The Preston Robert Tisch Brain Tumor Center at Duke
BTC : Gene Contributes to Brain Development and Cancer
Posted by wickr001 on 2004/2/21 18:59:00 (73558 reads)


Article by Jill Boy, Director of Communications,
Duke Comprehensive Cancer Center

A gene that is normally silenced after contributing to brain development was found to be expressed in cells from medulloblastoma, the most common form of pediatric brain malignancy in children. This study was reported in the February 1 issue of Cancer Research.

From left:
Shaoxi Liao, MD, PhD
Daniel Broderick
Qun Shi
Hai Yan, MD, PhD
David Cory Adamson, MD, PhD Karen Hunt
Chunhui Di

In their study, scientists discovered that multiple extra copies of the gene, called OTX2, had been switched back on among tumor cells removed from patients with medulloblastoma brain tumors. In the United States, medulloblastoma accounts for approximately 30 percent of all pediatric brain tumors.

Further, the scientists discovered that a potent derivative of Vitamin A, known as all trans-retinoic acid or ATRA, suppressed growth and induced cell death among the OTX2-laden tumor cells. More than half of medulloblastomas grown in the laboratory responded to ATRA treatment.

“The response that ATRA imposes upon these medulloblastoma brain tumor cell lines suggests that this type of tumor may respond favorably to ATRA-based therapy,” said Hai Yan, MD., Ph.D., the principle investigator of the study at the Brain Tumor Center at Duke University Medical Center.

“ATRA is already clinically approved for the treatment of acute promyelocytic leukemia. These studies lay the conceptual and practical framework for clinical trials using ATRA in the treatment of a commonly lethal pediatric disease.”

Among the researchers working with Yan to investigate the OTX2 gene in medulloblastomas were, Chunhui Di, Shaoxi Liao M.D, Ph.D, David C. Adamson, M.D., Ph.D., Timothy J. Parrett, M.D., Daniel K. Broderick, Qun Shi, Roger E. McLendon, M.D., and Darell D. Bigner, M.D., Ph.D. from the Brain Tumor Center, Department of Pathology, Duke University Medical Center, Durham, N.C.; Christoph Lengauer, Ph.D., Jordan M. Cummins, and Victor E.Velculescu, M.D., Ph.D. from The Johns Hopkins University Medical Institutions, Baltimore, Md.; and Daniel W. Fults, M.D. from the University of Utah School of Medicine, Salt Lake City, Utah.

This project is supported by The Pediatric Brain Tumor Foundation Institute at Duke, the Duke Brain Tumor SPORE grant, Duke Comprehensive Cancer Center Support Grant, NIH Grants, American Brain Tumor Association, Neurosurgery Research Education Foundation, and grants from the Accelerate Brain Tumor Cure Foundation and National Cancer Center.

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