placebo (P-score = 0.99). Thus, LDA was the optimal treatment relative to HDA and p

lacebo (P-score = 0.99) with moderate certainty of evidence due to some concerns in heterogeneity. But for trial sequential analysis, low-dose aspirin only showed its efficacy over placebo when the number of included participants exceeded the optimal information size, this was not the case for HDA.C

onclusions Low-dose aspirin has statistically significant efficacy in colorectal adenoma prevention, especially for long-term use but its efficacy over high-dose aspirin is uncertain based on available data which needs more trials to confirm.