Abstract
Carcinoids and neuroendocrine tumors (NETs) are a heterogeneous group of tumors that arise from the neuroendocrine cells of the GI tract, endocrine pancreas, and the respiratory system. NETs remain significantly understudied with respect to molecular mechanisms of pathogenesis, particularly the role of cell fate signaling systems such as Notch. The abundance of literature on the Notch pathway is a testament to its complexity in different cellular environments. Notch receptors can function as oncogenes in some contexts and tumor suppressors in others. The genetic heterogeneity of NETs suggests that to fully understand the roles and the potential therapeutic implications of Notch signaling in NETs, a comprehensive analysis of Notch expression patterns and potential roles across all NET subtypes is required.
Highlights
Notch has been studied for many years in the context of cancer, and over the years, the signaling pathways involved have become clearer
This study demonstrated a similar spectrum of mutant genes as those found in primary tumors, including TP53, RB1, EP300, and Notch, and TSC2, GNAS, KDR, STK11, and APC
Additional complexities arise in the form of transcriptional coactivators and corepressors that bind to Notch intracellular domain (NICD) to regulate gene expression, as a growing body of evidence suggests that Notch behaves as an oncogene or a tumor suppressor depending on cellular context
Summary
University of Texas MD Anderson Cancer Center, USA. Reviewed by: Nelson Shu-Sang Yee, The Pennsylvania State University College of Medicine, USA. Specialty section: This article was submitted to Cancer Molecular Targets and Therapeutics, a section of the journal
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