Intraepithelial neoplasia, surrogate endpoint biomarkers, and cancer chemoprevention
Intraepithelial neoplasia, surrogate endpoint biomarkers, and cancer chemoprevention
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上皮内肿瘤、替代终点生物标志物和癌症化学预防
DOI：
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发表时间：
1993
期刊：
影响因子：
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通讯作者：
G. Kelloff
中科院分区：
文献类型：
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作者：
C. Boone;G. Kelloff
瘤形成是分子、细胞和组织变化的进展，从关键细胞突变开始，通过克隆进化推进，涉及进一步的多个突变和扩增突变克隆。该过程的特征在于五个一般阶段：潜伏期，正常外观但紊乱的细胞的局灶性生长，异常外观细胞（发育不良），微侵袭，最后是转移。上皮中肿瘤进展的两种驱动力是诱变和有丝分裂。这些力经常同时发生，由上皮暴露于环境和内源性诱变剂和有丝分裂原产生。化学预防的主要策略是在发育异常前和发育异常的早期阶段阻断诱变剂和有丝分裂原的作用。
Neoplasia is a progression of molecular, cellular, and tissue changes starting with a critical cell mutation and advancing by clonal evolution, involving further multiple mutations and expanding mutated clones. This process is characterized by five general stages: latency, focal growth of normal‐appearing but disorganized cells, abnormal‐appearing cells (dysplasia), microinvasion, and finally, metastasis. The two driving forces of neoplastic progression in an epithelium are mutagenesis and mitogenesis. These forces frequently occur concurrently, produced by exposure of the epithelium to environmental and endogenous mutagens and mitogens. The major strategy of chemoprevention is to block the effects of both mutagens and mitogens during the early stages of predysplasia and dysplasia.