Open AccessMYCL1, FHIT, SPARC, p16 INK4 and TP53 genes associated to lung cancer in idiopathic pulmonary fibrosis
Author(s) -
Demopoulos K.,
Arvanitis D. A.,
Vassilakis D. A.,
Siafakas N. M.,
Spandidos D. A.
Publication year - 2002
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2002.tb00188.x
Subject(s) - loss of heterozygosity , idiopathic pulmonary fibrosis , fhit , lung cancer , pathology , biology , microsatellite , lung , pulmonary fibrosis , sputum , locus (genetics) , fibrosis , cancer , medicine , carcinogenesis , allele , gene , tumor suppressor gene , genetics , tuberculosis
Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic interstitial pneumonia limited to the lung and characterized by a fibroproliferative response with only minor signs of inflammation, which almost always causes rapid fibrotic destruction of the lung. In this study, we investigated genomic instability in IPF, using microsatellite DNA analysis, aiming to detect any specific genetic alterations for this disease. We used 40 highly polymorphic microsatellite DNA markers, in multiplex PCR assays, to examine 52 sputum specimens from IPF patients versus correspondent venous blood. Loss of heterozygosity (LOH) was found in 20 (38.5%) patients in at least one locus. These alterations were found on markers previously associated with lung cancer located on 1p34.3, 3p21.32‐p21.1, 5q32‐q33.1, 9p21 and 17p13.1 where MYCL1, FHIT, SPARC, p 16Ink4 and TP53 genes have been mapped respectively. These data provide new insights into IPF pathogenesis and a new perspective for its correlation with lung cancer.