JAK-STAT and G-protein-coupled receptor signaling pathways are frequently altered in epitheliotropic intestinal T-cell lymphoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-06

AUTHORS

M-L Nairismägi, J Tan, J Q Lim, S Nagarajan, C C Y Ng, V Rajasegaran, D Huang, W K Lim, Y Laurensia, G C Wijaya, Z M Li, I Cutcutache, W L Pang, S Thangaraju, J Ha, L P Khoo, S T Chin, S Dey, G Poore, L H C Tan, H K M Koh, K Sabai, H-L Rao, K L Chuah, Y-H Ho, S-B Ng, S-S Chuang, F Zhang, Y-H Liu, T Pongpruttipan, Y H Ko, P-L Cheah, N Karim, W-J Chng, T Tang, M Tao, K Tay, M Farid, R Quek, S G Rozen, P Tan, B T Teh, S T Lim, S-Y Tan, C K Ong

ABSTRACT

Epitheliotropic intestinal T-cell lymphoma (EITL, also known as type II enteropathy-associated T-cell lymphoma) is an aggressive intestinal disease with poor prognosis and its molecular alterations have not been comprehensively characterized. We aimed to identify actionable easy-to-screen alterations that would allow better diagnostics and/or treatment of this deadly disease. By performing whole-exome sequencing of four EITL tumor-normal pairs, followed by amplicon deep sequencing of 42 tumor samples, frequent alterations of the JAK-STAT and G-protein-coupled receptor (GPCR) signaling pathways were discovered in a large portion of samples. Specifically, STAT5B was mutated in a remarkable 63% of cases, JAK3 in 35% and GNAI2 in 24%, with the majority occurring at known activating hotspots in key functional domains. Moreover, STAT5B locus carried copy-neutral loss of heterozygosity resulting in the duplication of the mutant copy, suggesting the importance of mutant STAT5B dosage for the development of EITL. Dysregulation of the JAK-STAT and GPCR pathways was also supported by gene expression profiling and further verified in patient tumor samples. In vitro overexpression of GNAI2 mutants led to the upregulation of pERK1/2, a member of MEK-ERK pathway. Notably, inhibitors of both JAK-STAT and MEK-ERK pathways effectively reduced viability of patient-derived primary EITL cells, indicating potential therapeutic strategies for this neoplasm with no effective treatment currently available. More... »

PAGES

1311

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/leu.2016.13

DOI

http://dx.doi.org/10.1038/leu.2016.13

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1004786794

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26854024


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662 Department of Pathology, Singapore General Hospital, Singapore, Singapore.
663 Department of Pathology, University of Malaya, Kuala Lumpur, Malaysia.
664 Department of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
665 Institute of Molecular and Cell Biology, A*STAR, Singapore, Singapore.
666 Laboratory of Cancer Epigenome, Division of Medical Sciences, National Cancer Centre Singapore, Singapore, Singapore.
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674 Lymphoma Genomic Translational Research Laboratory, Division of Medical Oncology, National Cancer Centre Singapore, Singapore, Singapore.
675 Office of Education, Duke-NUS Medical School, Singapore, Singapore.
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679 schema:name Advanced Molecular Pathology Laboratory, Singapore Health Services, Singapore, Singapore.
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