Clinical Implications of Phosphorylated STAT3 Expression in De Novo Diffuse Large B-cell Lymphoma
Purpose: Activated signal transducer and activator of transcription 3 (STAT3) regulates tumor growth, invasion, cell proliferation, angiogenesis, immune response, and survival. Data regarding expression of phosphorylated (activated) STAT3 in diffuse large B-cell lymphoma (DLBCL) and the impact of ph...
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| Published in | Clinical cancer research Vol. 20; no. 19; pp. 5113 - 5123 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.10.2014
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Purpose: Activated signal transducer and activator of transcription 3 (STAT3) regulates tumor growth, invasion, cell proliferation, angiogenesis, immune response, and survival. Data regarding expression of phosphorylated (activated) STAT3 in diffuse large B-cell lymphoma (DLBCL) and the impact of phosphorylated STAT3 (pSTAT3) on prognosis are limited.
Experimental Design: We evaluated expression of pSTAT3 in de novo DLBCL using immunohistochemistry, gene expression profiling (GEP), and gene set enrichment analysis (GSEA). Results were analyzed in correlation with cell-of-origin (COO), critical lymphoma biomarkers, and genetic translocations.
Results: pSTAT3 expression was observed in 16% of DLBCL and was associated with advanced stage, multiple extranodal sites of involvement, activated B-cell–like (ABC) subtype, MYC expression, and MYC/BCL2 expression. Expression of pSTAT3 predicted inferior overall survival (OS) and progression-free survival (PFS) in patients with de novo DLBCL. When DLBCL cases were stratified according to COO or MYC expression, pSTAT3 expression did not predict inferior outcome, respectively. Multivariate analysis showed that the prognostic predictability of pSTAT3 expression was due to its association with the ABC subtype, MYC expression, and adverse clinical features. GEP demonstrated upregulation of genes, which can potentiate function of STAT3. GSEA showed the JAK–STAT pathway to be enriched in pSTAT3+ DLBCL.
Conclusions: The results of this study provide a rationale for the ongoing successful clinical trials targeting the JAK–STAT pathway in DLBCL. Clin Cancer Res; 20(19); 5113–23. ©2014 AACR. |
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| AbstractList | Purpose: Activated signal transducer and activator of transcription 3 (STAT3) regulates tumor growth, invasion, cell proliferation, angiogenesis, immune response, and survival. Data regarding expression of phosphorylated (activated) STAT3 in diffuse large B-cell lymphoma (DLBCL) and the impact of phosphorylated STAT3 (pSTAT3) on prognosis are limited.Experimental Design: We evaluated expression of pSTAT3 in de novo DLBCL using immunohistochemistry, gene expression profiling (GEP), and gene set enrichment analysis (GSEA). Results were analyzed in correlation with cell-of-origin (COO), critical lymphoma biomarkers, and genetic translocations.Results: pSTAT3 expression was observed in 16% of DLBCL and was associated with advanced stage, multiple extranodal sites of involvement, activated B-cell-like (ABC) subtype, MYC expression, and MYC/BCL2 expression. Expression of pSTAT3 predicted inferior overall survival (OS) and progression-free survival (PFS) in patients with de novo DLBCL. When DLBCL cases were stratified according to COO or MYC expression, pSTAT3 expression did not predict inferior outcome, respectively. Multivariate analysis showed that the prognostic predictability of pSTAT3 expression was due to its association with the ABC subtype, MYC expression, and adverse clinical features. GEP demonstrated upregulation of genes, which can potentiate function of STAT3. GSEA showed the JAK-STAT pathway to be enriched in pSTAT3+ DLBCL.Conclusions: The results of this study provide a rationale for the ongoing successful clinical trials targeting the JAK-STAT pathway in DLBCL. Clin Cancer Res; 20(19); 5113-23. copyright 2014 AACR. Purpose: Activated signal transducer