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DDX3X loss is an adverse prognostic marker in diffuse large B-cell lymphoma and is associated with chemoresistance in aggressive non-Hodgkin lymphoma subtypes.

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Kizhakeyil, Atish 
Zaini, Nurmahirah Binte Mohammed 
Poh, Zhi Sheng 
Wong, Brandon Han Siang 
Loh, Xinpeng 


Non-Hodgkin a diverse group of malignancies, encompassing the common difuse large B-cell lymphoma (DLBCL) to the rarer T-cell lymphomas. Chemoresistance is a major barrier to treatment and the mechanisms through which it occurs are incompletely understood [1]. Although eforts are made to target frequently dysregulated pathways in NHL subtypes, these diseases still evolve into aggressive forms resistant even to newer therapies [2].



DDX3X mutation, Drug resistance, Hematolymphoid malignancy, Prognosis, Tumour metastasis, Antineoplastic Agents, Biomarkers, Tumor, Cell Line, Tumor, Cyclin D1, DEAD-box RNA Helicases, Disease Progression, Drug Resistance, Neoplasm, Humans, Lymphoma, Large B-Cell, Diffuse, Lymphoma, Non-Hodgkin, Mitogen-Activated Protein Kinases, Mutation, Prognosis, STAT3 Transcription Factor, Exome Sequencing

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Mol Cancer

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Springer Science and Business Media LLC
Wellcome Trust (203151/Z/16/Z)
Medical Research Council (MR/M008584/1)
Cancer Research UK (A25117)
This research was supported, in part, by Start-Up Grant to NKV provided by Lee Kong Chian School of Medicine, Nanyang Technological University Singapore (L0412290), the Singapore Ministry of Education (MOE) under its MOE Academic Research Fund (AcRF) Tier 2 Grant (MOE2017-T2–2-004), and the National Research Foundation Singapore under its Open Fund Large Collaborative Grant (OFLCG18May-0028) and administered by the Singapore Ministry of Health’s National Medical Research Council (NMRC). N.F.G. acknowledges funding support from the Singapore Ministry of Health’s National Medical Research Council under its NMRC of Singapore Transition Award (NMRC/TA/0051/2016), Kay Kendall Leukaemia Fund Junior Clinical Research Training Fellowship (KKL649) and the Addenbrooke’s Charitable Trust Research Training Fellowship. D.H. was supported by the Medical Research Council (MR/M008584/1) and Blood Cancer UK and receives core funding from Wellcome (203151/Z/16/Z) and MRC to the Wellcome-MRC Cambridge Stem Cell Institute and from the CRUK Cambridge Centre (A25117). A.K. and Z.S.P. were provided with PhD fellowship by Lee Kong Chian School of Medicine, Nanyang Technological University Singapore. B.H.S.W. was provided with PhD fellowship by HealthTech NTU, Nanyang Technological University Singapore.