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注册报告:肿瘤微环境通过分泌肝细胞生长因子引发对RAF抑制剂的固有抗性。

Registered report: Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion.

作者信息

Blum David, LaBarge Samuel

机构信息

Bioexpression and Fermentation Facility, University of Georgia, Athens, United States.

City of Hope, Duarte, United States.

出版信息

Elife. 2014 Dec 10;3:e04034. doi: 10.7554/eLife.04034.

Abstract

The Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by conducting replications of 50 papers in the field of cancer biology published between 2010 and 2012. This Registered Report describes the proposed replication plan of key experiments from "Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion" by Straussman and colleagues, published in Nature in 2012 (Straussman et al., 2012). The key experiments being replicated in this study are from Figure 2A, C, and D (and Supplemental Figure 11) and Figure 4C (and Supplemental Figure 19) (Straussman et al., 2012). Figure 2 demonstrates resistance to drug sensitivity conferred by co-culture with some stromal cell lines and identifies the secreted factor responsible as HGF. In Figure 4, Straussman and colleagues show that blocking the HGF receptor MET abrogates HGF’s rescue of drug sensitivity. The Reproducibility Project: Cancer Biology is a collaboration between the Center for Open Science and Science Exchange, and the results of the replications will be published by eLife.

摘要

癌症生物学可重复性项目旨在通过对2010年至2012年间发表的癌症生物学领域50篇论文进行重复实验,来回应人们对科研可重复性日益增长的担忧。本注册报告描述了对施特劳斯曼及其同事于2012年发表在《自然》杂志上的论文《肿瘤微环境通过分泌HGF引发对RAF抑制剂的天然抗性》中关键实验的拟重复计划(施特劳斯曼等人,2012年)。本研究中要重复的关键实验来自图2A、C和D(以及补充图11)和图4C(以及补充图19)(施特劳斯曼等人,2012年)。图2展示了与某些基质细胞系共培养所赋予的对药物敏感性的抗性,并确定所分泌的因子为HGF。在图4中,施特劳斯曼及其同事表明,阻断HGF受体MET可消除HGF对药物敏感性的挽救作用。癌症生物学可重复性项目是开放科学中心和科学交流中心之间的合作项目,重复实验的结果将由《eLife》杂志发表。

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