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Genetic alterations in goblet cell carcinoids of the vermiform appendix and comparison with gastrointestinal carcinoid tumors.
Mod Pathol 2003; 16(12):1189-98MP

Abstract

Goblet cell carcinoid is a relatively rare neuroendocrine tumor of the vermiform appendix with poorly understood molecular pathogenesis. We studied the clinicopathologic features and genetic alterations, including allelic loss of chromosomes 11q, 16q, and 18q; sequencing of the K-ras, beta-catenin, and DPC4 (SMAD4) genes; and p53 overexpression and loss of DPC4 by immunohistochemistry; in 16 goblet cell carcinoids. We compared the allelic loss in goblet cell carcinoids to those in 18 gastrointestinal carcinoid tumors. For goblet cell carcinoids, appendiceal perforation was the most common (70%, 7/10) clinical presentation. The mean tumor size was 2.0 +/- 1.5 cm (range, 0.4 to 4.5 cm). The tumor invaded to appendiceal serosa in 50% (8/16) of patients, and two patients had metastasis in lymph nodes or adjoining viscera. With mean follow-up of 24 +/- 14 months (median, 23 mo), 1 of 10 patients had died of disease, and 2 others had tumor recurrence. All four patients with metastases, recurrences, and/or death from disease had serosal involvement at presentation (P =.02). Loss of heterozygosity of chromosome 11q was present in 25% of goblet cell carcinoids, 14% of ileal carcinoid tumors, and 9% of nonileal carcinoid tumors; of chromosome 16q in 38%, 29%, and 0 (P =.02); and of chromosome 18q in 56%, 86%, and 9% (P =.002), respectively. No mutations of K-ras, beta-catenin, or DPC4 genes; p53 overexpression; or loss of staining for DPC4 was present in any tumors. These findings suggest that allelic loss of chromosomes 11q, 16q, and 18q in goblet cell carcinoids and ileal carcinoids may have an important role in the pathogenesis of these tumors.

Authors+Show Affiliations

Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

14681318

Citation

Stancu, Mirela, et al. "Genetic Alterations in Goblet Cell Carcinoids of the Vermiform Appendix and Comparison With Gastrointestinal Carcinoid Tumors." Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, vol. 16, no. 12, 2003, pp. 1189-98.
Stancu M, Wu TT, Wallace C, et al. Genetic alterations in goblet cell carcinoids of the vermiform appendix and comparison with gastrointestinal carcinoid tumors. Mod Pathol. 2003;16(12):1189-98.
Stancu, M., Wu, T. T., Wallace, C., Houlihan, P. S., Hamilton, S. R., & Rashid, A. (2003). Genetic alterations in goblet cell carcinoids of the vermiform appendix and comparison with gastrointestinal carcinoid tumors. Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 16(12), pp. 1189-98.
Stancu M, et al. Genetic Alterations in Goblet Cell Carcinoids of the Vermiform Appendix and Comparison With Gastrointestinal Carcinoid Tumors. Mod Pathol. 2003;16(12):1189-98. PubMed PMID: 14681318.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Genetic alterations in goblet cell carcinoids of the vermiform appendix and comparison with gastrointestinal carcinoid tumors. AU - Stancu,Mirela, AU - Wu,Tsung-Teh, AU - Wallace,Charita, AU - Houlihan,Patrick S, AU - Hamilton,Stanley R, AU - Rashid,Asif, PY - 2003/12/19/pubmed PY - 2004/7/29/medline PY - 2003/12/19/entrez SP - 1189 EP - 98 JF - Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc JO - Mod. Pathol. VL - 16 IS - 12 N2 - Goblet cell carcinoid is a relatively rare neuroendocrine tumor of the vermiform appendix with poorly understood molecular pathogenesis. We studied the clinicopathologic features and genetic alterations, including allelic loss of chromosomes 11q, 16q, and 18q; sequencing of the K-ras, beta-catenin, and DPC4 (SMAD4) genes; and p53 overexpression and loss of DPC4 by immunohistochemistry; in 16 goblet cell carcinoids. We compared the allelic loss in goblet cell carcinoids to those in 18 gastrointestinal carcinoid tumors. For goblet cell carcinoids, appendiceal perforation was the most common (70%, 7/10) clinical presentation. The mean tumor size was 2.0 +/- 1.5 cm (range, 0.4 to 4.5 cm). The tumor invaded to appendiceal serosa in 50% (8/16) of patients, and two patients had metastasis in lymph nodes or adjoining viscera. With mean follow-up of 24 +/- 14 months (median, 23 mo), 1 of 10 patients had died of disease, and 2 others had tumor recurrence. All four patients with metastases, recurrences, and/or death from disease had serosal involvement at presentation (P =.02). Loss of heterozygosity of chromosome 11q was present in 25% of goblet cell carcinoids, 14% of ileal carcinoid tumors, and 9% of nonileal carcinoid tumors; of chromosome 16q in 38%, 29%, and 0 (P =.02); and of chromosome 18q in 56%, 86%, and 9% (P =.002), respectively. No mutations of K-ras, beta-catenin, or DPC4 genes; p53 overexpression; or loss of staining for DPC4 was present in any tumors. These findings suggest that allelic loss of chromosomes 11q, 16q, and 18q in goblet cell carcinoids and ileal carcinoids may have an important role in the pathogenesis of these tumors. SN - 0893-3952 UR - https://www.unboundmedicine.com/medline/citation/14681318/Genetic_alterations_in_goblet_cell_carcinoids_of_the_vermiform_appendix_and_comparison_with_gastrointestinal_carcinoid_tumors_ L2 - http://dx.doi.org/10.1097/01.MP.0000097362.10330.B1 DB - PRIME DP - Unbound Medicine ER -