and activator of transcription 3 (STAT3) regulates tumor growth, invasion, cell proliferation, angiogenesis, immune response, and survival. Data regarding expression of phosphorylated (activated) STAT3 in diffuse large B-cell lymphoma (DLBCL) and the impact of phosphorylated STAT3 (pSTAT3) on prognosis are limited. Experimental Design: We evaluated expression of pSTAT3 in de novo DLBCL using immunohistochemistry, gene expression profiling (GEP), and gene set enrichment analysis (GSEA). Results were analyzed in correlation with cell-of-origin (COO), critical lymphoma biomarkers, and genetic translocations. Results: pSTAT3 expression was observed in 16% of DLBCL and was associated with advanced stage, multiple extranodal sites of involvement, activated B-cell–like (ABC) subtype, MYC expression, and MYC/BCL2 expression. Expression of pSTAT3 predicted inferior overall survival (OS) and progression-free survival (PFS) in patients with de novo DLBCL. When DLBCL cases were stratified according to COO or MYC expression, pSTAT3 expression did not predict inferior outcome, respectively. Multivariate analysis showed that the prognostic predictability of pSTAT3 expression was due to its association with the ABC subtype, MYC expression, and adverse clinical features. GEP demonstrated upregulation of genes, which can potentiate function of STAT3. GSEA showed the JAK–STAT pathway to be enriched in pSTAT3+ DLBCL. Conclusions: The results of this study provide a rationale for the ongoing successful clinical trials targeting the JAK–STAT pathway in DLBCL. Clin Cancer Res; 20(19); 5113–23. ©2014 AACR. Activated signal transducer and activator of transcription 3 (STAT3) regulates tumor growth, invasion, cell proliferation, angiogenesis, immune response, and survival. Data regarding expression of phosphorylated (activated) STAT3 in diffuse large B-cell lymphoma (DLBCL) and the impact of phosphorylated STAT3 (pSTAT3) on prognosis are limited. We evaluated expression of pSTAT3 in de novo DLBCL using immunohistochemistry, gene expression profiling (GEP), and gene set enrichment analysis (GSEA). Results were analyzed in correlation with cell-of-origin (COO), critical lymphoma biomarkers, and genetic translocations. pSTAT3 expression was observed in 16% of DLBCL and was associated with advanced stage, multiple extranodal sites of involvement, activated B-cell-like (ABC) subtype, MYC expression, and MYC/BCL2 expression. Expression of pSTAT3 predicted inferior overall survival (OS) and progression-free survival (PFS) in patients with de novo DLBCL. When DLBCL cases were stratified according to COO or MYC expression, pSTAT3 expression did not predict inferior outcome, respectively. Multivariate analysis showed that the prognostic predictability of pSTAT3 expression was due to its association with the ABC subtype, MYC expression, and adverse clinical features. GEP demonstrated upregulation of genes, which can potentiate function of STAT3. GSEA showed the JAK-STAT pathway to be enriched in pSTAT3(+) DLBCL. The results of this study provide a rationale for the ongoing successful clinical trials targeting the JAK-STAT pathway in DLBCL. Activated signal transducer and activator of transcription 3 (STAT3) regulates tumor growth, invasion, cell proliferation, angiogenesis, immune response, and survival. Data regarding expression of phosphorylated (activated) STAT3 in diffuse large B-cell lymphoma (DLBCL) and the impact of phosphorylated STAT3 (pSTAT3) on prognosis are limited.PURPOSEActivated signal transducer and activator of transcription 3 (STAT3) regulates tumor growth, invasion, cell proliferation, angiogenesis, immune response, and survival. Data regarding expression of phosphorylated (activated) STAT3 in diffuse large B-cell lymphoma (DLBCL) and the impact of phosphorylated STAT3 (pSTAT3) on prognosis are limited.We evaluated expression of pSTAT3 in de novo DLBCL using immunohistochemistry, gene expression profiling (GEP), and gene set enrichment analysis (GSEA). Results were analyzed in correlation