Publication: 3p21, 5q21, 9p21 and 17p13 allelic deletions
accumulate in the dysplastic spectrum of laryngeal
carcinogenesis and precede malignant transformation
Authors
Sanz Ortega, J. ; Valor, C. ; Saez, M.C. ; Ortega, L. ; Sierra, E. ; Poch, J. ; Hernández, S. ; Sanz-Esponera, J.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
A tissue field of somatic genetic alterations
precede the histopathological phenotypic changes of
carcinoma. Loss of Heterozygosity (LOH) at the sites of
known or putative tumor suppressor genes is a common
genetic abnormality detected in precancerous conditions.
These genomic changes could be of potential use in the
diagnosis and prognosis of pre-malignant laryngeal
lesions. Recently the concept of laryngeal intraepithelial
neoplasia (LIN) was introduced. To evaluate patients
with an increased risk of developing invasive laryngeal
carcinoma via a dysplasia-carcinoma progression we
investigated 102 microdissected cell populations. Cell
populations were procured from 15 laryngectomy
specimens with different peritumoral histological
changes adjacent to the squamous cell carcinoma cells
and 15 laryngeal endoscopic biopsies with no evidence
of malignant transformation in a 6-10-year follow-up
period. Histological diagnoses were subdivided into
keratosis without dysplasia (KWD), with mild dysplasia
(LIN 1), with moderate dysplasia (LIN 2), and with
severe dysplasia or carcinoma in situ (LIN 3).
Microsatellite analysis was performed with the aim of
studying LOH of 5q21 (APC), 9p21 (p16), 3p21 and
17p13 (p53) chromosomal regions. Frequent allelic
losses were found in carcinoma cells at p53 (54%), p16
(66%), 3p21(87%) and 5q21(58%). Identical LOH
patterns were determined in 100% of the LIN3
peritumoral cells, 60% of LIN2, 50% of LIN 1 and 25%
of KWD. In contrast, histologically normal mucosae,
KWD and LIN1 lesions without malignant progression
showed no allelic loss. These results show that dysplasia
correlates with LOH at 3p21, 5q21, 9p21 and 17p13 in
early laryngeal carcinogenesis. These genomic changes
in pre-malignant laryngeal lesions could be of potential
use as markers for cancer risk assessment.
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