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An Open-Label Randomized Phase III Study of Intermittent Oral Capecitabine in Combination with Intravenous Oxaliplatin (Q3W) (“XELOX”) versus Bolus and Continuous Infusion Fluorouracil/Intravenous Leucovorin with Intravenous Oxaliplatin (Q2W) (“FOLFOX4”) as Treatment for Patients with Metastatic Colorectal Cancer who have Received Prior Treatment with CPT- 11 in Combination with 5-FU/LV as First L...

ABSTRACT: Primary objectives: To demonstrate that the combination of capecitabine plus oxaliplatin ("XELOX") is at least equivalent to the combination of 5-fluorouracil plus leucovorin plus oxaliplatin ("FOLFOX-4”) in terms of time to tumor progression or death (TTP) in patients with metastatic colorectal carcinoma who have received prior treatment with CPT-11 in combination with 5-FU as first line therapy. Primary endpoints: At least equivalence with respect time to tumor progression or death (TTP).

PROVIDER: 2515885 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description:RNA-binding proteins (RBPs) facilitate post-transcriptional control of eukaryotic gene expression at multiple levels. The RBP tristetraprolin (TTP/Zfp36) is a signal-induced phosphorylated anti-inflammatory protein guiding unstable mRNAs of pro-inflammatory proteins for degradation and preventing translation. Using iCLIP, we have identified numerous mRNA targets bound by wild-type TTP and by a non-MK2-phosphorylatable TTP mutant (TTP-AA) in 1h LPS-stimulated macrophages and correlated their interaction with TTP to changes at the level of mRNA abundance and translation in a transcriptome-wide manner. The close similarity of the transcriptome of TTP-deficient and TTP-expressing macrophages upon short LPS stimulation suggested an effective inactivation of TTP by MK2 under these conditions whereas retained RNA-binding capacity of TTP-AA to 3’UTRs caused profound changes in the transcriptome and translatome, altered NF-κB-activation and induced cell death. Increased TTP binding to the 3'UTR of feedback inhibitor mRNAs, such as Ier3, Dusp1 or Tnfaip3, in the absence of MK2-dependent TTP neutralization resulted in a strong reduction of their protein synthesis contributing to the deregulation of the NF-κB-signaling pathway. Taken together, our study uncovers a role for TTP in NF-κB-signaling and highlights the importance of fine-tuned TTP activity-regulation by MK2 in order to control feedback signaling during the inflammatory response.

2016-05-25 | GSE81249 | GEO