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有证据表明,体外X射线诱导的致癌转化过程中的第二个事件发生在细胞增殖期间。

Evidence that a second event in X-ray-induced oncogenic transformation in vitro occurs during cellular proliferation.

作者信息

Kennedy A R, Little J B

出版信息

Radiat Res. 1984 Aug;99(2):228-48.

PMID:6463204
Abstract

It has previously been hypothesized that radiation transformation in vitro is a two-step process; the first step is a frequent alteration occurring among a large fraction of the irradiated cells, while the second step, malignant transformation, is a rare event occurring with an approximate frequency of 10(-6) among the progeny of the irradiated cells. Data are reported here on the distributions of transformed-cell clone sizes in irradiated cultures reseeded at various times post-treatment. The results suggest that the second event in transformation occurs randomly during the growth of irradiated cultures of C3H 10T1/2 cells to confluence. When the same number of irradiated C3H 10T1/2 cells were seeded into petri dishes of different sizes [35 mm (8 cm2), 60 mm (21 cm2), 100 mm (55 cm2), 150 mm (145 cm2)], the number of foci which arose per dish was dependent on the final cell numbers at confluence in the various dish sizes, such that the number of foci/cm2 was constant. When irradiated cells and parental C3H 10T1/2 cells were mixed in different proportions at low density, the number of foci which ultimately arose was a function of the number of progeny of irradiated cells present in the culture at confluence. The results presented here confirm previous studies and give further evidence that the radiation-induced malignant transformation of cells occurs in an indirect, multistage fashion.

摘要

先前曾有人提出假说,体外辐射转化是一个两步过程;第一步是在大部分受辐照细胞中频繁发生的改变,而第二步,即恶性转化,是在受辐照细胞后代中以约10(-6)的频率发生的罕见事件。本文报道了在处理后不同时间重新接种的受辐照培养物中转化细胞克隆大小的分布数据。结果表明,转化过程中的第二个事件在C3H 10T1/2细胞受辐照培养物生长至汇合的过程中随机发生。当将相同数量的受辐照C3H 10T1/2细胞接种到不同大小的培养皿[35毫米(8平方厘米)、60毫米(21平方厘米)、100毫米(55平方厘米)、150毫米(145平方厘米)]中时,每个培养皿中出现的集落数取决于不同大小培养皿中汇合时的最终细胞数,使得每平方厘米的集落数是恒定的。当受辐照细胞和亲代C3H 10T1/2细胞以不同比例低密度混合时,最终出现的集落数是汇合时培养物中受辐照细胞后代数量的函数。本文给出的结果证实了先前的研究,并进一步证明细胞的辐射诱导恶性转化以间接的多阶段方式发生。

相似文献

1
Evidence that a second event in X-ray-induced oncogenic transformation in vitro occurs during cellular proliferation.有证据表明,体外X射线诱导的致癌转化过程中的第二个事件发生在细胞增殖期间。
Radiat Res. 1984 Aug;99(2):228-48.
2
Spontaneous formation of foci of morphologically transformed cells in populations of C3H 10T1/2 (clone 8) cells.在C3H 10T1/2(克隆8)细胞群体中形态转化细胞灶的自发形成。
Cancer Res. 1988 Nov 1;48(21):5969-76.
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Potential role of treatment artifact in the effect of cell density upon frequencies of C3H/10T1/2 cell transformation.
Cancer Res. 1985 Dec;45(12 Pt 1):6314-21.
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Induction of foci of morphologically transformed cells in synchronized populations of 10T1/2 cells by N-methyl-N'-nitro-N-nitrosoguanidine and the effect of spontaneous transformation on calculated transformation frequency.N-甲基-N'-硝基-N-亚硝基胍诱导同步化的10T1/2细胞群体中形态转化细胞灶的形成以及自发转化对计算出的转化频率的影响。
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The influence of cellular proliferative history on the susceptibility to oncogenic transformation.细胞增殖历史对致癌转化易感性的影响。
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6
Cell density dependence of focus formation in the C3H/10T1/2 transformation assay.
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Survival and oncogenic transformation of C3H/10T1/2 cells after extended X irradiation.延长X射线照射后C3H/10T1/2细胞的存活与致癌转化
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In vivo enhancement of genomic instability in minisatellite sequences of mouse C3H/10T1/2 cells transformed in vitro by X-rays.X射线体外转化的小鼠C3H/10T1/2细胞小卫星序列中基因组不稳定性的体内增强。
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Evidence suggesting that the dose-response relationship for radiation-induced transformation in vitro is due to the degree of initiation in individual cells.有证据表明,体外辐射诱导转化的剂量反应关系是由于单个细胞的起始程度所致。
Radiat Oncol Investig. 1997;5(3):144-9. doi: 10.1002/(SICI)1520-6823(1997)5:3<144::AID-ROI12>3.0.CO;2-6.
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Oncogenic transformation of C3H/10T1/2 clone 8 mouse embryo cells by halogenated pyrimidine nucleosides.卤代嘧啶核苷对C3H/10T1/2克隆8小鼠胚胎细胞的致癌转化作用。
Cancer Res. 1976 Jan;36(1):101-7.

引用本文的文献

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The risk linked to ionizing radiation: an alternative epidemiologic approach.与电离辐射相关的风险:一种替代的流行病学方法。
Environ Health Perspect. 2001 Sep;109(9):877-80. doi: 10.1289/ehp.01109877.
2
Oncogenic potential of bifunctional bioreductive drugs.双功能生物还原药物的致癌潜力。
Br J Cancer Suppl. 1996 Jul;27:S57-60.
3
Evidence that carcinogenesis involves an imbalance between epigenetic high-frequency initiation and suppression of promotion.有证据表明,致癌作用涉及表观遗传高频起始与促进抑制之间的失衡。
Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1332-6. doi: 10.1073/pnas.92.5.1332.
4
Is there a critical target gene for the first step in carcinogenesis?致癌作用第一步是否存在关键靶基因?
Environ Health Perspect. 1991 Jun;93:199-203. doi: 10.1289/ehp.9193199.