Version 1
: Received: 1 February 2018 / Approved: 2 February 2018 / Online: 2 February 2018 (06:57:47 CET)
How to cite:
Cintas, C.; Douche, T.; Guillermet-Guibert, J. Opportunities and Resistance to Signal-Targeted Therapies in Pancreatic Cancer: What Can we Learn from Proteomic Studies?. Preprints2018, 2018020013. https://doi.org/10.20944/preprints201802.0013.v1
Cintas, C.; Douche, T.; Guillermet-Guibert, J. Opportunities and Resistance to Signal-Targeted Therapies in Pancreatic Cancer: What Can we Learn from Proteomic Studies?. Preprints 2018, 2018020013. https://doi.org/10.20944/preprints201802.0013.v1
Cintas, C.; Douche, T.; Guillermet-Guibert, J. Opportunities and Resistance to Signal-Targeted Therapies in Pancreatic Cancer: What Can we Learn from Proteomic Studies?. Preprints2018, 2018020013. https://doi.org/10.20944/preprints201802.0013.v1
APA Style
Cintas, C., Douche, T., & Guillermet-Guibert, J. (2018). Opportunities and Resistance to Signal-Targeted Therapies in Pancreatic Cancer: What Can we Learn from Proteomic Studies?. Preprints. https://doi.org/10.20944/preprints201802.0013.v1
Chicago/Turabian Style
Cintas, C., Thibaut Douche and Julie Guillermet-Guibert. 2018 "Opportunities and Resistance to Signal-Targeted Therapies in Pancreatic Cancer: What Can we Learn from Proteomic Studies?" Preprints. https://doi.org/10.20944/preprints201802.0013.v1
Abstract
In metastatic pancreatic cancer patients non eligible to surgery, signal-targeted therapies so far failed to show a significant amelioration of survival. These therapeutic options were tested in Phase II/III clinical trials mostly in combination with the reference treatment Gemcitabine. These innovative therapies aim at annihilating the oncogene dependency; they also aim at renormalizing the tumoral stroma to allow immune cell function or re-vascularisation. Transcriptomics and genomics large scale analysis show the great heterogeneity of pancreatic cancers and failed to clearly delineate specific oncogene dependency besides oncogenic Kras. In this review, we will describe the most recent proteomic data in pancreatic tumors and its metastasis, which could help at identifying their major signalling dependencies, as well as explain why they are intrinsically resistant to signal-targeted therapies. We will also discuss why PI3K signalling, as a paradigm of pro-tumorigenic cell signalling and of tumoral adaptative resistance to drugs, is a relevant target in this context.
Medicine and Pharmacology, Oncology and Oncogenics
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