with cell-of-origin (COO), critical lymphoma biomarkers, and genetic translocations.EXPERIMENTAL DESIGNWe evaluated expression of pSTAT3 in de novo DLBCL using immunohistochemistry, gene expression profiling (GEP), and gene set enrichment analysis (GSEA). Results were analyzed in correlation with cell-of-origin (COO), critical lymphoma biomarkers, and genetic translocations.pSTAT3 expression was observed in 16% of DLBCL and was associated with advanced stage, multiple extranodal sites of involvement, activated B-cell-like (ABC) subtype, MYC expression, and MYC/BCL2 expression. Expression of pSTAT3 predicted inferior overall survival (OS) and progression-free survival (PFS) in patients with de novo DLBCL. When DLBCL cases were stratified according to COO or MYC expression, pSTAT3 expression did not predict inferior outcome, respectively. Multivariate analysis showed that the prognostic predictability of pSTAT3 expression was due to its association with the ABC subtype, MYC expression, and adverse clinical features. GEP demonstrated upregulation of genes, which can potentiate function of STAT3. GSEA showed the JAK-STAT pathway to be enriched in pSTAT3(+) DLBCL.RESULTSpSTAT3 expression was observed in 16% of DLBCL and was associated with advanced stage, multiple extranodal sites of involvement, activated B-cell-like (ABC) subtype, MYC expression, and MYC/BCL2 expression. Expression of pSTAT3 predicted inferior overall survival (OS) and progression-free survival (PFS) in patients with de novo DLBCL. When DLBCL cases were stratified according to COO or MYC expression, pSTAT3 expression did not predict inferior outcome, respectively. Multivariate analysis showed that the prognostic predictability of pSTAT3 expression was due to its association with the ABC subtype, MYC expression, and adverse clinical features. GEP demonstrated upregulation of genes, which can potentiate function of STAT3. GSEA showed the JAK-STAT pathway to be enriched in pSTAT3(+) DLBCL.The results of this study provide a rationale for the ongoing successful clinical trials targeting the JAK-STAT pathway in DLBCL.CONCLUSIONSThe results of this study provide a rationale for the ongoing successful clinical trials targeting the JAK-STAT pathway in DLBCL. |
| Author | Manyam, Ganiraju C. Chiu, April Winter, Jane N. Richards, Kristy L. Visco, Carlo Zu, Youli Tzankov, Alexandar Orazi, Attilio Young, Ken H. Huh, Jooryung Ok, Chi Young Møller, Michael B. Piris, Miguel A. Li, Ling Dybkær, Karen Montes-Moreno, Santiago Bertoni, Francesco Bhagat, Govind Ponzoni, Maurilio Medeiros, L. Jeffrey Zhao, Xiaoying Farnen, John P. Xu-Monette, Zijun Y. Hsi, Eric D. Ferreri, Andrés J.M. van Krieken, J. Han Choi, William W.L. Chen, Jiayu |
| AuthorAffiliation | 8 Memorial Sloan-Kettering Cancer Center, New York, NY, USA 10 The Methodist Hospital, Houston, TX, USA 15 Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands 7 Aalborg University Hospital, Aalborg, Denmark 18 San Raffaele H. Scientific Institute, Milan, Italy 5 San Bartolo Hospital, Vicenza, Italy 21 Odense University Hospital, Odense, Denmark 3 University Hospital, Basel, Switzerland 1 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA 11 Columbia University Medical Center and New York Presbyterian Hospital, New York, NY, USA 4 Department of Biostatistics and Bioinformatics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA 16 Asan Medical Center, Ulsan University College of Medicine, Seoul, Korea 9 Weill Medical College of Cornell University, New York, NY, USA 22 Feinberg School of Medicine, Northwestern University, Chicago, IL, USA 2 Medical School of Taizhou University, Taizhou, Zhejiang, China 19 Oncology Instit |
