Funding sources This publication was made possible in part by a National Institutes of Health SPORE Program Grant #5P50CA121973-05 to L.G., and grant number UL1 RR024153 from the National Center for Research Resources. B.O.D. was supported by the Howard Hughes Medical Fellows Program.
Lessons learned from gene expression profiling of cutaneous T-cell lymphoma
Article first published online: 2 DEC 2013
© 2013 British Association of Dermatologists
British Journal of Dermatology
Volume 169, Issue 6, pages 1188–1197, December 2013
How to Cite
Dulmage, B.O. and Geskin, L.J. (2013), Lessons learned from gene expression profiling of cutaneous T-cell lymphoma. British Journal of Dermatology, 169: 1188–1197. doi: 10.1111/bjd.12578
Conflicts of interest None declared.
- Issue published online: 2 DEC 2013
- Article first published online: 2 DEC 2013
- Accepted manuscript online: 12 AUG 2013 07:39AM EST
- Manuscript Accepted: 1 AUG 2013
- National Institutes of Health SPORE Program. Grant Number: #5P50CA121973-05
- National Center for Research Resources. Grant Number: UL1 RR024153
- Howard Hughes Medical Fellows Program
Gene expression studies of cutaneous T-cell lymphoma (CTCL) span a decade, yet the pathogenesis is poorly understood and diagnosis remains a challenge. This review examines the varied approaches to gene expression analysis of CTCL, with emphasis on cell populations, control selection and expression data collection. Despite discordant results, several dysregulated genes have been identified across multiple studies, including PLS3, KIR3DL2, TWIST1 and STAT4. Here, we provide an overview of the most consistently expressed genes across different studies and bring them together through common pathways biologically relevant to CTCL. Four pathways – evasion of activation-induced cell death, T helper 2 lymphocyte differentiation, transforming growth factor-β receptor expression, and tumour necrosis factor receptor ligands – appear to encompass the most frequently affected genes, hypothetically providing insight into the disease pathogenesis.