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Functions of paracrine PDGF signaling in the proangiogenic tumor stroma revealed by pharmacological targeting.通过药理学靶向揭示旁分泌血小板源性生长因子信号传导在促血管生成肿瘤基质中的作用。
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本文引用的文献

1
Progression of cancer from indolent to aggressive despite antigen retention and increased expression of interferon-gamma inducible genes.尽管存在抗原保留且干扰素-γ诱导基因表达增加,但癌症仍从惰性发展为侵袭性。
Cancer Immun. 2011 Jun 30;11:2.
2
Antigen specificity of immune suppression by myeloid-derived suppressor cells.髓系来源抑制细胞的免疫抑制的抗原特异性。
J Leukoc Biol. 2011 Jul;90(1):31-6. doi: 10.1189/jlb.0111021. Epub 2011 Apr 12.
3
Myeloid-derived suppressor cells express the death receptor Fas and apoptose in response to T cell-expressed FasL.髓源性抑制细胞表达死亡受体 Fas,并在 T 细胞表达 FasL 时发生凋亡。
Blood. 2011 May 19;117(20):5381-90. doi: 10.1182/blood-2010-11-321752. Epub 2011 Mar 30.
4
CD40 agonists alter tumor stroma and show efficacy against pancreatic carcinoma in mice and humans.CD40 激动剂可改变肿瘤基质,并在小鼠和人类中显示出对胰腺癌的疗效。
Science. 2011 Mar 25;331(6024):1612-6. doi: 10.1126/science.1198443.
5
T cells and stromal fibroblasts in human tumor microenvironments represent potential therapeutic targets.人类肿瘤微环境中的T细胞和基质成纤维细胞是潜在的治疗靶点。
Cancer Microenviron. 2010 Mar 31;3(1):29-47. doi: 10.1007/s12307-010-0044-5.
6
CD169-positive macrophages dominate antitumor immunity by crosspresenting dead cell-associated antigens.CD169 阳性巨噬细胞通过交叉呈递死亡细胞相关抗原主导抗肿瘤免疫。
Immunity. 2011 Jan 28;34(1):85-95. doi: 10.1016/j.immuni.2010.12.011. Epub 2010 Dec 30.
7
Successful colon cancer eradication after chemoimmunotherapy is associated with profound phenotypic change of intratumoral myeloid cells.化疗免疫治疗后成功根除结肠癌与肿瘤内髓样细胞的显著表型变化有关。
J Immunol. 2011 Jan 15;186(2):807-15. doi: 10.4049/jimmunol.1001483. Epub 2010 Dec 8.
8
Functional and clinical relevance of chondroitin sulfate proteoglycan 4.硫酸软骨素蛋白聚糖 4 的功能和临床意义。
Adv Cancer Res. 2010;109:73-121. doi: 10.1016/B978-0-12-380890-5.00003-X.
9
Suppression of antitumor immunity by stromal cells expressing fibroblast activation protein-alpha.基质细胞表达成纤维细胞激活蛋白-α抑制抗肿瘤免疫。
Science. 2010 Nov 5;330(6005):827-30. doi: 10.1126/science.1195300.
10
HIF-1α regulates function and differentiation of myeloid-derived suppressor cells in the tumor microenvironment.缺氧诱导因子 1α 调节肿瘤微环境中髓源性抑制细胞的功能和分化。
J Exp Med. 2010 Oct 25;207(11):2439-53. doi: 10.1084/jem.20100587. Epub 2010 Sep 27.

针对肿瘤微环境以治疗癌症。

Targeting stroma to treat cancers.

机构信息

Department of Pathology, Committee on Cancer Biology, Committee on Immunology, The University of Chicago, Chicago, IL 60637-5420, USA.

出版信息

Semin Cancer Biol. 2012 Feb;22(1):41-9. doi: 10.1016/j.semcancer.2011.12.008. Epub 2011 Dec 24.

DOI:10.1016/j.semcancer.2011.12.008
PMID:22212863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3321387/
Abstract

All cancers depend on stroma for support of growth. Leukemias, solid tumors, cancer cells causing effusions, metastases as well as micro-disseminated cancer cells release factors that stimulate stromal cells, which in turn produce ligands that stimulate cancer cells. Therefore, elimination of stromal support by destroying the stromal cells or by inhibiting feedback stimulation of cancer growth is in the focus of many evolving therapies. A stringent evaluation of the efficacy of stromal targeting requires testing in animal models. Most current studies emphasize the successes of stromal targeting rather than deciphering its limitations. Here we show that many of the stromal targeting approaches, while often reducing tumor growth rates, are rarely curative. Therefore, we will also discuss conditions where stromal targeting can eradicate large established tumors. Finally, we will examine still unanswered questions of this promising and exciting area of cancer research.

摘要

所有癌症的生长都依赖于基质的支持。白血病、实体瘤、引起渗出液的癌细胞、转移以及微播散的癌细胞释放出刺激基质细胞的因子,这些基质细胞反过来又产生刺激癌细胞的配体。因此,通过破坏基质细胞或抑制癌症生长的反馈刺激来消除基质支持是许多正在发展的治疗方法的重点。严格评估基质靶向的疗效需要在动物模型中进行测试。目前大多数研究强调基质靶向的成功,而不是破解其局限性。在这里,我们表明,许多基质靶向方法虽然经常降低肿瘤生长速度,但很少能治愈。因此,我们还将讨论在哪些情况下基质靶向可以根除已建立的大型肿瘤。最后,我们将研究这个有前途和令人兴奋的癌症研究领域仍未解答的问题。