• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

在小鼠中模拟间变性甲状腺癌。

Modeling anaplastic thyroid carcinoma in the mouse.

作者信息

Champa Devora, Di Cristofano Antonio

机构信息

Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1301 Morris Park Avenue, Room 302, Bronx, NY, 10461, USA.

出版信息

Horm Cancer. 2015 Feb;6(1):37-44. doi: 10.1007/s12672-014-0208-8. Epub 2014 Nov 25.

DOI:10.1007/s12672-014-0208-8
PMID:25420535
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4312228/
Abstract

Anaplastic thyroid carcinoma is the least common form of thyroid cancer; however, it accounts for the majority of deaths associated with this family of malignancies. A number of genetically engineered immunocompetent mouse models recapitulating the genetic and histological features of anaplastic thyroid cancer have been very recently generated and represent an invaluable tool to dissect the mechanisms involved in the progression from indolent, well-differentiated tumors to aggressive, undifferentiated carcinomas and to identify novel therapeutic targets. In this review, we focus on the relevant characteristics associated with these models and on what we have learned in terms of anaplastic thyroid cancer biology, genetics, and response to targeted therapy.

摘要

间变性甲状腺癌是甲状腺癌最不常见的形式;然而,它占与这类恶性肿瘤相关死亡人数的大多数。最近已经构建了一些能够重现间变性甲状腺癌的遗传和组织学特征的基因工程免疫活性小鼠模型,这些模型是剖析惰性、高分化肿瘤向侵袭性、未分化癌进展所涉及机制以及鉴定新治疗靶点的宝贵工具。在本综述中,我们重点关注与这些模型相关的特征,以及我们在间变性甲状腺癌生物学、遗传学和靶向治疗反应方面所学到的知识。

相似文献

1
Modeling anaplastic thyroid carcinoma in the mouse.在小鼠中模拟间变性甲状腺癌。
Horm Cancer. 2015 Feb;6(1):37-44. doi: 10.1007/s12672-014-0208-8. Epub 2014 Nov 25.
2
The next generation of orthotopic thyroid cancer models: immunocompetent orthotopic mouse models of BRAF V600E-positive papillary and anaplastic thyroid carcinoma.下一代原位甲状腺癌模型:BRAF V600E 阳性乳头状和间变性甲状腺癌的免疫活性原位小鼠模型。
Thyroid. 2014 Apr;24(4):705-14. doi: 10.1089/thy.2013.0483. Epub 2014 Jan 24.
3
Targeted therapy: a new hope for thyroid carcinomas.靶向治疗:甲状腺癌的新希望。
Crit Rev Oncol Hematol. 2015 Apr;94(1):55-63. doi: 10.1016/j.critrevonc.2014.10.012. Epub 2014 Nov 1.
4
Phosphatidylinositol 3-kinase/akt and ras/raf-mitogen-activated protein kinase pathway mutations in anaplastic thyroid cancer.间变性甲状腺癌中的磷脂酰肌醇3激酶/蛋白激酶B及Ras/Raf-丝裂原活化蛋白激酶通路突变
J Clin Endocrinol Metab. 2008 Jan;93(1):278-84. doi: 10.1210/jc.2007-1076. Epub 2007 Nov 7.
5
Pathology and genetics of thyroid carcinoma.甲状腺癌的病理学与遗传学
J Surg Oncol. 2006 Dec 15;94(8):662-9. doi: 10.1002/jso.20700.
6
Search for new genetic biomarkers in poorly differentiated and anaplastic thyroid carcinomas using next generation sequencing.使用新一代测序技术在低分化和未分化甲状腺癌中寻找新的遗传生物标志物。
Anticancer Res. 2015 Apr;35(4):2029-36.
7
Thyrocyte-specific inactivation of p53 and Pten results in anaplastic thyroid carcinomas faithfully recapitulating human tumors.甲状腺细胞特异性失活p53和Pten会导致间变性甲状腺癌,忠实地重现人类肿瘤。
Oncotarget. 2011 Dec;2(12):1109-26. doi: 10.18632/oncotarget.380.
8
Activation of the RAS/RAF/ERK signaling pathway contributes to resistance to sunitinib in thyroid carcinoma cell lines.RAS/RAF/ERK 信号通路的激活导致甲状腺癌细胞系对舒尼替尼产生耐药性。
J Clin Endocrinol Metab. 2012 Jun;97(6):E898-906. doi: 10.1210/jc.2011-3269. Epub 2012 Mar 22.
9
Creation and characterization of a doxycycline-inducible mouse model of thyroid-targeted RET/PTC1 oncogene and luciferase reporter gene coexpression.强力霉素诱导的甲状腺靶向RET/PTC1癌基因和荧光素酶报告基因共表达小鼠模型的构建与鉴定
Thyroid. 2007 Dec;17(12):1181-8. doi: 10.1089/thy.2007.0224.
10
Inhibitors of Raf kinase activity block growth of thyroid cancer cells with RET/PTC or BRAF mutations in vitro and in vivo.Raf激酶活性抑制剂在体外和体内均可阻断具有RET/PTC或BRAF突变的甲状腺癌细胞的生长。
Clin Cancer Res. 2006 Mar 15;12(6):1785-93. doi: 10.1158/1078-0432.CCR-05-1729.

