• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

12-O-十四烷酰佛波醇-13-乙酸酯体外增强辐射转化机制的研究

Investigation of the mechanism for enhancement of radiation transformation in vitro by 12-O-tetradecanoylphorbol-13-acetate.

作者信息

Kennedy A R, Little J B

机构信息

Department of Physiology, Harvard University, School of Public Health, Boston, MA 02115, USA.

出版信息

Carcinogenesis. 1980;1(12):1039-47. doi: 10.1093/carcin/1.12.1039.

DOI:10.1093/carcin/1.12.1039
PMID:11272108
Abstract

We have performed experiments designed to investigate the mechanism for the enhancement of radiation transformation in vitro by 12-O-tetradecanoylphorbol-13-acetate (TPA). Two types of experiments, involving C3H 10T1/2 cells and 100 rad X-ray exposures with subsequent TPA treatment, are reported here. In one set of experiments, cultures were initially seeded at differing initial cell densities prior to irradiation. In the other series of experiments, cultures exposed to 100 rads and TPA contained the same initial cell densities (about 300 viable cells per dish); these cultures were allowed to reach confluence and were then reseeded at various cell densities to allow a second cycle of growth to confluence (which involved different numbers of cell divisions). We have observed that the number of transformed foci which ultimately developed per dish treated with 100 rads and TPA remains approximately constant even though the cell density (initial or reseeded) is varied over several orders of magnitude. The yield of transformants per dish which occurred following this treatment was similar to those previously observed in cultures irradiated with higher doses (400-600 rads) of X-rays alone. Our results suggest that a similar mechanism for the induction of malignant transformation may be involved for high doses of radiation alone or for a low dose of radiation followed by TPA treatment.

摘要

我们进行了旨在研究12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)增强体外辐射转化机制的实验。本文报道了两类涉及C3H 10T1/2细胞以及100拉德X射线照射并随后进行TPA处理的实验。在一组实验中,培养物在辐照前最初以不同的初始细胞密度接种。在另一系列实验中,接受100拉德和TPA处理的培养物具有相同的初始细胞密度(每皿约300个活细胞);这些培养物培养至汇合状态,然后以不同的细胞密度重新接种,以进行第二轮生长至汇合(这涉及不同数量的细胞分裂)。我们观察到,尽管细胞密度(初始或重新接种的)在几个数量级范围内变化,但每皿经100拉德和TPA处理后最终形成的转化灶数量大致保持恒定。此处理后每皿转化体的产量与之前在仅接受较高剂量(400 - 600拉德)X射线照射的培养物中观察到的产量相似。我们的结果表明,单独高剂量辐射或低剂量辐射后进行TPA处理可能涉及类似的诱导恶性转化机制。

相似文献

1
Investigation of the mechanism for enhancement of radiation transformation in vitro by 12-O-tetradecanoylphorbol-13-acetate.12-O-十四烷酰佛波醇-13-乙酸酯体外增强辐射转化机制的研究
Carcinogenesis. 1980;1(12):1039-47. doi: 10.1093/carcin/1.12.1039.
2
Enhanced transformation of mouse 10T1/2 cells by 12-O-tetradecanoylphorbol-13-acetate following exposure to X-rays or to fission-spectrum neutrons.在暴露于X射线或裂变谱中子后,12-O-十四烷酰佛波醇-13-乙酸酯对小鼠10T1/2细胞的转化作用增强。
Cancer Res. 1982 Feb;42(2):477-83.
3
Studies of the rad-equivalence of ethylene oxide in the presence and absence of 12-O-tetradecanoylphorbol-13-acetate (TPA) in C3H/10T1/2 cells.关于在C3H/10T1/2细胞中存在和不存在12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)时环氧乙烷的辐射等效性研究。
Toxicol Lett. 1990 Oct;53(3):307-13. doi: 10.1016/0378-4274(90)90235-e.
4
Effect of time and duration of exposure to 12-O-tetradecanoylphorbol-13-acetate on x-ray transformation of C3H 10T 1/2 cells.12-氧-十四烷酰佛波醇-13-乙酸酯作用时间和暴露时长对C3H 10T 1/2细胞X射线转化的影响
Cancer Res. 1980 Jun;40(6):1915-20.
5
Ultraviolet light in the oncogenic transformation of cultured C3H/10T1/2 mouse embryo cells.紫外线在培养的C3H/10T1/2小鼠胚胎细胞致癌转化中的作用
Natl Cancer Inst Monogr. 1978 Dec(50):71-3.
6
Continuous-wave ultrasound and neoplastic transformation in vitro.连续波超声与体外肿瘤转化
Ultrasound Med Biol. 1989;15(4):335-40. doi: 10.1016/0301-5629(89)90045-8.
7
60 Hz magnetic field acts as co-promoter in focus formation of C3H/10T1/2 cells.60赫兹磁场在C3H/10T1/2细胞的焦点形成中起到协同促进作用。
Carcinogenesis. 1993 May;14(5):955-60. doi: 10.1093/carcin/14.5.955.
8
Enhancement of 3-methylcholanthrene-induced neoplastic transformation by 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone in the two-stage transformation assay in C3H 10T1/2 cells.在C3H 10T1/2细胞的两阶段转化试验中,3-氯-4-(二氯甲基)-5-羟基-2(5H)-呋喃酮对3-甲基胆蒽诱导的肿瘤转化的增强作用。
Arch Toxicol. 2001 Dec;75(10):613-7. doi: 10.1007/s00204-001-0285-7.
9
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.
10
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.

引用本文的文献

1
Cooperative effects of photodynamic treatment of cells in microcolonies.微菌落中细胞光动力治疗的协同效应。
Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1773-8. doi: 10.1073/pnas.94.5.1773.
2
The effect of phorbol ester treatment on migration of C3H 10T1/2 and BT5C glioma cells: possible application to carcinogenesis.佛波酯处理对C3H 10T1/2和BT5C胶质瘤细胞迁移的影响:在致癌作用中的可能应用。
J Cancer Res Clin Oncol. 1994;120(3):156-8. doi: 10.1007/BF01202194.
3
Initiation and promotion at different ages and doses in 2200 mice. III. Linear extrapolation from high doses may underestimate low-dose tumour risks.
对2200只小鼠进行不同年龄和剂量下的启动和促进研究。三、高剂量的线性外推法可能低估低剂量肿瘤风险。
Br J Cancer. 1981 Jul;44(1):24-34. doi: 10.1038/bjc.1981.143.
4
Modification by anisotonic treatment of repair and fixation of radiation damage in cell killing and transformation.通过非等渗处理对细胞杀伤和转化中辐射损伤的修复与固定进行修饰。
Br J Cancer Suppl. 1984;6:239-42.
5
Nanomolar concentrations of Bowman-Birk soybean protease inhibitor suppress x-ray-induced transformation in vitro.纳摩尔浓度的鲍曼-伯克大豆蛋白酶抑制剂在体外可抑制X射线诱导的细胞转化。
Proc Natl Acad Sci U S A. 1985 Aug;82(16):5395-9. doi: 10.1073/pnas.82.16.5395.
6
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.