( roof of the principlefor the therapeut...)Introgen's Advexin Demonstrates Clinical Benefit in Inherited,Cancer,Health

roof of the principle for the therapeutic application of targeted ADVEXIN therapy in tumors with p53 abnormalities that are among the most common and fundamental molecular defects in cancer," said Neil Senzer, M.D., Scientific Director, Mary Crowley Medical Research Center, and lead author of the article. "ADVEXIN's mechanism of action is targeted to restoring p53 tumor suppressor function that is abnormal in Li-Fraumeni tumors and in many other types of cancer."

ADVEXIN is being developed for European markets by Gendux AB, a subsidiary of Introgen Therapeutics, Inc. The European Medicines Agency (EMEA) has designated, and the European Union has confirmed, ADVEXIN p53 therapy as an Orphan Drug for the treatment of LFS. A Letter of Intent to the EMEA regarding Marketing Authorization Application for the approval of ADVEXIN to treat LFS was filed under the Exceptional Circumstances Approval procedures in the EU.

Collaborators on this publication included clinicians from Mary Crowley Medical Research Center, Sammons Cancer Center, Baylor University Medical Center, The Royal Marsden Hospital NHS Foundation Trust, Imperial College London Hammersmith Campus, and the Institute of Cancer Research in the United Kingdom.

About Li-Fraumeni Syndrome

Approximately 400 families are affected by LFS annually. The majority of LFS families contain mutations in the p53 tumor suppressor gene. Affected individuals often develop multiple primary tumors, which typically occur at a young age. Conventional therapy of patients with the Li-Fraumeni Syndrome is frequently unsuccessful due to the occurrence of multiple malignancies that share a common p53 genetic defect fundamental to cancer progression and the development of treatment resistance. Defects in p53-mediated cell death pathways cause these tumors to develop resistance to standard therapy, resulting in early death. Additionally, because affected individuals lack p53-mediated DNA repair function, treatment
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