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The functional interplay between systemic cancer and the hematopoietic stem cell niche.全身性癌症与造血干细胞微环境之间的功能相互作用。
Pharmacol Ther. 2016 Dec;168:53-60. doi: 10.1016/j.pharmthera.2016.09.006. Epub 2016 Sep 2.
2
Cancer Stem Cell-Secreted Macrophage Migration Inhibitory Factor Stimulates Myeloid Derived Suppressor Cell Function and Facilitates Glioblastoma Immune Evasion.癌症干细胞分泌的巨噬细胞迁移抑制因子刺激髓源性抑制细胞功能并促进胶质母细胞瘤的免疫逃逸。
Stem Cells. 2016 Aug;34(8):2026-39. doi: 10.1002/stem.2393. Epub 2016 May 27.
3
Vascular Mimicry: The Next Big Glioblastoma Target.血管拟态:胶质母细胞瘤的下一个重要靶点。
Biochem Physiol. 2015 Sep;4(3). doi: 10.4172/2168-9652.1000e140. Epub 2015 Aug 31.
4
Oxygen-Enhanced MRI Accurately Identifies, Quantifies, and Maps Tumor Hypoxia in Preclinical Cancer Models.氧增强磁共振成像在临床前癌症模型中准确识别、量化并绘制肿瘤缺氧情况。
Cancer Res. 2016 Feb 15;76(4):787-95. doi: 10.1158/0008-5472.CAN-15-2062. Epub 2015 Dec 9.
5
Lactate dehydrogenase-A inhibition induces human glioblastoma multiforme stem cell differentiation and death.乳酸脱氢酶-A抑制可诱导多形性胶质母细胞瘤干细胞分化和死亡。
Sci Rep. 2015 Oct 23;5:15556. doi: 10.1038/srep15556.
6
Bone marrow derived myeloid cells orchestrate antiangiogenic resistance in glioblastoma through coordinated molecular networks.骨髓来源的髓样细胞通过协调分子网络在胶质母细胞瘤中协调抗血管生成抗性。
Cancer Lett. 2015 Dec 28;369(2):416-26. doi: 10.1016/j.canlet.2015.09.004. Epub 2015 Sep 21.
7
Hypoxia Induces Production of L-2-Hydroxyglutarate.缺氧诱导L-2-羟基戊二酸的产生。
Cell Metab. 2015 Aug 4;22(2):304-11. doi: 10.1016/j.cmet.2015.06.023. Epub 2015 Jul 23.
8
Hypoxia-Mediated Increases in L-2-hydroxyglutarate Coordinate the Metabolic Response to Reductive Stress.缺氧介导的L-2-羟基戊二酸增加协调对还原应激的代谢反应。
Cell Metab. 2015 Aug 4;22(2):291-303. doi: 10.1016/j.cmet.2015.06.021. Epub 2015 Jul 23.
9
Galectin-3 Shapes Antitumor Immune Responses by Suppressing CD8+ T Cells via LAG-3 and Inhibiting Expansion of Plasmacytoid Dendritic Cells.半乳糖凝集素-3 通过 LAG-3 抑制 CD8+T 细胞并抑制浆细胞样树突状细胞的扩增来塑造抗肿瘤免疫反应。
Cancer Immunol Res. 2015 Apr;3(4):412-23. doi: 10.1158/2326-6066.CIR-14-0150. Epub 2015 Feb 17.
10
Periostin secreted by glioblastoma stem cells recruits M2 tumour-associated macrophages and promotes malignant growth.胶质母细胞瘤干细胞分泌的骨膜蛋白招募M2型肿瘤相关巨噬细胞并促进恶性生长。
Nat Cell Biol. 2015 Feb;17(2):170-82. doi: 10.1038/ncb3090. Epub 2015 Jan 12.

脑胶质瘤微环境中的缺氧:塑造癌症干细胞样细胞的表型。

Hypoxia in the glioblastoma microenvironment: shaping the phenotype of cancer stem-like cells.

机构信息

Neuro-Oncology Branch, National Cancer Institute and National Institute of Neurological Disorders and Stroke, Bethesda, Maryland ; Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland.

出版信息

Neuro Oncol. 2017 Jul 1;19(7):887-896. doi: 10.1093/neuonc/now258.

DOI:10.1093/neuonc/now258
PMID:28339582
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5570138/
Abstract

Glioblastoma is the most common and aggressive malignant primary brain tumor. Cellular heterogeneity is a characteristic feature of the disease and contributes to the difficulty in formulating effective therapies. Glioma stem-like cells (GSCs) have been identified as a subpopulation of tumor cells that are thought to be largely responsible for resistance to treatment. Intratumoral hypoxia contributes to maintenance of the GSCs by supporting the critical stem cell traits of multipotency, self-renewal, and tumorigenicity. This review highlights the interaction of GSCs with the hypoxic tumor microenvironment, exploring the mechanisms underlying the contribution of GSCs to tumor vessel dynamics, immune modulation, and metabolic alteration.

摘要

胶质母细胞瘤是最常见和最具侵袭性的恶性原发性脑肿瘤。细胞异质性是该疾病的一个特征,并导致难以制定有效的治疗方法。已鉴定出神经胶质瘤干细胞(GSCs)作为肿瘤细胞的一个亚群,被认为在很大程度上负责治疗耐药性。肿瘤内缺氧通过支持多能性、自我更新和致瘤性等关键干细胞特性来维持 GSCs。本文综述了 GSCs 与缺氧肿瘤微环境的相互作用,探讨了 GSCs 对肿瘤血管动力学、免疫调节和代谢改变的贡献的机制。