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肺癌靶向药物

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靶向药前做EGFR突变检测更准确

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      过去常依据抽烟、性别等作为肺癌病患接受靶向治疗的条件,但台大医院临床试验发现,经检测发现基因突变者,建议一开始就接受靶向药物,可提高肺癌病人疗效。
     台大医院肿瘤医学研究团队参与1项亚洲大型肺癌治疗研究临床试验。台大医院肿瘤医学部副主任杨志新表示,这项研究共收案亚洲9国,共1217位肺腺癌患者,其中有94%不抽烟,台湾有100多位患者参与研究,追踪4年。
     杨志新说,过去是以抽烟、性别等条件,作为选择病人接受靶向药物治疗依据,但这项研究发现,若肺癌细胞中有表皮生长因子接受器(EGFR)突变的病人,第1线(一开始)使用靶向治疗药物,比传统化学治疗效果好,病人生活品质也较好。
     台大医院内科部副主任余忠仁说,日本研究也发现,EGFR突变的病人,第1线使用靶向药物后,半数患者可存活30个月以上;过去没有使用靶向药物者,存活期只有10到12个月。
     杨志新说,希望健保局可以给付肺癌患者第1线使用靶向药物。另外,他说,基因检测在未来将扮演愈来愈重要角色,作为医师选择患者用药的依据。

EGFR是什么
  上皮生长因子受体(Epidermal Growth Factor Receptor; EGFR)是上皮生长因子(EGF)细胞增殖和信号传导的受体。EGFR属于ErbB受体家族的一种,该家族包括EGFR (ErbB-1), HER2/c-neu (ErbB-2), Her 3 (ErbB-3) 和 Her 4 (ErbB-4)。EGFR也被称作HER1、ErbB1,突变或过表达一般会引发肿瘤。EGFR是一种糖蛋白,属于酪氨酸激酶型受体,细胞膜贯通,分子量170Da。
    EGFR位于细胞膜表面,靠与配体结合来激活,包括EGF和TGFα(transforming growth factor α). 激活后,EGFR有单体转化为二聚体-尽管也有证据表明,激活前也存在二聚体。EGFR还可能和ErbB受体家族的其他成员聚合来激活,例如ErbB2/Her2/neu。
   EGFR二聚后可以激活它位于细胞内的激酶通路。包括Y992, Y1045, Y1068, Y1148 and Y1173等激活位点。 这个自磷酸化可以引导下游的磷酸化,包括MPAK,Akt和JNK通路, 诱导细胞增殖。 受体激活对于皮肤的免疫来说很重要。
   研究表明在许多实体肿瘤中存在EGFR的高表达或异常表达。EGFR与肿瘤细胞的增殖、血管生成、肿瘤侵袭、转移及细胞凋亡的抑制有关。其可能机制有:EGFR的高表达引起下游信号传导的增强;突变型EGFR受体或配体表达的增加导致EGFR的持续活化;自分泌环的作用增强;受体下调机制的破坏;异常信号传导通路的激活等。EGFR的过表达在恶性肿瘤的演进中起重要作用,胶质细胞、肾癌、肺癌、前列腺癌、胰腺癌、乳腺癌等组织中都有EGFR的过表达。对胶质细胞瘤的研究发现EGFR的高表达主要与其基因扩增有关。但有时EGFR表达水平的调节异常也存在于翻译及翻译后。EGFR在肿瘤中的高表达还可能与活化后降解减少有关,一些研究指出c-Src可通过抑制受体泛素化和内吞作用而上调EGFR水平。许多肿瘤中有突变型EGFR存在,现已发现许多种EGFR突变型。突变型EGFR的作用可能包括:具有配体非依赖型受体的细胞持续活化;由于EGFR的某些结构域缺失而导致受体下调机制的破坏;异常信号传导通路的激活;细胞凋亡的抑制等。突变体的产生是由于EGFR基因的缺失、突变和重排。EGFR的配体对细胞内信号传导有很大影响。EGFR的配体通过自分泌形式激活EGFR促进细胞增殖,他们的共表达往往预示肿瘤预后不良,例如,在乳腺浸润性导管癌的研究中发现,TGFα与EGFR共表达,且这种共表达与病人的生存率显著相关。Kopp等人对结/直肠癌的研究表明肿瘤的自分泌生长是EGFR的过表达及其配体表达共同作用的结果。
   此外,对EGFR与肿瘤的血管生成、高侵袭性及转移关系的研究发现EGFR可以通过Ang-1及VEGF等因子水平的调节而影响肿瘤血管生成。

