Comparative genomic hybridization in primary sinonasal adenocarcinomas

Abstract

BACKGROUND Little is known about the genetic alterations that occur in sinonasal adenocarcinomas. The goal of the current study was to detect recurrent chromosomal gains and losses in a series of 21 primary sinonasal adenocarcinomas using comparative genomic hybridization (CGH). METHODS The authors examined ethmoid sinus adenocarcinoma samples from 21 patients. All 21 adenocarcinomas were associated with work‐related exposure to wood dust. CGH was used to detect chromosomal abnormalities, and the results of CGH analysis were evaluated for correlations with clinicopathologic characteristics. RESULTS Chromosomal gains and losses were detected in all 21 adenocarcinomas. Gains were detected at high frequencies at 7q11–21 (n = 15 [71%]), 18p11 (n = 14 [66%]), 8q11–22 (n = 13 [62%]), 5p11–13 (n = 12 [57%]), 12q11–13 and 19p (n = 11 [52%]), 20q (n = 10 [47%]), X and 5p (n = 9 [43%]), and 3q26–27 (n = 8 [38%]); and losses were detected at 8p22–23 (n = 18 [86%]), 18q22–23 (n = 17 [80%]), 17p13 (n = 12 [57%]), and 5q31–qter (n = 11 [52%]). Aside from low‐level gains, 43 high‐level amplifications were observed in the current series of 21 tumors, most commonly at Xq13 (n = 7 [33%]). CONCLUSIONS CGH revealed that ethmoid sinus adenocarcinomas carry a large number of chromosomal losses and gains, including high‐level amplifications. To the authors' knowledge, the current study represents the first attempt to investigate sinonasal adenocarcinomas on a genetic level by using CGH. The pattern of chromosomal abnormalities in these tumors was different from the pattern in other tumors within the same anatomic region (e.g., squamous cell carcinomas and salivary gland tumors); this finding may be explained by differences in etiology. Nonetheless, sinonasal adenocarcinomas appear to be genetically similar to adenocarcinomas of the stomach and colon, which also have an etiology that differs from that of sinonasal adenocarcinomas. Further study is necessary to better understand the molecular genetic basis underlying the development of sinonasal adenocarcinomas. In the near future, this type of understanding may present new possibilities for prevention and treatment of malignant disease. Cancer 2004;100:335–41. © 2003 American Cancer Society.

Primary Intestinal-Type Adenocarcinoma of Tongue: A Case Report with Immunohistochemical and Molecular Profiles and Review of the Literature

“…The most plausible hypothesis is an origin from a transformed duct epithelium [12][13][14][15][16][17]. Transformation of the non-neoplastic respiratory epithelium of the sinonasal tract to an intestinal phenotype, adjacent to adenocarcinoma, has been reported [7,[18][19][20][21].…”

Mixed Exocrine-Neuroendocrine Carcinoma of the Nasal Cavity: Clinico-Pathologic and Molecular Study of a Case and Review of the Literature

“…Despite its histological similarity to colorectal carcinomas, the genetic and epigenetic changes frequently involved in colorectal tumorigenesis have been demonstrated at lower frequency in ITACs [14][15][16][17]. Other investigations reported a close relationship between dust exposure and specific gene alterations, including promoter methylation of p14 and p16 as well as TP53 mutation and/or loss of 17p13 region [18].…”

Genome‐wide analysis of genetic changes in intestinal‐type sinonasal adenocarcinoma

“…18,19 In this study, we analyzed 22 ITAC using a 30,000-oligonucleotide microarray CGH, a method with better resolution and sensitivity than chromosome CGH. 20 In addition, we investigated the DNA ploidy status and the possible occurrence of microsatellite instability (MSI).…”