【佳學(xué)基因靶向藥物基因檢測(cè)】EGFR?VEGF 的雙重抑制：治療具有 EGFR 突變的晚期非小細(xì)胞肺癌的有效方法（綜述）

基因檢測(cè)費(fèi)用熱點(diǎn)

與同行交流時(shí)腫瘤檢測(cè)的時(shí)間和空間對(duì)治療效果的影響知道《Int J Oncol》在?2023 Feb;62(2):26.發(fā)表了一篇題目為《Review》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Qian Wang,?Anqi Zeng,?Min Zhu,?Linjiang Song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。

腫瘤基因檢測(cè)及靶向藥物治療研究關(guān)鍵詞：

表皮生長(zhǎng)因子受體,血管內(nèi)皮生長(zhǎng)因子,聯(lián)合治療,雙重抑制,非小細(xì)胞肺癌,靶向治療。

腫瘤治療檢測(cè)基因臨床應(yīng)用結(jié)果

在全球范圍內(nèi)，肺癌的發(fā)病率和死亡率逐年上升。許多不良習(xí)慣和環(huán)境因素與肺癌有關(guān)，包括吸煙、接觸二手煙、職業(yè)接觸、呼吸系統(tǒng)疾病和遺傳。目前，低劑量螺旋CT常規(guī)是肺癌診斷的先進(jìn)。然而，病理檢查仍然是診斷肺癌的金標(biāo)準(zhǔn)。根據(jù)癌癥的分類和分期，可選擇手術(shù)、放療、化療、靶向治療和免疫治療等治療方案。 EGFR通路的激活可以促進(jìn)腫瘤細(xì)胞的存活和增殖，VEGF通路可以促進(jìn)血管的形成，從而促進(jìn)腫瘤的生長(zhǎng)。在具有 EGFR 突變的非小細(xì)胞肺癌 (NSCLC) 中，EGFR 激活可以通過(guò)缺氧非依賴性機(jī)制促進(jìn) VEGF 上調(diào)，從而促進(jìn)腫瘤生長(zhǎng)。 VEGF的上調(diào)可以使腫瘤細(xì)胞對(duì)EGFR抑制劑產(chǎn)生耐藥性。此外，VEGF信號(hào)的表達(dá)還受到其他因素的影響。因此，使用單一的EGFR抑制劑并不能有效抑制VEGF信號(hào)的表達(dá)。為了克服這個(gè)問(wèn)題，VEGF抑制劑和EGFR抑制劑聯(lián)合應(yīng)用成為了先進(jìn)方法。雙重抑制不僅可以克服腫瘤細(xì)胞對(duì)EGFR抑制劑的耐藥性，還可以顯著延長(zhǎng)NSCLC患者的無(wú)進(jìn)展生存期。本綜述討論了 EGFR 和 VEGF 通路之間的關(guān)聯(lián)，以及 EGFR-VEGF 通路雙重抑制的特征。血管內(nèi)皮生長(zhǎng)因子；聯(lián)合治療；雙重抑制；非小細(xì)胞肺癌；靶向治療。

腫瘤發(fā)生與革命國(guó)際數(shù)據(jù)庫(kù)描述：

On a global scale, the incidence and mortality rates of lung cancer are gradually increasing year by year. A number of bad habits and environmental factors are associated with lung cancer, including smoking, second?hand smoke exposure, occupational exposure, respiratory diseases and genetics. At present, low?dose spiral computed tomography is routinely the first choice in the diagnosis of lung cancer. However, pathological examination is still the gold standard for the diagnosis of lung cancer. Based on the classification and stage of the cancer, treatment options such as surgery, radiotherapy, chemotherapy, targeted therapy and immunotherapy are available. The activation of the EGFR pathway can promote the survival and proliferation of tumor cells, and the VEGF pathway can promote the formation of blood vessels, thereby promoting tumor growth. In non?small cell lung cancer (NSCLC) with EGFR mutation, EGFR activation can promote tumor growth by promoting VEGF upregulation through a hypoxia?independent mechanism. The upregulation of VEGF can make tumor cells resistant to EGFR inhibitors. In addition, the expression of the VEGF signal is also affected by other factors. Therefore, the use of a single EGFR inhibitor cannot completely inhibit the expression of the VEGF signal. In order to overcome this problem, the combination of VEGF inhibitors and EGFR inhibitors has become the method of choice. Dual inhibition can not only overcome the resistance of tumor cells to EGFR inhibitors, but also significantly increase the progression?free survival time of patients with NSCLC. The present review discusses the associations between the EGFR and VEGF pathways, and the characteristics of dual inhibition of the EGFR?VEGF pathway.Keywords:?EGFR; VEGF; combination therapy; dual inhibition; non?small cell lung cancer; targeted therapy.