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(American Journal of Pathology. 2000;157:1431-1438.)
© 2000 American Society for Investigative Pathology

Short Communications

Genomic Alterations in Well-Differentiated Gastrointestinal and Bronchial Neuroendocrine Tumors (Carcinoids)

Marked Differences Indicating Diversity in Molecular Pathogenesis

Jianming Zhao^*, Roland R. de Krijger, Dorette Meier^*, Ernst-Jan M. Speel^*, Parvin Saremaslani^*, Seraina Muletta-Feurer^*, Claudia Matter^*, Jürgen Roth, Philipp U. Heitz^* and Paul Komminoth^*

From the Department of Pathology^*
and the Division of Cell and Molecular Pathology,
University of Zurich, Zurich, Switzerland; and the Institute of Pathology,
University of Rotterdam, The Netherlands

Neuroendocrine tumors (carcinoids) are a heterogeneous group of neoplasms arising from the diffuse neuroendocrine system. Genetic changes underlying their tumorigenesis are primarily unknown. We used comparative genomic hybridization to screen 32 well-differentiated neuroendocrine tumors (21 gastrointestinal and 11 bronchial) and three associated metastases for genomic alterations. There were striking differences of genomic imbalances between the two subgroups of neuroendocrine tumors. Losses of chromosome 18q and 18p were shown in eight (38%) and seven (33%), respectively, out of 21 gastrointestinal tumors and in none of the 11 bronchial tumors. Conversely, deletions of 11q occurred in four of 11 (36%) bronchial tumors but only in one gastrointestinal tumor. These comparative genomic hybridization findings were confirmed by interphase cytogenetics. Our data indicate that neuroendocrine tumors of the two subgroups develop via different molecular pathways. Inactivation of one or several tumor suppressor genes on chromosome 18 may be important for the biological behavior of gastrointestinal tumors, whereas gene inactivation on 11q seems to be associated with tumor development of the bronchi.

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