引用本文的文献

1
Development of animal models to study aggressive thyroid cancers.用于研究侵袭性甲状腺癌的动物模型的开发。
Eur Thyroid J. 2025 Feb 10;14(1). doi: 10.1530/ETJ-24-0361. Print 2025 Feb 1.
2
Recommendations on Surveillance for Differentiated Thyroid Carcinoma in Children with PTEN Hamartoma Tumor Syndrome.关于PTEN错构瘤综合征患儿分化型甲状腺癌监测的建议。
Eur Thyroid J. 2020 Sep;9(5):234-242. doi: 10.1159/000508872. Epub 2020 Jul 28.
3
PI3K/mTOR inhibition potentiates and extends palbociclib activity in anaplastic thyroid cancer.PI3K/mTOR 抑制增强并延长了帕博西尼在间变性甲状腺癌中的活性。
Endocr Relat Cancer. 2019 Apr 1;26(4):425-436. doi: 10.1530/ERC-19-0011. Epub 2019 Jan 1.
4
Selective Ablation of Tumor Suppressors in Parafollicular C Cells Elicits Medullary Thyroid Carcinoma.滤泡旁C细胞中肿瘤抑制因子的选择性消融引发甲状腺髓样癌。
J Biol Chem. 2017 Mar 3;292(9):3888-3899. doi: 10.1074/jbc.M116.765727. Epub 2017 Jan 24.
5
Targeting lipid metabolism for the treatment of anaplastic thyroid carcinoma.靶向脂质代谢治疗间变性甲状腺癌。
Expert Opin Ther Targets. 2016;20(2):159-66. doi: 10.1517/14728222.2016.1086341. Epub 2015 Sep 28.
6
Mouse models of thyroid cancer: A 2015 update.甲状腺癌小鼠模型:2015年更新
Mol Cell Endocrinol. 2016 Feb 5;421:18-27. doi: 10.1016/j.mce.2015.06.029. Epub 2015 Jun 27.

本文引用的文献

1
Synergistic signaling of KRAS and thyroid hormone receptor β mutants promotes undifferentiated thyroid cancer through MYC up-regulation.KRAS与甲状腺激素受体β突变体的协同信号传导通过上调MYC促进未分化甲状腺癌。
Neoplasia. 2014 Sep;16(9):757-69. doi: 10.1016/j.neo.2014.08.003.
2
Update on anaplastic thyroid carcinoma: morphological, molecular, and genetic features of the most aggressive thyroid cancer.甲状腺未分化癌的研究进展:最具侵袭性的甲状腺癌的形态学、分子和遗传学特征。
Int J Endocrinol. 2014;2014:790834. doi: 10.1155/2014/790834. Epub 2014 Aug 21.
3
Anaplastic Thyroid Carcinoma: Current Treatments and Potential New Therapeutic Options with Emphasis on TfR1/CD71.间变性甲状腺癌:当前的治疗方法和潜在的新治疗选择,重点是 TfR1/CD71。
Int J Endocrinol. 2014;2014:685396. doi: 10.1155/2014/685396. Epub 2014 Jul 1.
4
Targeting RAS-MAPK-ERK and PI3K-AKT-mTOR signal transduction pathways to chemosensitize anaplastic thyroid carcinoma.针对 RAS-MAPK-ERK 和 PI3K-AKT-mTOR 信号转导通路提高间变性甲状腺癌化疗敏感性。
Transl Res. 2014 Nov;164(5):411-23. doi: 10.1016/j.trsl.2014.06.005. Epub 2014 Jun 23.
5
Obatoclax overcomes resistance to cell death in aggressive thyroid carcinomas by countering Bcl2a1 and Mcl1 overexpression.奥巴托克斯通过对抗Bcl2a1和Mcl1的过表达克服侵袭性甲状腺癌对细胞死亡的抗性。
Endocr Relat Cancer. 2014 Oct;21(5):755-67. doi: 10.1530/ERC-14-0268. Epub 2014 Jul 10.
6
Thyroid-stimulating hormone, thyroglobulin, and thyroid hormones and risk of differentiated thyroid carcinoma: the EPIC study.促甲状腺激素、甲状腺球蛋白、甲状腺激素与分化型甲状腺癌风险:EPIC 研究。
J Natl Cancer Inst. 2014 Jun;106(6):dju097. doi: 10.1093/jnci/dju097.
7
Activating BRAF and PIK3CA mutations cooperate to promote anaplastic thyroid carcinogenesis.激活BRAF和PIK3CA突变协同促进间变性甲状腺癌发生。
Mol Cancer Res. 2014 Jul;12(7):979-86. doi: 10.1158/1541-7786.MCR-14-0158-T. Epub 2014 Apr 25.
8
p53 constrains progression to anaplastic thyroid carcinoma in a Braf-mutant mouse model of papillary thyroid cancer.p53 限制了 BRAF 突变型甲状腺乳头状癌小鼠模型向间变性甲状腺癌的进展。
Proc Natl Acad Sci U S A. 2014 Apr 22;111(16):E1600-9. doi: 10.1073/pnas.1404357111. Epub 2014 Apr 7.
9
Mechanism and consequences of RAF kinase activation by small-molecule inhibitors.小分子抑制剂激活RAF激酶的机制及后果
Br J Cancer. 2014 Aug 12;111(4):640-5. doi: 10.1038/bjc.2014.139. Epub 2014 Mar 18.
10
Blocks to thyroid cancer cell apoptosis can be overcome by inhibition of the MAPK and PI3K/AKT pathways.通过抑制丝裂原活化蛋白激酶(MAPK)和磷脂酰肌醇-3激酶/蛋白激酶B(PI3K/AKT)信号通路,可以克服甲状腺癌细胞凋亡的障碍。
Cell Death Dis. 2014 Mar 6;5(3):e1104. doi: 10.1038/cddis.2014.78.