Expression of p53 and CEA in Atypical Adenomatous Hyperplasia of the Lung

Pueblitz, Siegfried; Hieger, Leroy R.

doi:10.1097/00000478-199707000-00018

Cited by 13 publications

(2 citation statements)

References 2 publications

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“…[29][30][31][32] AAH, as a preinvasive lesion, may progress and develop, through a BAC stage, into invasive adenocarcinoma, with the accumulation of several sequential molecular abnormalities. [3][4][5][6][7][8][9][10][11][12][13][33][34][35][36] However, there are no data to suggest what percentage of AAH cases actually progress to invasive adenocarcinoma. 36 The prognosis of resected lung carcinoma with AAH was not different from that without AAH.…”

Section: Discussionmentioning

confidence: 99%

Telomere Length and Telomerase Expression in Atypical Adenomatous Hyperplasia and Small Bronchioloalveolar Carcinoma of the Lung

et al. 2007

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Telomeres are located at the ends of every human chromosome and are subject to shortening at each cycle of cell division in cell senescence and early carcinogenesis. We examined the expression of telomeric DNA in 21 atypical adenomatous hyperplasias (AAHs) and 40 bronchioloalveolar carcinomas (BACs) measuring 2 cm or less in greatest diameter using fluorescent in situ hybridization and the expression of human telomerase reverse transcriptase (hTERT) messenger RNA (mRNA) in 35 AAHs and 37 BACs. The mean numbers of telomeric signals per nucleus were 5.0 in AAH and 7.4 in BAC, each significantly less than for normal cells (14.7; P < .0001), but the mean number of telomeric signals for AAH and BAC was not statistically different (P = .22). In "benign" lung samples, the pattern of expression of hTERT mRNA was barely detected in the nonciliated cells of the bronchioles and alveolar type II cells. Positive expression of hTERT mRNA was recognized in 66% of AAHs and 97% of BACs. Our results demonstrate telomere shortening, indicating its presence in the earliest phase of pulmonary carcinogenesis. Telomere length and telomerase may be involved in carcinogenesis in the lung.

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Section: Discussionmentioning

confidence: 99%

Telomere Length and Telomerase Expression in Atypical Adenomatous Hyperplasia and Small Bronchioloalveolar Carcinoma of the Lung

et al. 2007

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“…In our case, the diagnosis of MMPH was confirmed by the presence of solid condensed areas and of poor alveolar structures distinguished from AH or AAH. AAH, showing occasional immunoreactivity for CEA and p53 [12,19], consists of epithelial cells with nuclear atypia and high nuclear-to-cytoplasmic ratio, and shows alveolar structures with fewer intra-alveolar macrophages than MMPH [16]. So-called sclerosing hemangioma often presents a solitary mass lesion [14,20,21] and shows a mixed pattern with a well-demarcated circumferential margin.…”

Section: Discussionmentioning

confidence: 99%

Multifocal micronodular pneumocyte hyperplasia in a postmenopausal woman with tuberous sclerosis

et al. 2000

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We report a peculiar case of multifocal micronodular pneumocyte hyperplasia (MMPH) without association of pulmonary lymphangioleiomyomatosis (LAM) in a 56-year-old postmenopausal woman with tuberous sclerosis. This case is surmised to be a forme fruste of tuberous sclerosis. Computed tomography demonstrated multiple micronodules, measuring up to 5 mm in size, present in the bilateral lung fields, but no cystic changes. A proliferation of pleomorphic type-II pneumocytes lining the thickened alveolar septa in an adenomatoid pattern, with an associated increase in alveolar macrophages, was observed without typical nuclear atypia. In fully developed lesions, the ingrowth of more proliferating type-II pneumocytes into the thickened alveolar septa and macrophages filling the alveolar lumens were characteristic findings. Proliferation of immature smooth muscle cells suggesting LAM was not observed. Positive immunohistochemical stains for cytokeratin, epithelial membrane antigen, and surfactant apoproteins A and B, and negative staining for HMB45, alpha-1 smooth muscle actin, desmin, and carcinoembryonic antigen confirmed the characteristics of alveolar lining cells in each MMPH lesion. MMPH associated with tuberous sclerosis in the postmenopausal woman appears to be similar to that described in premenopausal women. The present case is familial rather than sporadic and suggests no relationship between the development of MMPH and the underlying hormonal state.

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Preinvasive Disease

Kerr

Fraire

2008

Dail and Hammar’s Pulmonary Pathology

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Expression of p53 and CEA in Atypical Adenomatous Hyperplasia of the Lung

Cited by 13 publications

References 2 publications

Telomere Length and Telomerase Expression in Atypical Adenomatous Hyperplasia and Small Bronchioloalveolar Carcinoma of the Lung

Telomere Length and Telomerase Expression in Atypical Adenomatous Hyperplasia and Small Bronchioloalveolar Carcinoma of the Lung

Multifocal micronodular pneumocyte hyperplasia in a postmenopausal woman with tuberous sclerosis

Preinvasive Disease

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