Comparative genomic hybridization in primary sinonasal adenocarcinomas.
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.
Ariza
Manuela
M
Instituto Universitario de Oncologia del Principado de Asturias, University of Oviedo, JM Caso 14, 33006 Oviedo, Asturias, Spain.
Llorente
José Luis
JL
Alvarez-Marcas
Cesar
C
Baragaño
Lucia
L
Salas
Ana
A
Rodriguez Prado
Nuria
N
Hermsen
Mario
M
Suárez
Carlos
C
Sampedro
Andres
A
D000230:Adenocarcinoma / Q000235:genetics*; D000368:Aged; D002869:Chromosome Aberrations; D006801:Humans; D008297:Male; D008875:Middle Aged; D009669:Nose Neoplasms / Q000235:genetics*; D009693:Nucleic Acid Hybridization; D009784:Occupational Diseases / Q000235:genetics*; D010255:Paranasal Sinus Neoplasms / Q000235:genetics*; D014934:Wood