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首页> 外文期刊>Cancer and Clinical Oncology >Normal Human Cells Acquiring Proliferative Advantage to Hyperplasia-Like Growth-Morphology: Aberrant Progeny Cells Associated With Endopolyploid and Haploid Divisions
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Normal Human Cells Acquiring Proliferative Advantage to Hyperplasia-Like Growth-Morphology: Aberrant Progeny Cells Associated With Endopolyploid and Haploid Divisions

机译：正常人细胞获得增生样生长形态的增殖优势：与内多倍体和单倍体分裂相关的异常子代细胞

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Today, cancer-patients can seek individual genomic tailored therapy, but at?? escalating costs. However, cancer-incidence reduction would reduce such health-cost. The essence of this report is a cell-culture experimental approach for the production of genetically unstable cells from normal cells which with accumulation of “mutations” might reveal early, neoplastic-like pathology. Summarily the experimental focus was on: 1) establishment of a simple nutritional method (amino acid deprivation) for young-cell-response with depoly-ploidization of endopolyploid cells to diploid CIN-cells, 2) a first time observation of a fast growing new, small cell-type, appearing time-correlated with haploid segregations in normal, fibroblast metaphases? and 3) growth characteristics of the progeny cells in 1) and 2) which from their young-cell derivation, could be growth-extended in cultural passages. This would hypothetically model early tumorigenic progression from normal cells. These studies revealed gain of proliferative advantage (GPA), multilayered, changed patterns of growth, focal 3-D cell-heaps with cell polarity change, and star-like mitotic forms. Comparatively, these developments were typical of hyperplasias. The transiency of the originating genome reductive mechanisms may have prevented earlier detections. It is discussed that present growth-changes were responses to homozygous-caused loss of heterozygosity (LOH) of putative pro-proliferation genetics, whereas leukemic and some solid tumor cells showed hemizygous-caused LOH in near-haploid clonal proliferations. The practical outcome is an experimentally simple, nutrition-based model system for SNP-based haplo-karyotyping of the two aberrant cell-types with GPA, which is a cancer, fundamental trait. Never before have cellular mechanism been shown to initiate in normal, human cells, neoplastic-like proliferative responses.
机译：今天，癌症患者可以寻求个体化的基因组定制疗法，但是成本上升。但是，减少癌症发病率将降低这种健康成本。该报告的实质是一种细胞培养实验方法，用于从正常细胞中生产出遗传不稳定的细胞，这种细胞具有“突变”的积累，可能揭示出早期的肿瘤样病理。总的来说，实验重点是：1）建立简单的营养方法（氨基酸剥夺），将内源多倍体细胞多聚倍化为二倍体CIN细胞，2）首次观察快速生长的新细胞，小细胞类型，在正常成纤维细胞中期与单倍体分离时间相关？ 3）1）和2）中子代细胞的生长特性，从它们的年轻细胞衍生而来，可以在文化传代中进行生长扩展。假设这将模拟正常细胞的早期致瘤进展。这些研究揭示了增殖优势（GPA）的获得，多层生长模式的改变，具有细胞极性变化的局部3-D细胞堆以及星形有丝分裂形式的获得。比较而言，这些发展是典型的增生。原始基因组还原机制的瞬态性可能阻止了较早的检测。讨论了当前的生长变化是对假定的增殖基因的纯合子引起的杂合性丧失的响应，而白血病和一些实体肿瘤细胞在近单倍体克隆增殖中显示出由半合子引起的LOH。实际结果是基于实验的简单，基于营养的模型系统，用于对两种异常细胞类型进行基于SNP的单倍染色体核型分析，GPA是癌症的基本特征。在正常的人类细胞中，从未显示出细胞机制可以启动肿瘤样增殖反应。

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