==== 汉译英 ====

The basis used to smoke, and gender as a targeted therapy for lung cancer patients receiving conditions, but clinical trials at National Taiwan University Hospital found that gene mutations detected by the proposed start receiving targeted drugs can enhance the efficacy of lung cancer patients.
     National Taiwan University Hospital Oncology research team involved in one of Asia's large-scale clinical trials of lung cancer treatment. Department of National Taiwan University Hospital, deputy director of medical oncology at the new Yang said that the study enrolled a total of 9 countries in Asia, a total of 1217 patients with lung cancer, of which 94% do not smoke, Taiwan has more than 100 patients participated in the study, tracking 4 years.
     Yang said a new, the past is smoking, gender and other conditions, as an alternative basis for patients receiving targeted drug therapy, but this study found that if the lung cancer cells in the epidermal growth factor receptor (EGFR) mutations in patients 1 line ( start) the use of targeted therapies, effective than traditional chemotherapy, the patient quality of life are better.
     Deputy Director of Department of Medicine, National Taiwan University Hospital, Chong-Jen Yu said the Japanese study also found that, EGFR mutations in patients with 1 line of targeted drugs, half of these patients can survive for more than 30 months; in the past did not use targeted drugs, survival is only 10 to 12 months.
     Yang said a new hope BNHI can benefit lung cancer patients to use 1 line of targeted drugs. In addition, he said, genetic testing will play in the future more and more important role, as the basis for physicians select patients with medication.

What EGFR
Epidermal growth factor receptor (Epidermal Growth Factor Receptor; EGFR) is the epidermal growth factor (EGF) cell proliferation and signal transduction receptor. EGFR is an ErbB receptor family, the family, including EGFR (ErbB-1), HER2/c-neu (ErbB-2), Her 3 (ErbB-3) and Her 4 (ErbB-4). EGFR is also known as HER1, ErbB1, mutations or overexpression generally triggered tumor. EGFR is a glycoprotein belonging to tyrosine kinase receptor, through the cell membrane, molecular weight 170Da.
    EGFR in the cell surface, by binding to ligand activation, including EGF and TGFα (transforming growth factor α). Activated, EGFR monomer into a dimer - Although there is evidence that activation of the former there are dimers. EGFR and ErbB receptor family may also be other members of the polymer to activate, for example ErbB2/Her2/neu.
 EGFR dimerization can activate it after the kinase pathway in cells. Including Y992, Y1045, Y1068, Y1148 and Y1173 and other active site. This can lead from the downstream phosphorylation of phosphorylation, including MPAK, Akt and JNK pathway and induce cell proliferation. The skin's immune receptor activation is very important.
 Research shows that there are many solid tumors or abnormal high expression of EGFR expression. EGFR and tumor cell proliferation, angiogenesis, tumor invasion, metastasis and inhibition of apoptosis. Its possible mechanism: EGFR high expression of the downstream signal transduction enhanced; mutant EGFR receptor or ligand causes increased expression of the sustained activation of EGFR; the role of an autocrine loop enhancement; receptor down mechanism of the damage; abnormal signal transduction pathway activation. EGFR overexpression in malignant tumors play an important role in the evolution of glial cells, kidney, lung, prostate, pancreatic, breast and other tissues have overexpression of EGFR. On glial cell tumors found high expression of EGFR gene amplification and its related major. But sometimes abnormal regulation of EGFR expression also exists in the translation and translated. The high EGFR expression in tumors may also be degraded with the decrease after activation, some studies pointed out that the c-Src can inhibit receptor ubiquitination and endocytosis and increased EGFR levels. Many tumors have mutant EGFR exist, has been found in many types of EGFR mutations. The role of EGFR mutations may include: a ligand-independent activation of receptor cells continue; the absence of EGFR, resulting in some domain of the damage mechanism of receptor down; abnormal signal transduction pathway activation; inhibition of apoptosis and so on. Mutant was the result of EGFR gene deletion, mutation and rearrangement. EGFR ligands on intracellular signal transduction have a great impact. EGFR ligand activation of EGFR by autocrine form of promotion of cell proliferation, and their co-expression often indicates poor prognosis tumors, for example, breast cancer, the study found, TGFα and EGFR co-expression, and this co-expression with patient The survival rate was significantly related. Kopp et al Results / cancer studies have shown that autocrine growth of tumors is overexpression of EGFR ligand expression and result of the role.
 In addition, EGFR and tumor angiogenesis, invasion and metastasis of high studies have found EGFR by Ang-1 and VEGF levels and other factors affect the regulation of tumor angiogenesis.

Tags: EGFR突变检测, 靶向药

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更新日期: 2011-02-08 01:44
作者: : mcyclub
修订: 1.1

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