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Int J Clin Exp Pathol 2011;4(1):97-99
Commentary Article
Bronchioloalveolar neoplasia
Hitoshi Kitamura, Koji Okudela
Department of Pathology, Graduate School of Medicine, Yokohama City University, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan
Received December 8, 2010; accepted December 11, 2010; Epub November 12, 2010; published January 1, 2011
Abstract: Bronchioloalveolar carcinoma (BAC) arising in the peripheral lung is the prototype of human lung adenocarcinoma 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. (IJCEP1012006).
Keywords: Bronchioloalveolar carcinoma; atypical adenomatous hyperplasia; KRAS gene; epidermal growth factor receptor gene; molecular
targeting therapy; murine model
Full text PDF
Address all correspondence to:
Hitoshi Kitamura, MD, PhD
Department of Pathology
Graduate School of Medicine
Yokohama City University
3-9 Fukuura, Kanazawa-ku
Yokohama 236-0004, Japan
Tel: +81-45-787-2583
Fax: +81-45-789-0588
E-mail: pathola@med.yokohama-cu.ac.jp
Commentary Article
Bronchioloalveolar neoplasia
Hitoshi Kitamura, Koji Okudela
Department of Pathology, Graduate School of Medicine, Yokohama City University, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan
Received December 8, 2010; accepted December 11, 2010; Epub November 12, 2010; published January 1, 2011
Abstract: Bronchioloalveolar carcinoma (BAC) arising in the peripheral lung is the prototype of human lung adenocarcinoma 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. (IJCEP1012006).
Keywords: Bronchioloalveolar carcinoma; atypical adenomatous hyperplasia; KRAS gene; epidermal growth factor receptor gene; molecular
targeting therapy; murine model
Full text PDF
Address all correspondence to:
Hitoshi Kitamura, MD, PhD
Department of Pathology
Graduate School of Medicine
Yokohama City University
3-9 Fukuura, Kanazawa-ku
Yokohama 236-0004, Japan
Tel: +81-45-787-2583
Fax: +81-45-789-0588
E-mail: pathola@med.yokohama-cu.ac.jp
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