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Updated: Jun 16, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
Potential for functional redundancy in EGF and TGFalpha signaling in desmoid cells: a cDNA microarray analysis
Sylvia H Trang1, David E Joyner, Timothy A Damron
1SARC Laboratory, Sarcoma Services, Department of Orthopaedics and Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA.
Abstract:
Genes that replace or duplicate the function of other genes are considered functionally redundant. In this cDNA microarray study, using an Agilent microarray platform and GeneSifter analysis software, we evaluated (1) the degree of downstream transcriptional redundancy and (2) the level of genetic uniqueness apparent in desmoid tumor cells stimulated in vitro for 3 h or for 24 h with 100 ng/ml of exogenous recombinant human EGF (rhEGF) or with recombinant human transforming growth factor alpha (rhTGFalpha). Our intent was to identify genes costimulated, or genes unique to, desmoid cells stimulated in vitro with rhEGF and rhTGFalpha. This experimental approach demonstrated a 55% transcriptional redundancy in the number of desmoid genes significantly upregulated or downregulated following 3 h of stimulation with rhEGF or with rhTGFalpha, and a 65% transcriptional redundancy following 24 h of growth factor stimulation. Approximately 150 genes costimulated by rhEGF and rhTGFalpha were identified. This study suggests that EGF and TGFalpha retain some level of functional redundancy, possibly resulting from their divergence from a common ancestral gene.
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