Nowell P C
Virchows Arch B Cell Pathol. 1978 Nov 17;29(1-2):145-50. doi: 10.1007/BF02899348.
Cytogenetic studies indicate that most tumors are clonal (i.e. unicellular in origin) and have karyotypic alterations. These are not consistent, but non-random abnormalities are being increasingly identified by banding techniques, pointing to the sites on human chromosomes where genes important in neoplastic development are located. It is postulated that tumor progression occurs as a result of genetic lability within the neoplastic clone, leading to emergence of increasingly mutant subpopulations (often recognizable cytogenetically) with more malignant properties. In the context of this hypothesis, acute leukemia, chronic leukemia, and preleukemia can be viewed as differing only in the rate at which an abnormal hemic clone is expanding, with progression to a more aggressive phase (e.g. the "blast crisis" of chronic granulocytic leukemia) reflecting emergence of a new predominant subpopulation as the result of an additional genetic change. These concepts, and the cytogenetic data from which they have been derived, may help our understanding of basic tumor biology, and have some practical applications in the diagnosis of human neoplasms.
细胞遗传学研究表明，大多数肿瘤是克隆性的（即起源于单细胞），并且具有核型改变。这些改变并不一致，但通过显带技术越来越多地发现非随机异常，这指向了人类染色体上与肿瘤发生发展相关重要基因所在的位点。据推测，肿瘤进展是肿瘤克隆内基因不稳定的结果，导致出现具有更恶性特征的突变亚群（通常可通过细胞遗传学识别）。在这一假说的背景下，急性白血病、慢性白血病和白血病前期仅在异常造血克隆的扩增速率上有所不同，进展到更具侵袭性的阶段（如慢性粒细胞白血病的“急变期”）反映了由于额外的基因变化而出现了新的优势亚群。这些概念以及得出它们的细胞遗传学数据，可能有助于我们理解肿瘤生物学基础，并在人类肿瘤的诊断中有一些实际应用。
