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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
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