Department of Pathology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois 60611, USA.
Arch Pathol Lab Med. 2013 Apr;137(4):481-91. doi: 10.5858/arpa.2012-0287-RA.
Lung carcinoma is the result of sequential accumulation of genetic and epigenetic changes. Lung adenocarcinoma is a heterogeneous disease with diverse somatic mutations, and several of them include the so-called driver mutations, which may serve as "druggable" therapeutic targets. Thus, development of personalized approaches for the treatment of non-small cell lung carcinoma (NSCLC) mandates that pathologists make a precise histologic classification inclusive of routine molecular analysis of such tumors.
To address the molecular mechanisms underlying NSCLC and how this knowledge reflects the multidisciplinary approach in the diagnosis and management of these patients. We will also summarize the current available and investigational personalized therapies for patients with resectable early-stage, unresectable locally advanced, and metastatic NSCLC.
Peer-reviewed published literature and personal experience.
There are multiple mechanisms involved in the pathogenesis of lung cancer, which operate in parallel and involve pathways of activation and inhibition of various cellular events. Further research is essential to characterize the histologic and mutational profiles of lung carcinomas, which will ultimately translate into improved and more personalized therapeutic management of patients with lung cancer.
肺癌是遗传和表观遗传改变逐步积累的结果。肺腺癌是一种具有多种体细胞突变的异质性疾病,其中一些突变包括所谓的驱动突变,这些突变可能成为“可靶向”的治疗靶点。因此,为非小细胞肺癌(NSCLC)患者制定个性化治疗方法需要病理学家对这些肿瘤进行精确的组织学分类,包括常规的分子分析。
探讨 NSCLC 的分子机制,以及这些知识如何反映在这些患者的诊断和管理中的多学科方法。我们还将总结目前针对可切除早期、不可切除局部晚期和转移性 NSCLC 患者的可用和研究中的个性化治疗方法。
同行评议的已发表文献和个人经验。
肺癌的发病机制涉及多种机制,这些机制并行运作,涉及各种细胞事件的激活和抑制途径。进一步的研究对于描述肺癌的组织学和突变特征至关重要,这将最终转化为改善和更具个性化的肺癌患者治疗管理。