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EMD 525797 in Combination With Cetuximab and Irinotecan in K-ras Wild Type Metastatic Colorectal Cancer

ABSTRACT: The purpose of this study is to assess the safety and clinical activity of the experimental drug EMD 525797 (study drug), a monoclonal antibody targeting alfa integrins, in combination with irinotecan and cetuximab in K-ras wildtype metastatic colorectal cancer patients.

DISEASE(S): Metastatic Colorectal Cancer,Colorectal Neoplasms

PROVIDER: 2080397 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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EMD 525797 in combination with Cetuximab and Irinotecan in k-ras Wildtype Metastatic Colorectal Cancer

Project description:Primary objectives: The primary objectives are: • To characterize the safety and tolerability profile of repeated administration of different EMD 525797 dose levels in combination with cetuximab and irinotecan in subjects with k-ras WT mCRC after failure of first-line therapy with an oxaliplatin-containing regimen (Safety Part); • To assess the anti-cancer activity of 2 EMD 525797 doses in terms progression-free survival time in subjects with k-ras WT mCRC after failure of first-line therapy with an oxaliplatin-containing regimen (Randomized Part). Primary endpoints: Safety Part: • To characterize the safety and tolerability profile of repeated administration of different EMD 525797 dose levels in combination with cetuximab and irinotecan in subjects with k-ras WT mCRC after failure of first-line therapy with an oxaliplatin-containing regimen. Randomized Part: • To assess the anti-cancer activity of 2 EMD 525797 doses in terms of progression-free survival time in subjects with k-ras WT mCRC after failure of first-line therapy with an oxaliplatin-containing regimen.

| 2526396 | ecrin-mdr-crc

Comparison between gene expression in heart from Emd KO and control mice

2006-12-02 | GSE6399 | GEO

Transcription profiling of mouse heart from Emd KO and controls

Project description:The present research is devoted to the identification of gene(s) severely affected by EMD mutations, leading to striated muscle laminopathies and more specifically the cardiomyopathy. For this purpose, we developped a large-scale gene expression approach on heart and skeletal tissues from Emd KO mouse model. Experiment Overall Design: In the project presented here we performed differential expression in heart from a mouse model of EDMD: a Emd KO mouse created via homologous recombination by Y.Hayashi in Japan (Ozawa, 2006). The emd knock-out mouse showed significantly delayed PR time, that could correspond to impaired atrial-ventricle node conduction. Genes were identified as differentially expressed if they met a false discovery rate threshold of 0.05 in a two-sample t-test (q-value) and showed at least a two-fold difference in expression independent of absolute signal intensity.

2008-06-14 | E-GEOD-6399 | biostudies-arrayexpress

FLOX + Cetuximab (Erbitux) for Patients With Metastatic Colorectal Cancer and Wild Type K-RAS Tumor

Project description:The Nordic FLOX-regime consists of a combination of bolus 5-FU, leukovorin and oxaliplatin (Eloxatin). Cetuximab (Erbitux) is an antibody against the epidermal growth factor receptor (EGFR). The combination of FLOX and weekly Erbitux has been investigated in the Nordic VII study where 571 patients were randomized to FLOX (regime A) or FLOX + Erbitux (regime B or C). Effect-data has not yet been published but the combination is well tolerated, and other studies have shown that Erbitux administered with chemotherapy seem to be more efficient than chemotherapy alone. The main purpose with this study is to investigate the effect of FLOX and Erbitux given every second week as first line treatment for patients with metastatic colorectal cancer and K-RAS wildtype tumor. The latest accessible data regarding treatment towards EGFR and K-RAS mutations shows that patients with K-RAS wildtype responds better to treatment than patients with K-RAS mutations.

| 2054067 | ecrin-mdr-crc

Modeling the Transcriptional Consequences of Epidermal Growth Factor Receptor Ablation in Ras-Initia

Project description:EGFR targeted therapy is in clinical use to treat squamous cell carcinoma of the head and neck and other cancers of lining epithelium. Activating Ras mutations are a negative prognostic factor for response to EGFR ablation therapy in multiple cancer types. Furthermore, the major adverse consequence of this therapy is an acneiform papulopustular eruption on normal skin. To better understand Ras signaling in an EGFR depleted environment, we performed gene expression profiling on oncogenic Ras transformed and wildtype mouse keratinocytes with EGFR ablated chronically by genetic deletion or acutely by drug treatment. We were able to identify a 25 gene signature specific to the Ras-EGFR ablation interaction and a distinct 19 gene EGFR ablation signature on normal keratinocytes. EGFR ablation in the context of wildtype Ras reduces ontologies favoring cell cycle control and transcription while ablation in the context of oncogenic Ras enriches ontologies for ion channels and membrane transporters, particularly focused on calcium homeostasis. The study showed substantial differences in ontologies between chronic EGFR ablation and acute pharmacological ablation, both with and without Ras activation. Pathway and biochemical analysis indicates that activation of p38α is a response to both acute and chronic abrogation of EGFR signaling under conditions of Ras activation. This was confirmed in oncogenic RAS transformed human keratinocytes and in tumors developing in orthografts of EGFR ablated mouse keratinocytes transformed by oncogenic Ras. EGFR ablation in the absence of oncogenic Ras revealed Erk and IL-1β related pathways. These findings reveal previously unrecognized interactions between Ras and EGFR signaling in squamous tumor cells that could influence the therapeutic response to EGFR ablation therapy.

2012-01-11 | GSE29415 | GEO