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Molecular Pathogenesis Laboratory, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, and Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892
Address all correspondence and requests for reprints to: Alexander O. Vortmeyer, Molecular Pathogenesis Laboratory, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Building 10, Room 5D37, 10 Center Drive, Bethesda, Maryland 20892. E-mail: vortmeyera{at}ninds.nih.gov.
The histogenesis of pancreatic islet cell tumors was investigated by morphological identification of putative precursor lesions in pancreatic tissue from patients with multiple endocrine neoplasia type 1 (MEN1), tissue microdissection, and genetic analysis. MEN1 mutation and absence of the MEN1 wild-type allele in different precursor lesions strongly suggest that pancreatic islet cell tumors are derived from the ductal/acinar system but not from pancreatic islet tissue. Pluripotent cells within the exocrine pancreas appear capable of formation into small atypical accumulations of MEN1-deficient cells with both exocrine and endocrine phenotype. The findings suggest presence of multiple developmental aberrations in MEN1 pancreas that potentially serve as precursor material for neuroendocrine tumors.
Abbreviations: A1–A4, Atypical structure types 1–4; HE, hematoxylin and eosin; I, structures morphologically consistent with islets; LOH, loss of heterozygosity; MEN1, multiple endocrine neoplasia type 1; N, structures morphologically consistent with normal exocrine pancreas; T, structures consistent with neuroendocrine islet cell tumor.
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