Overview of Cancer Stem Cells and Stemness for Community Oncologists.
Overview of Cancer Stem Cells and Stemness for Community Oncologists.
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DOI：
10.1007/s11523-017-0508-3
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发表时间：
2017-08
影响因子：
5.4
通讯作者：
Liu H
中科院分区：
文献类型：
--
作者：
Lathia JD;Liu H
过去癌症研究的进展导致了对癌症发病机制的不断了解和新药的开发，这些新药显著改善了患者的预后。然而，许多患者仍然遇到治疗抵抗、复发或转移，最终死于疾病进展。实验证据表明，癌细胞亚群，称为癌症干细胞（CSCs），具有类似于正常干细胞的“干性”特性，包括自我更新、分化和增殖潜力。这些干细胞特性在分化过程中丢失，并由STAT3、NANOG、NOTCH、WNT和HEDGEHOG等通路控制，这些通路在CSCs中由于遗传和表观遗传变化而高度失调。在针对这些CSCs的临床前模型中，通过破坏干细胞通路并结合当前的治疗方式，已经观察到有希望的结果。这使得基于抗csc的临床试验处于多个发展阶段。在这篇综述中，我们讨论了csc和干细胞通路在癌症治疗中的作用以及它们与临床观察的关系。由于CSCs和控制它们的干细胞通路可以解释治疗期间观察到的负面临床结果，因此肿瘤学家了解它们如何促进癌症进展以及如何靶向它们以改善患者预后是很重要的。
Advances in cancer research in the past have led to an evolving understanding of cancer pathogenesis and the development of novel drugs that significantly improve patient outcomes. However, many patients still encounter treatment resistance, recurrence, or metastasis and eventually die from progressing disease. Experimental evidence indicates that a subpopulation of cancer cells, called cancer stem cells (CSCs), possess “stemness” properties similar to normal stem cells, including self-renewal, differentiation, and proliferative potential. These stemness properties are lost during differentiation and are governed by pathways such as STAT3, NANOG, NOTCH, WNT, and HEDGEHOG, which are highly dysregulated in CSCs due to genetic and epigenetic changes. Promising results have been observed in preclinical models targeting these CSCs through the disruption of stemness pathways in combination with current treatment modalities. This has led to anti-CSC–based clinical trials in multiple stages of development. In this review, we discuss the role of CSCs and stemness pathways in cancer treatment and how they relate to clinical observations. Because CSCs and the stemness pathways governing them may explain the negative clinical outcomes observed during treatment, it is important for oncologists to understand how they contribute to cancer progression and how they may be targeted to improve patient outcomes.
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影响因子：
11.2
作者：
Boman, Bruce M.;Fields, Jeremy Z.;Runquist, Olaf A.
通讯作者：
Runquist, Olaf A.
影响因子：
11.2
作者：
Adorno-Cruz V;Kibria G;Liu X;Doherty M;Junk DJ;Guan D;Hubert C;Venere M;Mulkearns-Hubert E;Sinyuk M;Alvarado A;Caplan AI;Rich J;Gerson SL;Lathia J;Liu H
通讯作者：
Liu H
影响因子：
11.5
作者：
Berlin, Jordan;Bendell, Johanna C.;Low, Jennifer A.
通讯作者：
Low, Jennifer A.
影响因子：
--
作者：
Boesch M;Zeimet AG;Reimer D;Schmidt S;Gastl G;Parson W;Spoeck F;Hatina J;Wolf D;Sopper S
通讯作者：
Sopper S
影响因子：
64.8
作者：
Boumahdi, Soufiane;Driessens, Gregory;Blanpain, Cedric
通讯作者：
Blanpain, Cedric