Interestingly, even when using all 22 SAGE libraries the 293-signature results in a good separation of most IPF from the normal lung parenchyma samples demonstrating the strength of the 293-signature (Figure S2B).
The largest study [ 45] included over 2,000 participants, but most of the participants had normal lung function.
OVA-induced lung tissues were characterized by peribronchial and perivascular inflammation caused by leukocyte infiltration compared with normal lung tissues; most infiltrating inflammatory cells were eosinophils.
Immunohistochemical analyses of human lung sections reveal that fibroblasts within fibroblastic foci of idiopathic pulmonary fibrosis do not express Thy-1, whereas most fibroblasts from normal lungs are Thy-1+ [19].
In this context, it was shown that fibroblasts in IPF lungs are Thy-1 negative, whereas most fibroblasts from normal lungs are Thy-1 positive [ 37].
Tsujino and colleagues [ 57] reported decreased numbers of CD151-positive AECs in patients with IPF, although most AECs in normal lungs express CD151, indicating that a downregulation of this tetraspanin may play a role in the pathogenesis of IPF.
Most normal epithelial tissues, including breast, prostate, lung, and ovary, express high levels of nuclear p27 protein, especially in the terminally differentiated layers.
Serum, sputum, Bronchoalveolar Lavage Fluid (BALF), nasal lavage and bronchial epithelial cell expression of CC16 is reported to be lower in smokers with normal lung function in most of the studies [ 5, 10- 18].
Within the panel of data available to us, MGB2 appears to be a specific biomarker for ovarian tumours with low expression in most normal epithelial tissues and prostate and lung tumours.
Using this approach, we have demonstrated that S100A2 gene products are over-represented in the tumours of most NSCLC patients compared to matched normal lung tissue (Heighway et al, 2002).
