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摘要:
小细胞肺癌(SCLC)约占肺癌的15%,致死率高。SCLC的病理、分子生物学机制和临床预后特征与非小细胞肺癌(NSCLC)不尽相同。大多数SCLC表达神经内分泌特征(整合了神经和内分泌特性),其分子机制可能与TP53和RB1的失活,以及包括Notch信号在内的多个信号通路的频繁中断有关。近年来,随着分子机制研究深入和相关的基因工程小鼠模型的开发以及建立患者来源的异种移植物模型的研究进展,为发现SCLC潜在的治疗靶点,改善疗效和预后带来了新希望。
Abstract:Small cell lung cancer (SCLC) is a lethal tumor with high incidence and accounts for approximately 15% of lung cancer. It is different from NSCLC in pathological, molecular, biological mechanisms and clinical characteristics. The majority of SCLC have neuroendocrine characteristics including both neuroendocrine and endocrine features. The molecular mechanism may be related to the inactivation of TP53 and RB1, and the disruption of multiple signaling pathways including Notch signaling. In recent years, the comprehensive molecular analyses and the development of genetically engineered mouse models (GEMMs) and patient-derived xenografts (PDXs) have provided new hope for the treatment of SCLC.
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作者贡献施甜甜: 查阅文献、文章撰写王玉栋: 文章的审核校正
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