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Type I collagen deletion in αSMA myofibroblasts augments immune suppression and accelerates progression of pancreatic cancer.Ⅰ型胶原在 αSMA 肌成纤维细胞中的缺失增强了免疫抑制作用,并加速了胰腺癌的进展。
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基于双重组酶的小鼠模型有助于解析癌症生物学和治疗靶点。

Dual Recombinase-Based Mouse Models Help Decipher Cancer Biology and Targets for Therapy.

机构信息

Division of Translational Cancer Research, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany.

Chair of Translational Cancer Research and Institute of Experimental Cancer Therapy, Klinikum rechts der Isar, School of Medicine, Technische Universität München, Munich, Germany.

出版信息

Cancer Res. 2023 Jul 14;83(14):2279-2282. doi: 10.1158/0008-5472.CAN-22-2119.

DOI:10.1158/0008-5472.CAN-22-2119
PMID:37449355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10351565/
Abstract

The advent of next-generation sequencing (NGS) and single-cell profiling technologies has revealed the complex and heterogenous ecosystem of human tumors under steady-state and therapeutic perturbation. Breakthroughs in the development of genetically engineered mouse models (GEMM) of human cancers that are based on the combination of two site-specific recombinase systems [dual-recombinase system (DRS)] offer fundamental new possibilities to elucidate and understand critical drivers of the diverse tumor phenotypes and validate potential targets for therapy. Here, we discuss opportunities DRS-based cancer GEMMs offer to model, trace, manipulate, and functionally investigate established cancers, their interactions with the host, and their response to therapy.

摘要

下一代测序 (NGS) 和单细胞分析技术的出现,揭示了人类肿瘤在稳态和治疗扰动下的复杂和异质生态系统。基于两种位点特异性重组酶系统(双重组酶系统 (DRS))的人类癌症基因工程小鼠模型 (GEMM) 的开发取得了突破,为阐明和理解不同肿瘤表型的关键驱动因素以及验证治疗的潜在靶点提供了基本的新可能性。在这里,我们讨论了基于 DRS 的癌症 GEMM 在模拟、跟踪、操作和功能研究已建立的癌症、它们与宿主的相互作用以及它们对治疗的反应方面提供的机会。