摘要
癌变与组织再生过程中存在着一个微妙的平衡。大量的恶性肿瘤被认为是受损的或不完整的再生过程的外显,导致持续分裂的细胞。再生能力组织和动物有能力阻止和抵消生长异常,并可能有化学癌变的低脆弱性。癌症细胞存活取决于不同的氧化还原相关机制(除其它事项外),这些机制是现代发展疗法的靶点。这些治疗方式的缺点是特异性和耐药性的缺乏。因为这些氧化还原相关机制的多数在成功协调细胞功能与繁殖中起着重要作用,再生产过程给当代癌症研究提供了一个独特的平行环境。这篇综述着重于癌变与再生的相互联系和一个再生力和氧化还原控制机制的理解如何促成新治疗靶向的识别来阻止癌细胞的生长和存活。
关键词: 抗癌症治疗,癌变,氧化还原相关机制,再生,干细胞
图形摘要
Current Drug Targets
Title:Redox-Related Mechanisms to Rebalance Cancer-Deregulated Cell Growth
Volume: 17 Issue: 12
Author(s): An-Sofie Stevens, Nicky Pirotte, Annelies Wouters, Andromeda Van Roten, Frank Van Belleghem, Maxime Willems, Ann Cuypers and Tom Artois and Karen Smeets
Affiliation:
关键词: 抗癌症治疗,癌变,氧化还原相关机制,再生,干细胞
摘要: A delicate balance exists between the process of carcinogenesis and tissue regeneration. A number of malignant tumours are considered the outcome of an impaired or incomplete regeneration process, resulting in persistently dividing cells. Regeneration-competent tissues and animals are able to prevent and counteract growth abnormalities and seem to have a low vulnerability to chemical carcinogenesis. Cancer cell survival depends, among other things, on various redox-related mechanisms, which are targets of currently developed therapies. Disadvantages of these therapies are a lack of specificity and drug resistance. As the majority of these redox-related mechanisms also play an important role in successful and coordinated cell functioning and reproduction, the regeneration process offers a unique parallel context for modern cancer research. This review focuses on the interconnections between regeneration and carcinogenesis and how an understanding of regenerative forces and redox-controlled mechanisms could contribute to the identification of new therapeutic targets to block the growth and survival of cancer cells.
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Cite this article as:
An-Sofie Stevens, Nicky Pirotte, Annelies Wouters, Andromeda Van Roten, Frank Van Belleghem, Maxime Willems, Ann Cuypers and Tom Artois and Karen Smeets , Redox-Related Mechanisms to Rebalance Cancer-Deregulated Cell Growth, Current Drug Targets 2016; 17 (12) . https://dx.doi.org/10.2174/1389450116666150506112817
DOI https://dx.doi.org/10.2174/1389450116666150506112817 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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