Loss of heterozygosity patterns of sclerosing hemangioma of the lung and bronchioloalveolar carcinoma indicate a similar molecular pathogenesis.

Abstract

The histogenesis and origin of sclerosing hemangioma (SH) of lung were uncertain for many years. Many immunohistochemical, ultrastructural, and recent molecular studies support the hypothesis that SH is a neoplasm originating from the cells of the terminal lobular unit, similar to the nonmucinous variant of bronchioloalveolar carcinoma (BAC). Most cases of SH are benign, but they can metastasize to the regional lymph nodes. To compare the patterns of allelic loss of tumor suppressor genes in SH and BAC by microdissection-based genotypic analysis. Microdissection-based loss of heterozygosity analysis of 9 cases of SH and 14 cases of BAC, using a panel of 7 polymorphic microsatellite markers located on 1p, 5q, 9p, 10q, and 17p. Microsatellite marker and chromosomal arm-based fractional allelic loss (FAL) were calculated in each case. Our results showed similar patterns of allelic loss between the 2 groups of tumors on an individual case basis. Chromosomal arms 5q and 10q showed frequent allelic loss in SH (66.7% and 62.5%, respectively), whereas in BAC, chromosomal arm 17p (52.6%) was frequently affected. A statistically significant difference in allelic loss between SH and BAC was located only on chromosomal arm 5q (P =.04). Microsatellite marker D5S615 was significantly more frequently affected in SH than in BAC (66.7% vs 28.6%; P =.04). Our molecular data support the hypothesis of common origin of SH and BAC. A putative tumor suppressor gene that might play a role in tumorigenesis of SH may be located on the chromosomal arm 5q.