【佳學(xué)基因檢測(cè)】針對(duì)人類疾病中 FGF 信號(hào)網(wǎng)絡(luò)的基因檢測(cè)治療

腫瘤基因檢測(cè)哪家醫(yī)院賊好解析

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(duì)人類疾病中 FGF 信號(hào)網(wǎng)絡(luò)的治療》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Masaru Katoh等完成。促進(jìn)了腫瘤的正確治療與個(gè)性化用藥的發(fā)展，進(jìn)一步強(qiáng)調(diào)了基因信息檢測(cè)與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究?jī)?nèi)容關(guān)鍵詞：

厄達(dá)非替尼,免疫檢查點(diǎn)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(cè)臨床應(yīng)用結(jié)果

成纖維細(xì)胞生長(zhǎng)因子 (FGF) 通過(guò)其受體 FGFR1、FGFR2、FGFR3 或 FGFR4 發(fā)出信號(hào)，調(diào)節(jié)細(xì)胞命運(yùn)、血管生成、免疫和代謝。失調(diào)的 FGF 信號(hào)傳導(dǎo)會(huì)導(dǎo)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(fù)的前 FGF 信號(hào)療法，而用于治療心血管疾病、糖尿病和骨關(guān)節(jié)炎的 FGF 類似物和基因療法正在開(kāi)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(kāi)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(hào)傳導(dǎo)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(fēng)險(xiǎn)和成本效益問(wèn)題。 FGFR 靶向治療應(yīng)針對(duì)癌癥治療進(jìn)行優(yōu)化，重點(diǎn)關(guān)注基因組檢測(cè)和反復(fù)。厄達(dá)非替尼；免疫檢查點(diǎn)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(cè)的研究結(jié)果：超過(guò) 3700 名患者被納入這項(xiàng)薈萃調(diào)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(dá)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(guān)。 A3B的高表達(dá)與臨床病理特征沒(méi)有顯著相關(guān)性?；蚪獯a基因檢測(cè)的研究結(jié)論：APOBEC3B過(guò)表達(dá)僅在某些癌癥類型中與較差的OS、DFS和RFS有關(guān)，不能預(yù)測(cè)所有癌癥的普遍作用。

腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國(guó)際數(shù)據(jù)庫(kù)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.