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Id Gene Expression as a Key Mediator of Tumor Cell Biology¹

Preuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research Center, Department of Neurological Surgery, School of Medicine, University of California San Francisco, San Francisco, California 94143

² To whom requests for reprints should be addressed, at Preuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research Center, Department of Neurological Surgery, HSE 722, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0520.

Id genes encode members of the helix-loop-helix (HLH) family of transcription factors that inhibit transcription by forming inactive heterodimers with basic HLH (bHLH) proteins. There are four members of the Id gene family recognized in mammals, and the proteins they encode share homology primarily in their HLH domain. bHLH proteins typically form heterodimers with other bHLH proteins, and their basic domain binds to a DNA sequence element, the E-box, activating transcription. Products of Id genes lack the basic DNA binding domain of the bHLH transcription factors, and when they heterodimerize with bHLH proteins, the complexes are inactive. Generally, high levels of Id mRNA are detected in proliferative undifferentiated, embryonal cells and lower levels are detected in well-differentiated, mature, adult tissues. In vitro, these genes are generally expressed at lower levels in cells after the induction of differentiation. Recently, high levels of expression of Id genes have been identified in cell lines derived from a wide variety of different tumors and in tumor tissues as well. These findings suggest that not only the inappropriate proliferation of tumors but also the anaplastic characteristics that contribute to their malignant behavior may be regulated by Id gene expression.

¹ Presented at the "General Motors Cancer Research Foundation Twentieth Annual Scientific Conference: Developmental Biology and Cancer," June 9–10, 1998, Bethesda, MD. This work was supported in part by grants from the Pediatric Brain Tumor Foundation of the United States, the Preuss Foundation, the Betz Foundation, and the Nissen family.

Received 9/18/98. Accepted 2/ 1/99.