共查询到17条相似文献,搜索用时 93 毫秒
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目的:探讨辽宁沈阳地区非小细胞肺癌(NSCLC)患者表皮生长因子受体(EGFR)基因突变情况及其与临床病理特征的关系。方法:采用扩增耐突变系统(Amplification Refractory Mutation System,ARMS)检测辽宁沈阳地区471例NSCLC患者EGFR基因第18,19,20及21外显子突变情况。结果:471例NSCLC患者共检出EGFR突变253例(53.7%),其中19缺失和L858R突变占总突变数的42.3%,51.8%。女性患者突变率67.9%明显高于男性(37.4%),两者之间差异有统计学意义(P=0.000)。腺癌患者突变率57.2%明显高于非腺癌患者(18.6%),差异有统计学意义(P=0.000)。结论:辽宁沈阳地区NSCLC患者EGFR突变多见于女性,腺癌患者,突变类型以19缺失和21外显子的L858R突变为主。 相似文献
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肺癌的发病率和死亡率已居我国恶性肿瘤的第一位。以表皮生长因子受体,酪氨酸激酶为靶点的酪氨酸激酶抑制剂(EGFR-TKI)治疗肺癌已广泛引起关注。但部分患者在服用EGFR-TKI初期即出现原发耐药,有些患者在服用EGFR-TKI一段时间后产生继发性耐药,本文综述EGFR-TKl分子耐药机制的研究现状,探讨EGFR-TKl分子耐药机制重要的临床意义。 相似文献
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肺癌是当前死亡率最高的恶性肿瘤之一。表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKIs)明显提高了晚期非小细胞肺癌(NSCLC)患者的生活质量,延长了生存期。EGFR基因优势突变的NSCLC患者临床获益明显,然而由于耐药产生,患者的中位无进展生存期(PFS)仅1年左右。最近,有文献报道EGFR TKIs耐药的机制之一是NSCLC转化为小细胞肺癌(SCLC)。本文对这种现象进行了分析总结,探讨了其转化的可能机制。根据EGFR-TKIs耐药后的处理方法和病理表型转化患者的治疗报道,探讨NSCLC EGFR-TKIs耐药后转化为SCLC患者的治疗策略。 相似文献
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近年来,随着医学分子生物学的飞速发展,分子靶向治疗理念的提出使肿瘤治疗进入一个新阶段。在对非小细胞肺癌(NSCLC)的分子学研究中,表皮生长因子受体(EGFR)突变成为目前研究最热门的分子靶点,针对这一靶点的表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKIs)如吉非替尼、厄洛替尼等,已经广泛应用于临床治疗。然而,有一部分患者对EGFR-TKIs的治疗并不敏感或对其产生耐药性,影响了EGFR-TKIs的临床疗效。本文就EGFR-TKIs的耐药机制以及解除耐药的相应策略进行综述。 相似文献
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摘 要:表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI )至今已上市近二十年。第一代EGFR-TKI在提高EGFR突变晚期非小细胞肺癌(NSCLC)的客观缓解率(ORR)、延长无进展生存期(PFS)方面起了重大的贡献。第二代EGFR-TKI在延长总生存期(OS)方面带来了惊喜。第三代EGFR-TKI克服了第一二代药物的耐药,其一线PFS可能打破现有治疗的格局。第四代EGFR-TKI已在研发中且EGFR-TKI研究已扩展到术后辅助治疗领域,期待其进一步的发展。 相似文献
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肺癌是全球新发癌症发病率最高的癌症,也是中国最常见和致死率最高的癌症。其中85%为非小细胞肺癌(NSCLC),手术是早期患者的主要治疗手段,术后的标准辅助治疗为化疗。但部分患者从辅助化疗中获益十分有限,而且化疗的不良反应也严重影响了患者的生活质量和依从性。表皮生长因子受体-酪氨酸激酶抑制剂(EGFR-TKIs)的出现改变了晚期NSCLC患者的治疗模式,而术后辅助EGFR-TKIs治疗也已成为了国内外的研究热点。本文将对NSCLC术后EGFR-TKIs治疗的效果、安全性以及尚未解决的问题进行探讨。 相似文献
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背景与目的活化的表皮生长因子受体(epidermal growth factor receptor,EGFR)突变鉴定和EGFR酪氨酸激酶抑制剂(EGFR-tyrosinekinaseinhibitors,EGFR-TKIs)的应用已经极大地改变了非小细胞肺癌(non-small-cell lung cancer,NSCLC)的治疗策略。然而,耐药性的产生限制了EGFR-TKI治疗的长期疗效。本研究旨在探讨EGFR激活突变的晚期NSCLC患者中8种驱动基因的突变与EGFR-TKIs原发耐药性的相关性。方法回顾分析2004年4月至2011年3月,在中山大学肿瘤防治中心首次接受EGFR-TKIs治疗的416例Ⅲ/Ⅳ期或复发的NSCLC患者的临床资料。通过常规临床技术检测到多种与EGFR-TKIs疗效相关的基因突变,包括BIM、ALK、KRAS、PIK3CA、PTEN、MET、IGF1R和ROS1基因突变。采用Kaplan-Meier生存分析和logrank检验,比较不同组间的无进展生存(progression-free survival,PFS)和总生存(overall survival,... 相似文献
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Makoto Nishio Terufumi Kato Seiji Niho Noboru Yamamoto Toshiaki Takahashi Naoyuki Nogami Hiroyasu Kaneda Yuka Fujita Keith Wilner Mizuki Yoshida Mitsuhiro Isozaki Shinsuke Wada Fumito Tsuji Kazuhiko Nakagawa 《Cancer science》2020,111(5):1724-1738
In a subgroup of Japanese patients in the ARCHER 1050 randomized phase 3 trial, we evaluated the efficacy and safety and determined the effects of dose modifications on adverse events (AE) and therapy management of first‐line oral dacomitinib 45 mg compared with oral gefitinib 250 mg, each once daily in 28‐d cycles, in patients with EGFR‐activating mutation–positive (EGFR‐positive; exon 19 deletion or exon 21 L858R substitution mutations) advanced non‐small cell lung cancer (NSCLC). The primary endpoint was progression‐free survival (PFS; RECIST, version 1.1, by blinded independent review). In 