HISTOLOGY AND HISTOPATHOLOGY

Cellular and Molecular Biology

Review

Apoptosis regulating genes in neuroendocrine tumors

W-H. Liu1 and D-G. Wang2

1The Schepens Eye Research Institute and the Department of Ophthalmology, Harvard Medical School, Boston, and 2Center for Molecular Medicine, School of Medicine, University of Connecticut Health Center, Farmington, USA

Offprint requests to: Dr Da-Gong Wang, M.D., Ph.D. Center for Molecular Medicine, School of Medicine, The University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3101. USA.

 

Summary. Neuroendocrine tumors (NETs) are a heterogeneous group of neoplasms. They are relatively uncommon and characterised by a relatively indolent clinical course. The indolent nature of NETs has long been enigmatic and recent advances in apoptosis research have led to speculation regarding the role of programmed cell death in NET tumorigenesis. It is hoped that a fundamental molecular understanding will help explain these variant behaviors that are so evident to the clinician, and ultimately yield novel and more effective therapies.
Recent studies have demonstrated that deregulation of programmed cell death may be a critical component in the multistep tumorigenesis of NETs and that the frequent expression of the BCL-2 oncoprotein in these tumors may contribute to their pathogenesis. The genetic complementation of simultaneously deregulated BCL-2 and c-MYC may be implicated in the multistep tumorigenesis of human NETs. It is also clear that numerous cellular gene products can and will be shown to impact upon apoptosis in NETs; some of these may even be molecules identified as oncoproteins or tumor suppressors. The major challenge will be to ascribe primary pathogenetic significance to tumor-associated derangements in expression of these molecules, and hopefully to then exploit our knowledge toward therapeutic benefit. Histol. Histopathol. 15, 851-859 (2000)

Key words: Neuroendocrine tumor, Apoptosis, Tumorigenesis

DOI: 10.14670/HH-15.851