Immunoexpressions of Thyroid Transcription Factor-1 and bcl-2 in Congenital Cystic Adenomatoid Malformation.
- Author:
Na Rae KIM
1
;
Dong Hoon KIM
;
Gou Young KIM
;
Dae Shick KIM
;
Joungho HAN
Author Information
1. Department of Pathology, Kangnam General Hospital Public Corporation, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Cystic adenomatoid malformation of lung, congenital;
Thyroid transcription
- MeSH:
Apoptosis;
Bronchi;
Congenital Abnormalities;
Cystic Adenomatoid Malformation of Lung, Congenital*;
Epithelial Cells;
Epithelium;
Humans;
Lung;
Lymphocytes;
Morphogenesis;
Pregnancy;
Thyroid Gland*
- From:Korean Journal of Pathology
2003;37(1):10-14
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Congenital cystic adenomatoid malformation (CCAM) is a congenital abnormality of branching morphogenesis of the lung. Thyroid transcription factor-1 (TTF-1) is detected in human respiratory epithelial cells from 11 weeks of gestation, and at full term, TTF-1 expression is confined within type II epithelial cells and in some respiratory nonciliated bronchiolar epithelial cells. Immunoexpression of bcl-2 is intimately related to apoptosis during the development. METHODS: To elucidate the nature of the lesion, TTF-1 expression was evaluated in twenty-four cases of CCAM (eight cases of type 1 and sixteen cases of type 2) along with immunostaining for bcl-2. For the control group, four cases of fetal lungs (19 week-, 21 week-, 27 week- and 40 week-gestational age) were also evaluated. In all cases of CCAM, TTF-1 was detected in the nuclei of epithelial cells lining the cysts. RESULTS: TTF-1 was expressed in the majority of the bronchiolar-like epithelial cells of the cysts in CCAM types 1, and 2, where almost 100% of the lining cells of the cysts were TTF-1 positive with variable intensity, while negative TTF-1 expressions were found in the alveolar-like epithelium of the adjacent alveoli or distal nonciliated bronchi. For bcl-2 immunostaining, no lining epithelial cells of the cysts were stained except for the infiltrating lymphocytes. In the control group, strong immunoreactivities found in early fetal stages were absent in the full-term aged lung (40 gestational weeks). CONCLUSION: These results support the hypothesis that CCAM types 1 and 2 reflect the abnormalities in lung morphogenesis and differentiation that are distinct from those for normally developed alveolar epithelium or adjacent bronchial epithelium, thus retaining the abnormal TTF-1 immunoreactions. Though restricted to CCAM types 1 and 2 in this study, CCAM might be related to TTF-1 rather than apoptosis in the morphogenesis of the developing lung.
