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Sie sind hier: FRIAS School of Life Sciences … Wissenschaftliche … Amor Hajri

Amor Hajri

Tumor cell biology and animal tumor models in preclinical oncology
Institute of Biology III
Senior scientist with Junior Fellow Katja Arndt

    CV

    Dr. Hajri Amor completed his Diploma of clinical Biology in the Faculty of Medicine –Tunis. Thereafter, he continued his education in France in Strasbourg at the University of Louis Pasteur where he obtained in 1986 his Master of Biochemistry and Molecular/cellular biology. In 1987, he received his Postgraduate Degree “Molecular and Cellular Pharmacology” and in 1992, he received his PhD “Pharmacology/ Oncology” from the faculty of Pharmacy at the university of Louis Pasteur. After post-doc experience, “Sandoz/Basel-INSERM U61/Strasbourg” (1993-1994), he joined the digestive cancer research institute where he developed his own research laboratory. He is a membership of European Pancreatic Club, American Society of Gene Therapy, secretary of French club of pancreas and he is a reviewer of the editorial review board of many cancer and gene therapy journals. In April 2009, Dr. Hajri Amor joined the group of Dr. Katja Arndt as “senior scientist”.

     

    FRIAS Project

    The transcription factors promote cancer development, cell survival and proliferation, and induce tumor angiogenesis. Associated with this is the fact that they mediate signals coming from multiple different pathways, hence inhibiting their function will likely interfere with the function of numerous signaling molecules. The main objective of our project is to investigate the role of AP-1 in controlling proliferative signal transduction pathways in tumor cell growth using proteome and transcriptome analysis. In parallel, our aim is to explore new approaches to specifically inhibit AP-1/Fos-Jun transcription factors in cancer in order to validate them as a specific drug targets. In this perspective, we will characterize the mechanisms of inhibition and evaluate the antitumor effect of different AP-1 peptide inhibitors designed and developed in the laboratory of Dr Arndt K. These peptides that specifically bind the oncogenic transcription factors c-Jun, c-Fos and c-Myc, compete not only with the native protein-protein interaction but also with the DNA binding. They are hence able to inhibit the expression of target specific gene expression related to tumor progression and invasion; and thus could be a promising agents for cancer therapy. Ultimately, our challenge will be the delivery of these AP1inhibitors and tumor targeting. The current translational research project involves an expertise in experimental oncology using in vitro cell cultures and in vivo tumor xenograft models (ectopic, orthotopic and metastatic).

     

    Selected Publications

    1. S. Réjiba, L.H. Reddy, C. Bigand, C. Parmentier, P. Couvreur, A. Hajri: Squalenoyl gemcitabine nanomedicine overcomes the low efficacy of gemcitabine therapy in pancreatic cancer Nanomedicine-uk, 2011 (in Druck)
    2. S. RÉJIBA, C. PARMENTIER, C. BIGAND, A. HAJRI (2009) Gemcitabin-based  chemogene therapy of pancreatic cancer using Ad-dCK::UMK GDEPT and TS/RRM2 siRNAs strategies, Neoplasia, 11, 637-650
    3. AL. ANGELOVA, M. APRAHAMIAN, SP. GREKOVA, A. HAJRI, B. LEUCHS, NA. GIESE, C. DINSART, A. HERRMANN, J. ROMMELAERE, Z,. RAYKOV (2009) Improvement of Gemcitabine-Based Therapy of Pancreatic Carcinoma by Means of Oncolytic Parvovirus H-1PV, Clin Cancer Res, 15, 511-519
    4. S. WACK, S. RÉJIBA, M. APRAHAMIAN, A. HAJRI (2008) Telomerase transcriptional targeting of inducible Bax/TRAIL gene therapy improves gemcitabine treatment of pancreatic cancer, Mol Ther., 16, 252-260
    5. S. RÉJIBA, S. WACK, M. APRAHAMIAN, A. HAJRI (2007) K-ras oncogene silencing strategy reduces tumor growth and enhances gemcitabine chemotherpay efficiancy for pancreatic cancer treatment, Cancer Sci., 98, 1128-1136
    6. S. DEHARVENGT, S. WACK, M. APRAHAMIAN, A. HAJRI (2005) Transcriptional tumor-selective promoter targeting of E. coli purine nucleoside phosphorylase for pancreatic cancer suicide gene therapy, J Gene Med, 7, 672-680
    7. S. DEHARVENGT, S. WACK, M. UHRING, M. APRAHAMIAN, A. HAJRI (2004) Suicide gene produg therapy for pancreatic adenocarcinoma by E. Coli purine nucleoside phosphorylase and 6-methylpurine 2´-deoxyriboside, Pancreas, 28(2), E54-64
    8. A. HAJRI, S. WACK, P. LEHN, JP. VIGNERON, JM. LEHN, M. APRAHAMIAN (2004) Combined suicide gene therapy for pancreatic peritoneal carcinomatosis using BGTC liposomes, Cancer Gene Ther., 11(1), 16-27