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This article is part of the supplement: Abstracts of the 16th International Charles Heidelberger Symposium on Cancer Research

Open Access Poster presentation

EGFR/erb-1, HER2/erb-2, CK7, LP34, Ki67 and p53 expression in preneoplastic lesions of bronchial epithelium

Lina Carvalho1234*, Joana E Santo1, Ana Alarcão12, Patricia Couceiro12, Maria R Silva123, Ana Gomes24, Maria J d’Aguiar1, Lia Teixeira1 and Vitor Sousa1234

Author Affiliations

1 Instituto de Anatomia Patológica – Faculdade de Medicina da Universidade de Coimbra, Coimbra, Portugal

2 Centro de Investigação em Meio Ambiente, Genética e Oncobiologia (CIMAGO), Coimbra, Portugal

3 Centro de Pneumologia – Faculdade de Medicina da Universidade de Coimbra, Coimbra, Portugal

4 Serviço de Anatomia Patológica dos Hospitais da Universidade de Coimbra, Coimbra, Portugal

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BMC Proceedings 2010, 4(Suppl 2):P64  doi:10.1186/1753-6561-4-S2-S64

The electronic version of this article is the complete one and can be found online at:

Published:24 September 2010

© 2010 Carvalho et al; licensee BioMed Central Ltd.

Poster presentation

A prognostic interpretation of preneoplastic lesions would have impact in bronchial carcinoma early diagnosis and through the study of Erb-B family receptors as they have an important role in lung carcinogenesis. The existence of drugs as tirosine kinase inhibitors (TKis) stressed the importance of studying gene alterations for selected chemoprevention schemes and characterization of carcinogenesis.

Bronchial preneoplastic lesions were characterized by immunohistochemistry using the antibodies LP34 (high weigh molecular cytokeratin), CK7, Chromogranin A, Ki67, p53, C-erbB-2 and EGFR. HER2 and EGFR gene copy number was also evaluated by fluorescent in situ hybridization (FISH) in those lesions.

The expected results defined the origin cell for basal cell hyperplasia and squamous metaplasia as adaptative lesions and dysplasia. By known experiences and published data, beyond the stem cell, the spectral evolution of bronchial preneoplastic lesions was demonstrated by characterizing basal cells (LP34) and their neoplastic potentiality.

Dysplasias showed a higher expression of EGFR, Ki67 and p53 with a stepwise increase with the gravity of the respective grading. C-erbB-2 immunohistochemical overexpression was a rare event in preneoplastic lesions. Polysomy was the main mechanism for EGFR and HER2/neu higher gene copy number and together with increased proliferation index (Ki67) will account to preview bronchial carcinogenesis.