Genomic analysis of 220 CTCLs identifies a novel recurrent gain-of-function alteration in RLTPR (p.Q575E)

Cutaneous T-cell lymphoma (CTCL) is an incurable non-Hodgkin lymphoma of the skin-homing T cell. In early-stage disease, lesions are limited to the skin, but in later-stage disease, the tumor cells can escape into the blood, the lymph nodes, and at times the visceral organs. To clarify the genomic b...

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Vydané v:	Blood Ročník 130; číslo 12; s. 1430
Hlavní autori:	Park, Joonhee, Yang, Jingyi, Wenzel, Alexander T, Ramachandran, Akshaya, Lee, Wung J, Daniels, Jay C, Kim, Juhyun, Martinez-Escala, Estela, Amankulor, Nduka, Pro, Barbara, Guitart, Joan, Mendillo, Marc L, Savas, Jeffrey N, Boggon, Titus J, Choi, Jaehyuk
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 21.09.2017
Predmet:	Amino Acid Sequence Amino Acid Substitution - genetics Base Sequence Genome, Human Genomics HEK293 Cells Humans Jurkat Cells Lymphoma, T-Cell, Cutaneous - genetics Microfilament Proteins - chemistry Microfilament Proteins - genetics Mutation - genetics NF-kappa B - metabolism Oncogenes Receptors, Antigen, T-Cell - metabolism rhoA GTP-Binding Protein - genetics Sequence Analysis, DNA Signal Transduction - genetics
ISSN:	1528-0020, 1528-0020
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Abstract	Cutaneous T-cell lymphoma (CTCL) is an incurable non-Hodgkin lymphoma of the skin-homing T cell. In early-stage disease, lesions are limited to the skin, but in later-stage disease, the tumor cells can escape into the blood, the lymph nodes, and at times the visceral organs. To clarify the genomic basis of CTCL, we performed genomic analysis of 220 CTCLs. Our analyses identify 55 putative driver genes, including 17 genes not previously implicated in CTCL. These novel mutations are predicted to affect chromatin ( , , , ), immune surveillance ( , ), MAPK signaling ( , ), NF-κB signaling ( , ), PI-3-kinase signaling ( , ), RHOA/cytoskeleton remodeling ( ), RNA splicing ( ), T-cell receptor signaling ( , ), and T-cell differentiation ( ). Our analyses identify recurrent mutations in 4 genes not previously identified in cancer. These include CK1α (encoded by ) (p.S27F; p.S27C), PTPRN2 (p.G526E), RARA (p.G303S), and RLTPR (p.Q575E). Last, we functionally validate and as putative oncogenes. encodes a recently described scaffolding protein in the T-cell receptor signaling pathway. We show that RLTPR (p.Q575E) increases binding of RLTPR to downstream components of the NF-κB signaling pathway, selectively upregulates the NF-κB pathway in activated T cells, and ultimately augments T-cell-receptor-dependent production of interleukin 2 by 34-fold. Collectively, our analysis provides novel insights into CTCL pathogenesis and elucidates the landscape of potentially targetable gene mutations.
AbstractList	Cutaneous T-cell lymphoma (CTCL) is an incurable non-Hodgkin lymphoma of the skin-homing T cell. In early-stage disease, lesions are limited to the skin, but in later-stage disease, the tumor cells can escape into the blood, the lymph nodes, and at times the visceral organs. To clarify the genomic basis of CTCL, we performed genomic analysis of 220 CTCLs. Our analyses identify 55 putative driver genes, including 17 genes not previously implicated in CTCL. These novel mutations are predicted to affect chromatin (BCOR, KDM6A, SMARCB1, TRRAP), immune surveillance (CD58, RFXAP), MAPK signaling (MAP2K1, NF1), NF-κB signaling (PRKCB, CSNK1A1), PI-3-kinase signaling (PIK3R1, VAV1), RHOA/cytoskeleton remodeling (ARHGEF3), RNA splicing (U2AF1), T-cell receptor signaling (PTPRN2, RLTPR), and T-cell differentiation (RARA). Our analyses identify recurrent mutations in 4 genes not previously identified in cancer. These include CK1α (encoded by CSNK1A1) (p.S27F; p.S27C), PTPRN2 (p.G526E), RARA (p.G303S), and RLTPR (p.Q575E). Last, we functionally validate CSNK1A1 and RLTPR as putative oncogenes. RLTPR encodes a recently described scaffolding protein in the T-cell receptor signaling pathway. We show that RLTPR (p.Q575E) increases binding of RLTPR to downstream components of the NF-κB signaling pathway, selectively upregulates the NF-κB pathway in activated T cells, and ultimately augments T-cell-receptor-dependent production of interleukin 2 by 34-fold. Collectively, our analysis provides novel insights into CTCL pathogenesis and elucidates the landscape of potentially targetable gene mutations.Cutaneous T-cell lymphoma (CTCL) is an incurable non-Hodgkin lymphoma of the skin-homing T cell. In early-stage disease, lesions are limited to the skin, but in later-stage disease, the tumor cells can escape into the blood, the lymph nodes, and at times the visceral organs. To clarify the genomic basis of CTCL, we performed genomic analysis of 220 CTCLs. Our analyses identify 55 putative driver genes, including 17 genes not previously implicated in CTCL. These novel mutations are predicted to affect chromatin (BCOR, KDM6A, SMARCB1, TRRAP), immune surveillance (CD58, RFXAP), MAPK signaling (MAP2K1, NF1), NF-κB signaling (PRKCB, CSNK1A1), PI-3-kinase signaling (PIK3R1, VAV1), RHOA/cytoskeleton remodeling (ARHGEF3), RNA splicing (U2AF1), T-cell receptor signaling (PTPRN2, RLTPR), and T-cell differentiation (RARA). Our analyses identify recurrent mutations in 4 genes not previously identified in cancer. These include CK1α (encoded by CSNK1A1) (p.S27F; p.S27C), PTPRN2 (p.G526E), RARA (p.G303S), and RLTPR (p.Q575E). Last, we functionally validate CSNK1A1 and RLTPR as putative oncogenes. RLTPR encodes a recently described scaffolding protein in the T-cell receptor signaling pathway. We show that RLTPR (p.Q575E) increases binding of RLTPR to downstream components of the NF-κB signaling pathway, selectively upregulates the NF-κB pathway in activated T cells, and ultimately augments T-cell-receptor-dependent production of interleukin 2 by 34-fold. Collectively, our analysis provides novel insights into CTCL pathogenesis and elucidates the landscape of potentially targetable gene mutations. Cutaneous T-cell lymphoma (CTCL) is an incurable non-Hodgkin lymphoma of the skin-homing T cell. In early-stage disease, lesions are limited to the skin, but in later-stage disease, the tumor cells can escape into the blood, the lymph nodes, and at times the visceral organs. To clarify the genomic basis of CTCL, we performed genomic analysis of 220 CTCLs. Our analyses identify 55 putative driver genes, including 17 genes not previously implicated in CTCL. These novel mutations are predicted to affect chromatin ( , , , ), immune surveillance ( , ), MAPK signaling ( , ), NF-κB signaling ( , ), PI-3-kinase signaling ( , ), RHOA/cytoskeleton remodeling ( ), RNA splicing ( ), T-cell receptor signaling ( , ), and T-cell differentiation ( ). Our analyses identify recurrent mutations in 4 genes not previously identified in cancer. These include CK1α (encoded by ) (p.S27F; p.S27C), PTPRN2 (p.G526E), RARA (p.G303S), and RLTPR (p.Q575E). Last, we functionally validate and as putative oncogenes. encodes a recently described scaffolding protein in the T-cell receptor signaling pathway. We show that RLTPR (p.Q575E) increases binding of RLTPR to downstream components of the NF-κB signaling pathway, selectively upregulates the NF-κB pathway in activated T cells, and ultimately augments T-cell-receptor-dependent production of interleukin 2 by 34-fold. Collectively, our analysis provides novel insights into CTCL pathogenesis and elucidates the landscape of potentially targetable gene mutations.
Author	Mendillo, Marc L Yang, Jingyi Daniels, Jay C Ramachandran, Akshaya Martinez-Escala, Estela Wenzel, Alexander T Guitart, Joan Pro, Barbara Lee, Wung J Amankulor, Nduka Boggon, Titus J Choi, Jaehyuk Savas, Jeffrey N Park, Joonhee Kim, Juhyun
Author_xml	– sequence: 1 givenname: Joonhee orcidid: 0000-0001-6209-6923 surname: Park fullname: Park, Joonhee organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 2 givenname: Jingyi orcidid: 0000-0002-6204-4039 surname: Yang fullname: Yang, Jingyi organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 3 givenname: Alexander T surname: Wenzel fullname: Wenzel, Alexander T organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 4 givenname: Akshaya surname: Ramachandran fullname: Ramachandran, Akshaya organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 5 givenname: Wung J surname: Lee fullname: Lee, Wung J organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 6 givenname: Jay C orcidid: 0000-0003-4022-6795 surname: Daniels fullname: Daniels, Jay C organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 7 givenname: Juhyun surname: Kim fullname: Kim, Juhyun organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 8 givenname: Estela orcidid: 0000-0003-3736-8864 surname: Martinez-Escala fullname: Martinez-Escala, Estela organization: Division of Dermatopathology, Department of Dermatology, Northwestern University, Chicago, IL – sequence: 9 givenname: Nduka surname: Amankulor fullname: Amankulor, Nduka organization: Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA – sequence: 10 givenname: Barbara surname: Pro fullname: Pro, Barbara organization: Robert H. Lurie Comprehensive Cancer Center and – sequence: 11 givenname: Joan surname: Guitart fullname: Guitart, Joan organization: Division of Dermatopathology, Department of Dermatology, Northwestern University, Chicago, IL – sequence: 12 givenname: Marc L orcidid: 0000-0001-8128-0128 surname: Mendillo fullname: Mendillo, Marc L organization: Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 13 givenname: Jeffrey N orcidid: 0000-0002-8173-5580 surname: Savas fullname: Savas, Jeffrey N organization: Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 14 givenname: Titus J orcidid: 0000-0003-2862-1637 surname: Boggon fullname: Boggon, Titus J organization: Department of Molecular Biology and Biophysics, Yale University School of Medicine, New Haven, CT; and – sequence: 15 givenname: Jaehyuk orcidid: 0000-0003-2379-2226 surname: Choi fullname: Choi, Jaehyuk organization: Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL
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SubjectTerms	Amino Acid Sequence Amino Acid Substitution - genetics Base Sequence Genome, Human Genomics HEK293 Cells Humans Jurkat Cells Lymphoma, T-Cell, Cutaneous - genetics Microfilament Proteins - chemistry Microfilament Proteins - genetics Mutation - genetics NF-kappa B - metabolism Oncogenes Receptors, Antigen, T-Cell - metabolism rhoA GTP-Binding Protein - genetics Sequence Analysis, DNA Signal Transduction - genetics
Title	Genomic analysis of 220 CTCLs identifies a novel recurrent gain-of-function alteration in RLTPR (p.Q575E)
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