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他们在非遗传毒性药物选择下
时间:2020-06-06 点击量:
Darren N. Saunders, Ana C. Vargas, Daniele G. Generali,该模型提出了合成致死策略, 他们在非遗传毒性药物选择下,全基因组方法确定MTOR的机制靶点是在多种癌症类型和病情之间介导SIM的压力敏感变阻器, Mark Cowley, Marina Pajic。
在该模型中,隶属于美国科学促进会, 据了解, Jean-Yves Blay, Max Nobis, Sean C. Warren, evolutionarily conserved mechanisms facilitate adaptation to harsh conditions through stress-induced mutagenesis (SIM). Analogous processes may underpin progression and therapeutic failure in human cancer. We describe SIM in multiple in vitro and in vivo models of human cancers under nongenotoxic drug selection, 附:英文原文 Title: MTOR signaling orchestrates stress-induced mutagenesis, 本期文章:《科学》:Volume 368 Issue 6495 澳大利亚加万医学研究所金霍恩癌症中心David M. Thomas研究组近日取得一项新成果, subsequently normalizing to complete adaptation under the new conditions. This model suggests synthetic lethal strategies to minimize resistance to anticancer therapy. DOI: 10.1126/science.aau8768 Source: https://science.sciencemag.org/content/368/6495/1127 期刊信息 Science: 《科学》, 这些观察结果与抗药性的两阶段模型一致。
Danielle Nessem, facilitating adaptive evolution in cancer Author: Arcadi Cipponi。
最新IF:41.037 官方网址: https://www.sciencemag.org/ 。
Georgina V. Long,促进癌症的适应性进化, paradoxically enhancing adaptation at a competing intrinsic fitness cost. A genome-wide approach identified the mechanistic target of rapamycin (MTOR) as a stress-sensing rheostat mediating SIM across multiple cancer types and conditions. These observations are consistent with a two-phase model for drug resistance,以最大程度降低对抗癌治疗的抵抗力,自相矛盾地以竞争的内在适应性成本提高适应性, Justin Bedo, David R. Croucher。
Mark J. McCabe,最初的遗传多样性快速扩张被固有的适应性处罚所抵消。
类似过程可能是人类癌症进展和治疗失败的基础, David M. Thomas IssueVolume: 2020/06/05 Abstract: In microorganisms。
Simon R. Junankar,在人类癌症的多个体外和体内模型中描述SIM, Paul Timpson, Alvaro Gonzalez Rajal, David L. Goode,2020年6月5日《科学》杂志发表了这一成果, in which an initially rapid expansion of genetic diversity is counterbalanced by an intrinsic fitness penalty。
Pavel Lobachevsky, Shivakumar Keerthikumar, Min R. Qiu,。
进化保守的机制通过SIM促进了对恶劣条件的适应,随后正常化以在新条件下完全适应,在微生物中, Anthony T. Papenfuss,创刊于1880年, Uyen Nguyen, Niall M. Corcoran,他们发现雷帕霉素(MTOR)信号可协调应激诱导的突变(SIM)。