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一个正常的人体细胞是如何变成癌细胞的?

How does a normal human cell become a cancer cell?

作者信息

Gan D D, Macaluso M, Cinti C, Khalili K, Giordano A

机构信息

Center for NeuroVirology and Cancer Biology, Dept. of Biology, Temple University, Philadelphia, PA 19122, USA.

出版信息

J Exp Clin Cancer Res. 2003 Dec;22(4):509-16.

PMID:15053291
Abstract

The mechanism by which cells become cancerous has been studied in several different species and cell types. Here, we will focus on the mechanism by which a normal human cell becomes a cancer cell and specifically discuss genes that researchers have used to transform cells. Studying how those genes affect cellular immortalization and transformation will help researchers understand more about cancer biology, find new treatments for cancer and/or improve cell survival during gene therapy.

摘要

细胞癌变的机制已在几种不同的物种和细胞类型中进行了研究。在此,我们将重点关注正常人类细胞转变为癌细胞的机制,并具体讨论研究人员用于转化细胞的基因。研究这些基因如何影响细胞永生化和转化,将有助于研究人员更深入地了解癌症生物学,找到新的癌症治疗方法和/或改善基因治疗期间的细胞存活情况。

相似文献

1
How does a normal human cell become a cancer cell?一个正常的人体细胞是如何变成癌细胞的?
J Exp Clin Cancer Res. 2003 Dec;22(4):509-16.
2
Immortalization and transformation of primary human airway epithelial cells by gene transfer.通过基因转移使原代人呼吸道上皮细胞永生化和转化。
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Derivation of human tumor cells in vitro without widespread genomic instability.体外衍生无广泛基因组不稳定的人类肿瘤细胞。
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Immortal ALT+ human cells do not require telomerase reverse transcriptase for malignant transformation.永生化的ALT+人类细胞在恶性转化过程中不需要端粒酶逆转录酶。
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Knock-in of mutant K-ras in nontumorigenic human epithelial cells as a new model for studying K-ras mediated transformation.在非致瘤性人上皮细胞中敲入突变型K-ras作为研究K-ras介导的转化的新模型。
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Differential transcriptional regulation of human telomerase in a cellular model representing important genetic alterations in esophageal squamous carcinogenesis.在一个代表食管鳞状细胞癌发生过程中重要基因改变的细胞模型中,人端粒酶的差异转录调控
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Progressive loss of malignant behavior in telomerase-negative tumorigenic adrenocortical cells and restoration of tumorigenicity by human telomerase reverse transcriptase.端粒酶阴性致瘤性肾上腺皮质细胞恶性行为的渐进性丧失及人端粒酶逆转录酶对致瘤性的恢复
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Signal transducer and activator of transcription 3 (STAT3) regulates human telomerase reverse transcriptase (hTERT) expression in human cancer and primary cells.信号转导及转录激活因子3(STAT3)在人类癌症和原代细胞中调节人类端粒酶逆转录酶(hTERT)的表达。
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引用本文的文献

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Nanomaterials (Basel). 2015 Aug 12;5(3):1317-1330. doi: 10.3390/nano5031317.
2
The role of the dysfunctional akt-related pathway in cancer: establishment and maintenance of a malignant cell phenotype, resistance to therapy, and future strategies for drug development.功能失调的Akt相关通路在癌症中的作用:恶性细胞表型的建立与维持、对治疗的抗性以及药物开发的未来策略
Scientifica (Cairo). 2013;2013:317186. doi: 10.1155/2013/317186. Epub 2013 Dec 5.
3
Deregulations in the cyclin-dependent kinase-9-related pathway in cancer: implications for drug discovery and development.
癌症中细胞周期蛋白依赖性激酶9相关通路的失调:对药物发现与开发的启示
ISRN Oncol. 2013 Jun 6;2013:305371. doi: 10.1155/2013/305371. Print 2013.
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Development of safer gene delivery systems to minimize the risk of insertional mutagenesis-related malignancies: a critical issue for the field of gene therapy.开发更安全的基因递送系统以将插入诱变相关恶性肿瘤的风险降至最低:这是基因治疗领域的一个关键问题。
ISRN Oncol. 2012;2012:616310. doi: 10.5402/2012/616310. Epub 2012 Nov 22.
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Cyclin T1 overexpression induces malignant transformation and tumor growth.Cyclin T1 过表达诱导恶性转化和肿瘤生长。
Cell Cycle. 2010 Aug 1;9(15):3119-26. doi: 10.4161/cc.9.15.12526.
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Genetic and epigenetic alterations in breast cancer: what are the perspectives for clinical practice?乳腺癌中的基因和表观遗传改变:临床实践的前景如何?
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