Small-cell lung cancer (SCLC) is a deadly tumour accounting for approximately 15% of lung cancers and is pathologically, molecularly, biologically and clinically very different from other lung cancers. While the majority of tumours express a neuroendocrine programme (integrating neural and endocrine properties), an important subset of tumours have low or absent expression of this programme. The probable initiating molecular events are inactivation of TP53 and RB1, as well as frequent disruption of several signalling networks, including Notch signalling. SCLC, when diagnosed, is usually widely metastatic and initially responds to cytotoxic therapy but nearly always rapidly relapses with resistance to further therapies. There were no important therapeutic clinical advances for 30 years, leading SCLC to be designated a 'recalcitrant cancer'. Scientific studies are hampered by a lack of tissue availability. However, over the past 5 years, there has been a worldwide resurgence of studies on SCLC, including comprehensive molecular analyses, the development of relevant genetically engineered mouse models and the establishment of patient-derived xenografts. These studies have led to the discovery of new potential therapeutic vulnerabilities for SCLC and therefore to new clinical trials. Thus, while the past has been bleak, the future offers greater promise.

小细胞肺癌（SCLC）是致命性肿瘤，约占肺癌的15％，并且在病理，分子，生物学和临床上均与其他肺癌大不相同。虽然大多数肿瘤表达神经内分泌程序（整合神经和内分泌特性），但重要的肿瘤子集却很少或没有该程序的表达。可能的引发分子事件是TP53和RB1的失活以及包括Notch信令在内的多个信令网络的频繁中断。当诊断为SCLC时，它通常是广泛转移的，最初对细胞毒性疗法有反应，但几乎总是迅速复发，并且对其他疗法有抵抗力。30年来，没有重要的临床治疗进展，导致SCLC被指定为“顽固性癌症”。缺乏组织可利用性阻碍了科学研究。但是，在过去的5年中，SCLC的研究在世界范围内重新兴起，包括全面的分子分析，相关的基因工程小鼠模型的开发以及患者来源的异种移植物的建立。这些研究导致发现了SCLC的新的潜在治疗漏洞，因此也进行了新的临床试验。因此，