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A gene expression signature that distinguishes desmoid tumours from nodular fasciitis
Author(s) -
Bacac M,
Migliavacca E,
Stehle JC,
McKee T,
Delorenzi M,
Coindre JM,
Guillou L,
Stamenkovic I
Publication year - 2006
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1915
Subject(s) - biology , microphthalmia associated transcription factor , cancer research , hedgehog , gli1 , receptor tyrosine kinase , wnt signaling pathway , lyn , pdgfb , kinome , transcription factor , pathology , tyrosine kinase , signal transduction , growth factor , platelet derived growth factor receptor , microbiology and biotechnology , gene , receptor , genetics , medicine
Nodular fasciitis (NF) is a rapidly growing cellular mass composed of fibroblasts/myofibroblasts, usually localized in subcutaneous tissues, that typically undergoes fibrosis and almost never recurs. Desmoid tumours (DTs) are rare forms of fibroblastic/myofibroblastic growth that arise in deep soft tissues, display a propensity for local infiltration and recurrence, but fail to metastasize. Given that both entities are primarily fibroblastic/myofibroblastic lesions with overlapping histological features, their gene expression profiles were compared to identify differentially expressed genes that may provide not only potential diagnostic markers, but also clues as to the pathogenesis of each disorder. Differentially expressed transcripts (89 clones displaying increased expression in DTs and 246 clones displaying increased expression in NF) included genes encoding several receptor and non‐receptor tyrosine kinases ( EPHB3, PTPRF, GNAZ, SYK, LYN, EPHA4, BIRC3 ), transcription factors ( TWIST1, PITX2, EYA2, OAS1, MITF, TCF20 ), and members of the Wnt signalling pathway ( AXIN2, WISP1, SFRP ). Remarkably, almost one‐quarter of the differentially expressed genes encode proteins associated with inflammation and tissue remodelling, including members of the interferon (IFN), tumour necrosis factor (TNF), and transforming growth factor beta (TGF‐β) signalling pathways as well as metalloproteinases (MMP1, 9, 13, 23), urokinase plasminogen activator (PLAU), and cathepsins. The observations provide the first comparative molecular characterization of desmoid tumours and nodular fasciitis and suggest that selected tyrosine kinases, transcription factors, and members of the Wnt, TGF‐β, IFN, and TNF signalling pathways may be implicated in influencing and distinguishing their fate. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.