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Int J Clin Exp Pathol. 2010 Nov 12;4(1):97-9.

Bronchioloalveolar neoplasia.

Author information

  • 1Department of Pathology, Graduate School of Medicine, Yokohama City University 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan. pathola@med.yokohama-cu.ac.jp

Abstract

Bronchioloalveolar carcinoma (BAC) arising in the peripheral lung is the prototype of human lung adenocar-cinoma and is considered to develop, at least in part, from its precursor atypical adenomatous hyperplasia (AAH). Molecular genetics investigations have revealed the significant roles of mutations in KRAS and epidermal growth factor receptor (EGFR) genes in the pathogenesis of AAH and BAC. Recently, selective molecular targeting therapies, such as those using EGFR tyrosine kinase inhibitors, have been introduced with remarkable success. In spite of the accumulation of research results into BAC/AAH, there remain three important issues to be addressed; 1) the etiology of BAC and AAH, 2) the genetic and/or epigenetic alteration(s) responsible for the progression of AAH to BAC, 3) the genetic backgrounds speculated as the cause of multiple AAH/BAC. These three issues are briefly reviewed and discussed, along with the murine pulmonary carcinogenesis model which is potentially useful for solving these issues.

KEYWORDS:

Bronchioloalveolar carcinoma; KRAS gene; atypical adenomatous hyperplasia; epidermal growth factor receptor gene; molecular targeting therapy; murine model

PMID:
21228931
[PubMed - indexed for MEDLINE]
PMCID:
PMC3016107
Free PMC Article
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