【佳學(xué)基因靶向藥物基因檢測(cè)】BRAF V600E 突變對(duì)神經(jīng)膠質(zhì)瘤的影響：分子因素、預(yù)后價(jià)值和治療進(jìn)展

基因腫瘤檢測(cè)哪家醫(yī)院賊好解析

閱讀的藥物化治療及藥物選擇發(fā)現(xiàn)《Front Oncol》在 2023 Jan 4;12:1067252.發(fā)表了一篇題目為《Glioblastoma: Emerging Treatments and Novel Trial Designs》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Vincenzo Di Nunno, Lidia Gatto, Alicia Tosoni, Stefania Bartolini, Enrico Franceschi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：

布拉夫, MAPK-甲乙酮,達(dá)拉非尼,恩科非尼,膠質(zhì)母細(xì)胞瘤;膠質(zhì)瘤;曲美替尼,維羅非尼。

腫瘤治療檢測(cè)基因臨床應(yīng)用結(jié)果

神經(jīng)膠質(zhì)瘤是分子異質(zhì)性腦腫瘤，是任何癌癥導(dǎo)致生命損失賊多年的原因。高級(jí)別膠質(zhì)瘤預(yù)后較差，盡管采用包括手術(shù)、放療和化療在內(nèi)的多模式治療，但仍表現(xiàn)出高反復(fù)率。需要基于生物標(biāo)志物評(píng)估和 BRAF 的正確醫(yī)學(xué)的新治療方法，BRAF 是 MAPK 信號(hào)通路的關(guān)鍵調(diào)節(jié)因子，影響細(xì)胞分化、增殖、遷移和促腫瘤發(fā)生活性，正在成為一個(gè)有前途的分子靶點(diǎn)。 V600E 是膠質(zhì)瘤中賊常見的 BRAF 改變，尤其是在兒童低級(jí)別星形細(xì)胞瘤、多形性黃色星形細(xì)胞瘤、乳頭狀顱咽管瘤、上皮樣膠質(zhì)母細(xì)胞瘤和神經(jīng)節(jié)膠質(zhì)瘤中。 BRAF 靶向治療在神經(jīng)膠質(zhì)瘤中的可能應(yīng)用正在不斷增長(zhǎng)，并且有初步證據(jù)表明 BRAF 抑制劑在攜帶 BRAF V600E 突變的腫瘤中獲得了延長(zhǎng)的疾病控制。將靶向治療引入治療算法的可能性代表了 BRAF V600E 突變反復(fù)性高級(jí)別和低級(jí)別神經(jīng)膠質(zhì)瘤患者的范式轉(zhuǎn)變，臨床實(shí)踐中應(yīng)考慮 BRAF 常規(guī)檢測(cè)。本綜述的重點(diǎn)是總結(jié) BRAF 在神經(jīng)膠質(zhì)瘤亞型中的分子圖譜和 BRAF V600E 突變腫瘤的新治療策略。 MAPK-甲乙酮；達(dá)拉非尼；恩科非尼；膠質(zhì)母細(xì)胞瘤;膠質(zhì)瘤;曲美替尼；維羅非尼。

腫瘤發(fā)生與革命國(guó)際數(shù)據(jù)庫(kù)描述：

Gliomas are molecularly heterogeneous brain tumors responsible for the most years of life lost by any cancer. High-grade gliomas have a poor prognosis and despite multimodal treatment including surgery, radiotherapy, and chemotherapy, exhibit a high recurrence rate. There is a need for new therapeutic approaches based on precision medicine informed by biomarker assessment and BRAF, a key regulator of MAPK signaling pathway, influencing cell differentiation, proliferation, migration and pro-tumorigenic activity, is emerging as a promising molecular target. V600E, is the most frequent BRAF alteration in gliomas, especially in pediatric low-grade astrocytomas, pleomorphic xanthoastrocytoma, papillary craniopharyngioma, epithelioid glioblastoma and ganglioglioma. The possible application of BRAF-targeted therapy in gliomas is continuously growing and there is preliminary evidence of prolonged disease control obtained by BRAF inhibitors in tumors harboring BRAF V600E mutation. The possibility of introducing targeted therapies into the treatment algorithm represents a paradigm shift for patients with BRAF V600E mutant recurrent high-grade and low-grade glioma and BRAF routine testing should be considered in clinical practice. The focus of this review is to summarize the molecular landscape of BRAF across glioma subtypes and the novel therapeutic strategies for BRAF V600E mutated tumors.Keywords: BRAF; MAPK-MEK; dabrafenib; encorafenib; glioblastoma; glioma; trametinib; vemurafenib.