Histopathology Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London, WC2A 3LY, UK.
Future Oncol. 2011 Aug;7(8):981-93. doi: 10.2217/fon.11.70.
The widely accepted paradigm for tumorigenesis begins with rate-limiting mutations in a key growth control gene resulting in immediate lesion growth. Tumor progression occurs as cells within the tumor acquire additional carcinogenic mutations. However, there is clear evidence that the road to cancer can begin long before the growth of a clinically detectable lesion - indeed, long before any of the usual morphological correlates of preneoplasia are recognizable. Field cancerization, the replacement of the normal cell population by a histologically nondysplastic but protumorigenic mutant cell clone, underlies the development of many cancer types, and in this article we review field cancerization in the GI tract. We present the evidence that field cancerization can underpin tumorigenesis in all gastrointestinal compartments, discuss the homeostatic mechanisms that could permit clone spread and highlight how an understanding of the mechanisms driving field cancerization is a means to study human stem cell biology. Finally, we discuss how appropriate recognition of the role of field cancerization in tumorigenesis could impact patient care.
肿瘤发生的广泛接受的模式始于关键生长控制基因中的限速突变，导致立即发生病变生长。肿瘤进展发生在肿瘤内的细胞获得额外的致癌突变时。然而，有明确的证据表明，癌症的发生途径可以在临床上可检测到的病变生长之前很久就开始——实际上，在可识别的癌前病变的任何通常形态学相关之前很久就开始了。 场癌变是指正常细胞群体被组织学上非发育不良但促肿瘤发生的突变细胞克隆所取代，它是许多癌症类型发展的基础，本文我们将回顾胃肠道中的场癌变。我们提出了证据表明，场癌变可以为所有胃肠道隔室的肿瘤发生提供基础，讨论允许克隆扩散的动态平衡机制，并强调了解驱动场癌变的机制如何成为研究人类干细胞生物学的一种手段。最后，我们讨论了适当认识场癌变在肿瘤发生中的作用如何影响患者护理。
