Atypical adenomatous hyperplasia of lung: Its incidence and analysis of clinical, glycohistochemical and structural features including newly defined growth regulators and vascularization(Article)
- aUICC-TPCC, Institute of Pathology, Humboldt University, Schumannstr. 20-23, D-10117 Berlin, Germany
- bInstitute of Pathology, University Novi Sad, Novi Sad, Serbia
- cInstitute of Pathology, Forschungszentrum Borstel, Borstel, Germany
- dInstitute of Physiological Chemistry, Faculty of Veterinary Medicine, Ludwig-Maximilians-University, Munich, Germany
Abstract
Background: Adenomatous hyperplasia of the peripheral lung has been suggested to be a preneoplastic lesion leading to peripherally localized lung carcinomas. The paucity of data about cellular and vascular characteristics of this lesion in comparison to normal lung prompted this investigation. Material and methods: We describe results of two investigations comprising 75 cases and 70 cases, respectively, with atypical adenomatous hyperplasia (AAH) of the lung, respectively: (a) a prospective study part with thorough analysis of surgical lung specimens (lobes and lungs) for light microscopical detection of the lesion; and (b) a retrospective study part with immuno- and lectin histochemical analysis of AAH and non-neoplastic lung parenchyma monitoring expression of growth-related markers and changes in vascularization patterns. Sections of the individual cases were examined by an image-analyzing system including automated measurement of staining intensities and structure analysis. Results: The prospective study part revealed an incidence of AAH in 2/31 cases with squamous cell carcinoma and in 5/32 cases with adenocarcinomas. No relation to pT- or pN stages was detectable, high grade AAHs were seen to be close to the tumor lesions (<2 cm distance) and those with low grade at greater distances. Statistically significantly increased levels of expression of anti-apoptotic bcl-2, macrophage migration inhibitory factor (MIF) capable to suppress p53 activities, heparin-binding lectin, interleukin-2, galectin-1 and of binding sites for the endogenous lectins galectins-1, -3 and -7 were determined. In addition, alveolar-lining cells, which express these markers, formed spatial clusters, which harbor different levels of structural entropy. AAH displayed an increased level of vascularization characterized by regular size and increased number of newly formed vessels. Interpretation: The prospective and retrospective study parts point to a close association of AAH with peripherally localized adenocarcinoma of the lung. AAH is characterized by pronounced alteration of expression of several growth-related markers and probably non-reversible changes in vascularization. © 2003 Elsevier Ireland Ltd.All rights reserved.
Indexed keywords
| EMTREE drug terms: | cancer growth factorgalectin 1galectin 3galectin 7interleukin 2lectinmacrophage migration inhibition factorproteinprotein bcl 2protein p53unclassified drug |
|---|---|
| EMTREE medical terms: | adultagedarticlebinding sitecancer gradingcancer incidencecontrolled studyfemalehistopathologyhumanhuman tissueimmunohistochemistrylung adenocarcinomalung adenomalung squamous cell carcinomamajor clinical studymalepriority journalprotein expressiontumor vascularization |
Chemicals and CAS Registry Numbers:
galectin 1, 258495-34-0; galectin 3, 208128-56-7; interleukin 2, 85898-30-2; protein, 67254-75-5; protein bcl 2, 219306-68-0
Funding details
| Funding sponsor | Funding number | Acronym |
|---|---|---|
| International Association for the Study of Lung Cancer See opportunities by IASLC | IASLC | |
| Wilhelm Sander-Stiftung |
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1
The financial support by the Wilhelm Sander-Stiftung (Munich), the Verein zur Förderung des biologisch-technologischen Fortschritts in der Medizin e.V., and the International Association for the Study of Lung Cancer (IASLC) is gratefully acknowledged.
- ISSN: 01695002
- CODEN: LUCAE
- Source Type: Journal
- Original language: English
- DOI: 10.1016/S0169-5002(03)00289-7
- PubMed ID: 14568684
- Document Type: Article
- Publisher: Elsevier Ireland Ltd
Kayser, K.; UICC-TPCC, Institute of Pathology, Humboldt University, Schumannstr. 20-23, Germany;
© Copyright 2017 Elsevier B.V., All rights reserved.
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