Chromosomal imbalances in wood dust‐related adenocarcinomas of the inner nose and their associations with pathological parameters

Abstract

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.

Colonic-Type Adenocarcinoma of the Base of the Tongue: A Case Report of a Rare Neoplasm

“…Supporting the likely possibility of malignant transformation of minor salivary duct epithelium is the analogous correlation seen with primary intestinal-type adenocarcinoma of the sinonasal tract, where evidence of respiratory epithelium transformation to an intestinal phenotype has been noted in adjacent nonneoplastic epithelium [2,[9][10][11]. Of interest is the occupational background of this patient, which suggests the possibility of this tumor being etiologically related to prolonged exposure to wood particles in a similar fashion as seen among woodworkers developing intestinal-type adenocarcinomas (ITACs) [6].…”

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].…”