ArticleThe American journal of pathology2001
Comparative genomic hybridization identifies loss of 18q22-qter as an early and specific event in tumorigenesis of midgut carcinoids.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 154 citations in OpenAlex.
- Composite gangliocytoma/neuroma and neuroendocrine tumor: a clinicopathologic, immunohistochemical, and molecular genetic study of 11 cases.Virchows Archiv : an international journal of pathology · 2026Article
- Molecular alterations in high-grade neuroendocrine tumors of the small intestine.The Journal of pathology · 2026Article
- Characterization of tumor-associated microbiome in multifocal small intestinal neuroendocrine tumors (SI-NETs).ESMO gastrointestinal oncology · 2025Article
- Loss of MBD2 is associated with tumor growth in small intestinal neuroendocrine tumors.Endocrine connections · 2025Article
- Functional Copy-Number Alterations as Diagnostic and Prognostic Biomarkers in Neuroendocrine Tumors.International journal of molecular sciences · 2024Article
- Molecular Classification of Gastrointestinal and Pancreatic Neuroendocrine Neoplasms: Are We Ready for That?Endocrine pathology · 2024Review
- Multifaceted modeling of small intestinal neuroendocrine tumors.Endocrine oncology (Bristol, England) · 2024Review
- Neuroendocrine Tumors: Genomics and Molecular Biomarkers with a Focus on Metastatic Disease.Cancers · 2023Review
- Multiomic sequencing of paired primary and metastatic small bowel carcinoids.F1000Research · 2023Article
- Fortuitous discovery of an early neuroendocrine tumor during appendicular peritonitis.Annals of medicine and surgery (2012) · 2022Article
- Molecular factors, diagnosis and management of gastrointestinal tract neuroendocrine tumors: An update.World journal of clinical cases · 2022Review
- Whole genome sequencing reveals the independent clonal origin of multifocal ileal neuroendocrine tumors.Genome medicine · 2022Article
- New insights in diagnosis and treatment of gastroenteropancreatic neuroendocrine neoplasms.World journal of gastroenterology · 2022Review
- A Well-Differentiated Grade-3 Neuroendocrine Tumor in the Ascending Colon: A Case Report.The American journal of case reports · 2022Article
- Case Report: Precision genetic diagnosis in a case of Dyggve-Melchior-Clausen syndrome reveals paternal isodisomy and heterodisomy of chromosome 18 with imprinting clinical implications.Frontiers in genetics · 2022Article
- Gastrin: From Physiology to Gastrointestinal Malignancies.Function (Oxford, England) · 2022Review
- EZH2 presents a therapeutic target for neuroendocrine tumors of the small intestine.Scientific reports · 2021Article
- Molecular Pathology of Well-Differentiated Gastro-entero-pancreatic Neuroendocrine Tumors.Endocrine pathology · 2021Review
- Proteomics identifies neddylation as a potential therapy target in small intestinal neuroendocrine tumors.Oncogene · 2019Article
- Clinical applications of (epi)genetics in gastroenteropancreatic neuroendocrine neoplasms: Moving towards liquid biopsies.Reviews in endocrine & metabolic disorders · 2019Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carcinoid tumors are rare neuroendocrine tumors occurring in the lung or in the digestive tract where they are further subclassified as foregut, midgut, or hindgut carcinoids. To gain a better understanding of the genetic basis of the different types of carcinoid tumors, we have characterized numerical imbalances in a series of midgut carcinoids, and compared the results to previous findings in carcinoids from the lung. Numerical imbalances were revealed in 16 of the 18 tumors, and the most commonly detected aberrations were losses of 18q22-qter (67%), 11q22-q23 (33%), and 16q21-qter (22%), and gain of 4p14-qter (22%). The total number of alterations found in the metastases was significantly higher than in the primary tumors, indicating the accumulation of acquired genetic changes in the tumor progression. Losses of 18q and 11q were present both in primary tumors and metastases, whereas loss of 16q and gain of 4 were only detected in metastases. Furthermore, the pattern of comparative genomic hybridization alterations varied depending on the total number of detected alterations. Taken together, the findings would suggest a progression of numerical imbalances, in which loss of 18q and 11q represent early events, and loss of 16q and gain of 4p are late events in the tumor progression of midgut carcinoids. When compared to previously published comparative genomic hybridization abnormalities in lung carcinoids, loss of 11q was found to occur in both tumor types, whereas loss of 18q and 16q and gain of 4 were not revealed in lung carcinoids. The results indicate that inactivation of a putative tumor suppressor gene in 18q22-qter represents a frequent and early event that is specific for the development of midgut carcinoids.
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