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Chromosomal Aneuploidy Precedes Morphological Changes and Supports Multifocality in Head and Neck Lesions
Author(s) -
Ai Hong,
Barrera Jose E.,
Meyers Arlen D.,
Shroyer Kenneth R.,
VarellaGarcia Marileila
Publication year - 2001
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/00005537-200110000-00034
Subject(s) - aneuploidy , fluorescence in situ hybridization , pathology , biology , field cancerization , monosomy , dysplasia , chromosome instability , carcinoma in situ , comparative genomic hybridization , trisomy , head and neck squamous cell carcinoma , malignant transformation , microdissection , chromosome , carcinoma , cancer , cancer research , karyotype , medicine , head and neck cancer , genetics , gene
Objective To identify chromosome changes associated with the transformation of dysplastic lesions and to verify evidence for multifocality in synchronous premalignant lesions associated with head and neck squamous cell carcinoma (HNSCC). Study Design Chromosomal aneuploidy was evaluated in sections of formalin‐fixed, paraffin‐embedded tissues from 16 patients with HNSCC, including sites with normal squamous mucosa, dysplasia (low‐ and high‐grade), and invasive tumor. Methods A panel of 6 centromeric probes (chromosomes 1, 3, 7, 8, 9, and 17) was analyzed in dual‐color fluorescence in situ hybridization assays, using matched hematoxylin–eosin‐stained sections for histologic correlation. Results Imbalances for most of the targets tested were found in 20 of 24 invasive carcinoma sites, mainly represented by gain in copy number per cell. However, cell populations with chromosome losses and gains in multimodal patterns were concomitantly observed in a number of tumors, indicating a high degree of chromosome instability. The detection of chromosomal aneuploidy precedes the malignant transformation as indicated by findings of monosomy and trisomy in normal squamous mucosa, and in low‐grade and high‐grade dysplasia sites. Loss of chromosomes 3 and 17 prevailed in low‐grade dysplasias, and gain of chromosomes 7 and 8 were prevalent in high‐grade dysplasias. Synchronous low‐grade and high‐grade dysplastic lesions displayed discordant molecular signatures, suggesting a multifocal origin. Conclusions The interphase fluorescence in‐situ hybridization (FISH) assay with centromeric may detect early changes in the progression of dyplastic epithelia to invasive carcinoma and supports the field cancerization theory of multifocality.