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, Paul Komminoth

Onderzoeksoutput: Bijdrage aan tijdschriftArtikelpeer review

98 Citaten (Scopus)

Samenvatting

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 welldifferentiated 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.

Originele taal-2Engels
Pagina's (van-tot)1431-1438
Aantal pagina's8
TijdschriftAmerican Journal of Pathology
Volume157
Nummer van het tijdschrift5
DOI's
StatusGepubliceerd - 2000
Extern gepubliceerdJa

Vingerafdruk

Duik in de onderzoeksthema's van 'Genomic alterations in well-differentiated gastrointestinal and bronchial neuroendocrine tumors (carcinoids): Marked differences indicating diversity in molecular pathogenesis'. Samen vormen ze een unieke vingerafdruk.

Citeer dit