81 Japanese patients (40 dacomitinib, 41 gefitinib), PFS was longer with dacomitinib compared with gefitinib (hazard ratio [HR], 0.544 [95% confidence interval {CI}, 0.307‐0.961]; 2‐sided P = .0327; median 18.2 for dacomitinib [95% CI, 11.0‐31.3] mo, 9.3 [95% CI, 7.4‐14.7] mo for gefitinib). The most common Grade 3 AEs were dermatitis acneiform with dacomitinib (27.5%) and increased alanine aminotransferase with gefitinib (12.2%). A higher proportion of patients receiving dacomitinib (85.0%) compared with gefitinib (24.4%) had AEs leading to dose reduction. Incidence and severity of diarrhea, dermatitis acneiform, stomatitis and paronychia were generally reduced after dacomitinib dose reductions and dacomitinib treatment duration was generally longer in patients with a dose reduction in comparison with those without a dose reduction. Our results confirmed the efficacy and safety of first‐line dacomitinib in Japanese patients with EGFR‐positive advanced NSCLC. 相似文献
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Predictive efficacy of 11C‐PD153035 PET imaging for EGFR–tyrosine kinase inhibitor sensitivity in non‐small cell lung cancer patients 下载免费PDF全文
Jian Wang Jian‐Jing Liu Yan‐Jia Zhu Ying Zhang Qi Wang Wen‐Gui Xu 《International journal of cancer. Journal international du cancer》2016,138(4):1003-1012
To determine the correlation of 11C‐PD153035 uptake with epidermal growth factor receptor‐tyrosine kinase inhibitor (EGFR‐TKI) sensitivity and phosphorylated EGFR (pEGFR) expression in non‐small cell lung cancer (NSCLC) cell lines with different EGFR‐TKI sensitivities and in their corresponding xenografts. Four human NSCLC cell lines (HCC827, PC9, A549, and H1975) in the logarithmic phase were co‐incubated with 11C‐PD153035 to analyze the correlation of 11C‐PD153035 uptake with EGFR‐TKI sensitivity, and EGFR/pEGFR expression. Nude mice xenograft models bearing the four NSCLCs were prepared. 11C‐PD153035 positron‐emission tomography (PET)‐computed tomography (CT) was used to image the xenografts and observe radioactive uptakes. Correlation of the in vivo uptakes with EGFR‐TKI sensitivity, and EGFR/pEGFR expression was analyzed. HCC827 and PC9 cells, which were highly sensitive to EGFR‐TKIs, exhibited higher 11C‐PD153035 uptakes than the other cells. A549 cells, which were moderately sensitive to EGFR‐TKIs, showed higher uptake than the EGFR‐TKI–resistant H1975 cells, which showed little or no uptake. Radioactive uptakes were positively correlated with pEGFR expression in all cells. PET‐CT showed that radioactivity was highest in HCC827 xenografts. The radioactivity in PC9 xenografts was higher than that in A549 and H1975 xenografts. Tumor vs. non‐tumor tissue ratio values were positively correlated with pEGFR expression in HCC827 and PC9 xenografts, but not in A549 and H1975 xenografts. In conclusion, 11C‐PD153035 can serve as an EGFR imaging agent in vitro and in vivo, and predicts sensitivity to EGFR‐TKIs. This will provide an experimental basis for clinical applications of 11C‐PD153035 and individualized NSCLC therapy. 相似文献
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表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor-tyrosine kinease inhibitors ,EGFR-TKIs)对EGFR 敏感突变非小细胞肺癌(non small cell lung cancer,NSCLC )除了其卓越的疗效,也如其他药物一样最终不可避免地发生耐药。EGFR 基因突变是最常见的肺癌驱动基因之一,针对 EGFR-TKI 耐药后的处理,目前虽无固定治疗模式,但临床进行了大量的探索性研究及治疗对策的探讨,部分结果对临床治疗这类患者有一定启示。本文将就近年具有代表性的研究及进展做一论述。 相似文献
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