Chromosomal imbalances in wood dust-related adenocarcinomas of the inner nose and their associations with pathological parameters.
Comparative genomic hybridization (CGH) was used to screen 42 wood dust-related sinonasal adenocarcinomas for chromosomal alterations. The tumour collection comprised 39 papillary-tubular cylinder cell adenocarcinomas (PTCCs; six cases G1, 23 G2, and ten G3), two alveolar goblet cell adenocarcinomas (AGCs), and one signet ring cell adenocarcinoma (SRC), according to the Kleinsasser and Schroeder classification. Copy number changes were detected in 41 tumours (97.6%). The one carcinoma without imbalances was a PTCC-G1. DNA gains were most frequently seen on chromosomes 12p (83%), 7q (74%), 8q (71%), and 20q (71%), 11q (61%), 22 (59%), and 1q (52%). Pronounced overrepresentations suggestive of high copy amplifications were detected on 8q (15 cases, 36%), 7q (six cases, 14%), 20q (five cases, 12%), 13q14 (three cases, 7%), 1q22, 5p, 12p and 20 (two cases, 5% each), and 2q24, 3q13, 3q22, 7p, 14q12, and 16q13 (one case, each 2%). Frequent chromosomal losses occurred at 5q (81%), 18q (76%), 4 (74%), 8p (61%), 9p (60%), 6q and 17p (52% each), and 3p, 13q, and 21 (50% each). There was a quantitative as well as a qualitative increase of alterations from PTCC-G1 to PTCC-G2 and finally PTCC-G3, confirming the usefulness of histopathological grading. While PTCC-G1 carried only a few alterations, namely gains on chromosomes 17 and 7 as well as losses of 4q and 13q, PTCC-G2 already carried many of the above-mentioned alterations, while PTCC-G3 showed significantly more gains of 7q, 8q, and 12p, and losses of 8p and 17p. Additionally, the latter subgroup was particularly prone to carry pronounced DNA gains. These data provide further evidence for a recurrent pattern of chromosomal imbalances in sinonasal adenocarcinomas and highlight distinct aberrations that are associated with tumour differentiation and progression.
Korinth
Dirk
D
Institute of Pathology, University Hospital Charité, Berlin, Germany.
Pacyna-Gengelbach
Manuela
M
Deutschmann
Nicole
N
Hattenberger
Sigurd
S
Bockmühl
Ulrike
U
Dietel
Manfred
M
Schroeder
Heinz-Georg
HG
Donhuijsen
Konrad
K
Petersen
Iver
I
D000230:Adenocarcinoma / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D002282:Adenocarcinoma, Bronchiolo-Alveolar / Q000209:etiology / Q000235:genetics / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018279:Carcinoma, Signet Ring Cell / Q000209:etiology / Q000235:genetics / Q000473:pathology; D002454:Cell Differentiation / Q000502:physiology; D002869:Chromosome Aberrations; D004273:DNA, Neoplasm / Q000235:genetics; D004391:Dust; D006801:Humans; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization / Q000379:methods; D009784:Occupational Diseases / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D016273:Occupational Exposure / Q000009:adverse effects; D010255:Paranasal Sinus Neoplasms / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D014934:Wood
D004273:DNA, Neoplasm; D004391:Dust