Registered report: Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion
- PMID: 25490933
- PMCID: PMC4270138
- DOI: 10.7554/eLife.04034
Registered report: Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion
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.
Keywords: RTK inhibitor resistance; Reproducibility Project: Cancer Biology; biochemistry; human; methodology.
Conflict of interest statement
DB: This is a Science Exchange associated lab.
RP:CB: EI, FT and JL are employed by and hold shares in Science Exchange Inc.
The other authors declare that no competing interests exist.
Comment on
-
Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion.Nature. 2012 Jul 26;487(7408):500-4. doi: 10.1038/nature11183. Nature. 2012. PMID: 22763439 Free PMC article.
References
-
- Caenepeel S, Cajulis E, Kendall R, Coxon A, Hughes P. Targeting HGF-mediated resistance to vemurafenib in V600E BRAF mutant melanoma cell lines. 2013 doi: 10.1158/1538-7445.AM2013-3405. Proceedings of the 104th Annual Meeting of the American Association for Cancer Research. Washington, DC. Cancer Res73:Abstract. - DOI
-
- Casbas-Hernandez P, D'Arcy M, Roman-Perez E, Brauer HA, McNaughton K, Miller SM, Chhetri RK, Oldenburg AL, Fleming JM, Amos KD, Makowski L, Troester MA. Role of HGF in epithelial-stromal cell interactions during progression from benign breast disease to ductal carcinoma in situ. Breast Cancer Research. 2013;15:R82. doi: 10.1186/bcr3476. - DOI - PMC - PubMed
-
- Etnyre D, Shambannagari MR, Puri N. Washington, DC: Cancer Research; 2013. Abstract 2078: Synergistic effects of c-Met and BRAF inhibitors and role of c-Met as a therapeutic target in human melanoma. AACR 104th Annual Meeting; 2013.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Research Materials
Miscellaneous
