【佳學基因檢測】針對人類疾病中 FGF 信號網(wǎng)絡的基因檢測治療

腫瘤基因檢測哪家醫(yī)院最好解析

閱讀腫瘤的正確化治療及靶向藥物選擇發(fā)現(xiàn)《Trends Pharmacol Sci》在. 2016 Dec;37(12):1081-1096.發(fā)表了一篇題目為《針對人類疾病中 FGF 信號網(wǎng)絡的治療》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Masaru Katoh等完成。促進了腫瘤的正確治療與個性化用藥的發(fā)展，進一步強調了基因信息檢測與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究內容關鍵詞：

厄達非替尼,免疫檢查點阻滯劑,英非拉替尼,小RNA,骨髓增生綜合征,FGF

腫瘤靶向治療基因檢測臨床應用結果

成纖維細胞生長因子 (FGF) 通過其受體 FGFR1、FGFR2、FGFR3 或 FGFR4 發(fā)出信號，調節(jié)細胞命運、血管生成、免疫和代謝。失調的 FGF 信號傳導會導致人類疾病，例如乳腺癌、軟骨發(fā)育不良、胃癌、肺癌和 X 連鎖低磷性佝僂病。重組 FGF 是用于組織和/或傷口修復的前 FGF 信號療法，而用于治療心血管疾病、糖尿病和骨關節(jié)炎的 FGF 類似物和基因療法正在開發(fā)中。 FGF 陷阱、抗 FGF/FGFR 單克隆抗體 (mAb) 和小分子 FGFR 抑制劑是正在開發(fā)的用于治療癌癥、軟骨發(fā)育不良和佝僂病的抗 FGF 信號傳導療法。在這里，我將討論靶向 FGFRs、ALK、EGFR 和 FLT3 的正確醫(yī)療的收益風險和成本效益問題。 FGFR 靶向治療應針對癌癥治療進行優(yōu)化，重點關注基因組檢測和反復。厄達非替尼；免疫檢查點阻滯劑；英非拉替尼；小RNA；骨髓增生綜合征..基因解碼基因檢測的研究結果：超過 3700 名患者被納入這項薈萃調查。 A3B 水平升高與 OS 低（合并 HR = 1.30；95% CI：1.09-1.55，P < 0.01）、DFS 差（合并 HR = 1.66；95% CI：1.17-2.35，P < 0.01）和RFS 差（HR = 1.51, 95% CI:1.11-2.04, P = 0.01）。亞組分析顯示，高 A3B 表達與肺（HR = 1.85，95% CI：1.40-2.45）和乳腺癌（HR = 1.38，95% CI：1.00-1.89）的較差 OS 相關。 A3B的高表達與臨床病理特征沒有顯著相關性?；蚪獯a基因檢測的研究結論：APOBEC3B過表達僅在某些癌癥類型中與較差的OS、DFS和RFS有關，不能預測所有癌癥的普遍作用。

腫瘤發(fā)生與反復轉移國際數(shù)據(jù)庫描述：

Fibroblast growth factor (FGF) signaling through its receptors, FGFR1, FGFR2, FGFR3, or FGFR4, regulates cell fate, angiogenesis, immunity, and metabolism. Dysregulated FGF signaling causes human diseases, such as breast cancer, chondrodysplasia, gastric cancer, lung cancer, and X-linked hypophosphatemic rickets. Recombinant FGFs are pro-FGF signaling therapeutics for tissue and/or wound repair, whereas FGF analogs and gene therapy are under development for the treatment of cardiovascular disease, diabetes, and osteoarthritis. FGF traps, anti-FGF/FGFR monoclonal antibodies (mAbs), and small-molecule FGFR inhibitors are anti-FGF signaling therapeutics under development for the treatment of cancer, chondrodysplasia, and rickets. Here, I discuss the benefit-risk and cost-effectiveness issues of precision medicine targeting FGFRs, ALK, EGFR, and FLT3. FGFR-targeted therapy should be optimized for cancer treatment, focusing on genomic tests and recurrence.Keywords: epithelial-to-mesenchymal transition; erdafitinib; immune-checkpoint blocker; infigratinib; miRNA; myeloproliferative syndrome..Results: Over 3700 patients were included in this meta-survey. Elevated levels of A3B were significantly related to low OS (pooled HR = 1.30; 95% CI:1.09-1.55, P < 0.01), poor DFS (pooled HR = 1.66; 95% CI:1.17-2.35, P < 0.01) and poor RFS (HR = 1.51, 95% CI:1.11-2.04, P = 0.01). Subgroup analysis revealed that high A3B expression was associated with poor OS in lung (HR = 1.85, 95% CI: 1.40-2.45), and breast cancers (HR = 1.38, 95% CI: 1.00-1.89). High expression of A3B did not display any significant association with clinicopathologic features.Conclusion: APOBEC3B overexpression is related to poor OS, DFS and RFS only in some cancer types and no generalized role could be predicted for all cancers.

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