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. 2001 Nov;159(5):1941-8.
doi: 10.1016/S0002-9440(10)63041-6.

Loss of heterozygosity on chromosomes 9q and 16p in atypical adenomatous hyperplasia concomitant with adenocarcinoma of the lung

K Takamochi  1 , T Ogura, K Suzuki, H Kawasaki, Y Kurashima, T Yokose, A Ochiai, K Nagai, Y Nishiwaki, H Esumi
Affiliations

Loss of heterozygosity on chromosomes 9q and 16p in atypical adenomatous hyperplasia concomitant with adenocarcinoma of the lung

K Takamochi et al. Am J Pathol. 2001 Nov.

Abstract

Atypical adenomatous hyperplasia (AAH) has recently been implicated as a precursor to lung adenocarcinoma. We previously reported loss of heterozygosity (LOH) in tuberous sclerosis (TSC) gene-associated regions to frequently be observed in lung adenocarcinoma with multiple AAHs. In this study, we analyzed LOH in four microsatellite loci on 9q, including the TSC1 gene-associated region, and four loci on 16p, including the TSC2 gene-associated region, in both 18 AAHs and 17 concomitant lung adenocarcinomas from 11 patients. Seven of 18 (39%) AAHs and 9 of 17 (53%) adenocarcinomas displayed LOH on 9q. Five (28%) AAHs and seven (41%) adenocarcinomas harbored LOH at loci adjacent to the TSC1 gene. Four of 18 (22%) AAHs and 6 of 17 (35%) adenocarcinomas displayed LOH on 16p. One (6%) AAH and five (29%) adenocarcinomas harbored LOH at loci adjacent to the TSC2 gene. These findings may indicate a causal relationship of LOH on 9q and 16p in a fraction of AAH lesions and adenocarcinomas of the lung. Especially, the frequencies of LOH on 9q and at the TSC1 gene-associated region were high. The TSC1 gene or another neighboring tumor suppressor gene on 9q might be involved in an early stage of the pathogenesis of lung adenocarcinoma.

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Figures

Figure 1.
Figure 1.
Histological features of AAH (H&E staining). A: The lesion has well-defined boundaries and no central scar formation or collapse. B: Low-grade AAH: the cell density is low to moderate, with the cells arranged in a single layer, intermittently or focally and continuously, on the alveolar septa. C: High-grade AAH: the cells are continuously and densely arranged in a single layer, but do not exhibit the piled-up structure often observed in adenocarcinoma. Original magnifications: ×2 (A), ×150 (B), ×100 (C).
Figure 2.
Figure 2.
Representative examples of microsatellite analyses of chromosomes 9q and 16p in AAHs and adenocarcinomas (AC). A: AAH-17 retained heterozygosity at D9S146. AC-16 showed LOH at D9S146. B: Both AAH-11 and AC-10 showed LOH at D16S291.
Figure 3.
Figure 3.
The distributions of deletions on 9q in AAHs and adenocarcinomas. AC, primary lung adenocarcinoma.
Figure 4.
Figure 4.
The distributions of deletions on 16q in AAHs and adenocarcinomas. AC, primary lung adenocarcinoma.
See this image and copyright information in PMC

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