| AuthorAffiliation_xml | – name: 2 Medical School of Taizhou University, Taizhou, Zhejiang, China – name: 5 San Bartolo Hospital, Vicenza, Italy – name: 4 Department of Biostatistics and Bioinformatics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA – name: 6 Hospital Universitario Marques de Valdecilla, Santander, Spain – name: 19 Oncology Institute of Southern Switzerland, Bellinzona, Italy – name: 10 The Methodist Hospital, Houston, TX, USA – name: 3 University Hospital, Basel, Switzerland – name: 14 University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, China – name: 18 San Raffaele H. Scientific Institute, Milan, Italy – name: 11 Columbia University Medical Center and New York Presbyterian Hospital, New York, NY, USA – name: 12 University of North Carolina School of Medicine, Chapel Hill, NC, USA – name: 9 Weill Medical College of Cornell University, New York, NY, USA – name: 16 Asan Medical Center, Ulsan University College of Medicine, Seoul, Korea – name: 8 Memorial Sloan-Kettering Cancer Center, New York, NY, USA – name: 13 Cleveland Clinic, Cleveland, OH, USA – name: 21 Odense University Hospital, Odense, Denmark – name: 7 Aalborg University Hospital, Aalborg, Denmark – name: 22 Feinberg School of Medicine, Northwestern University, Chicago, IL, USA – name: 20 Gundersen Lutheran Health System, La Crosse, WI, USA – name: 15 Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands – name: 17 Zhejiang University School of Medicine, Second University Hospital, Hangzhou, China – name: 1 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA |
| Author_xml | – sequence: 1 givenname: Chi Young surname: Ok fullname: Ok, Chi Young – sequence: 2 givenname: Jiayu surname: Chen fullname: Chen, Jiayu – sequence: 3 givenname: Zijun Y. surname: Xu-Monette fullname: Xu-Monette, Zijun Y. – sequence: 4 givenname: Alexandar surname: Tzankov fullname: Tzankov, Alexandar – sequence: 5 givenname: Ganiraju C. surname: Manyam fullname: Manyam, Ganiraju C. – sequence: 6 givenname: Ling surname: Li fullname: Li, Ling – sequence: 7 givenname: Carlo surname: Visco fullname: Visco, Carlo – sequence: 8 givenname: Santiago surname: Montes-Moreno fullname: Montes-Moreno, Santiago – sequence: 9 givenname: Karen surname: Dybkær fullname: Dybkær, Karen – sequence: 10 givenname: April surname: Chiu fullname: Chiu, April – sequence: 11 givenname: Attilio surname: Orazi fullname: Orazi, Attilio – sequence: 12 givenname: Youli surname: Zu fullname: Zu, Youli – sequence: 13 givenname: Govind surname: Bhagat fullname: Bhagat, Govind – sequence: 14 givenname: Kristy L. surname: Richards fullname: Richards, Kristy L. – sequence: 15 givenname: Eric D. surname: Hsi fullname: Hsi, Eric D. – sequence: 16 givenname: William W.L. surname: Choi fullname: Choi, William W.L. – sequence: 17 givenname: J. Han surname: van Krieken fullname: van Krieken, J. Han – sequence: 18 givenname: Jooryung surname: Huh fullname: Huh, Jooryung – sequence: 19 givenname: Xiaoying surname: Zhao fullname: Zhao, Xiaoying – sequence: 20 givenname: Maurilio surname: Ponzoni fullname: Ponzoni, Maurilio – sequence: 21 givenname: Andrés J.M. surname: Ferreri fullname: Ferreri, Andrés J.M. – sequence: 22 givenname: Francesco surname: Bertoni fullname: Bertoni, Francesco – sequence: 23 givenname: John P. surname: Farnen fullname: Farnen, John P. – sequence: 24 givenname: Michael B. surname: Møller fullname: Møller, Michael B. – sequence: 25 givenname: Miguel A. surname: Piris fullname: Piris, Miguel A. – sequence: 26 givenname: Jane N. surname: Winter fullname: Winter, Jane N. – sequence: 27 givenname: L. Jeffrey surname: Medeiros fullname: Medeiros, L. Jeffrey – sequence: 28 givenname: Ken H. surname: Young fullname: Young, Ken H. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25124685$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Adult Aged Antibodies, Monoclonal, Murine-Derived - therapeutic use Antineoplastic Combined Chemotherapy Protocols - therapeutic use Cohort Studies Cyclin D1 - genetics Cyclin D1 - metabolism Cyclophosphamide - therapeutic use Doxorubicin - therapeutic use Female Gene Expression Genes, bcl-2 Genes, myc Humans Lymphoma, Large B-Cell, Diffuse - drug therapy Lymphoma, Large B-Cell, Diffuse - genetics Lymphoma, Large B-Cell, Diffuse - metabolism Lymphoma, Large B-Cell, Diffuse - mortality Lymphoma, Large B-Cell, Diffuse - pathology Male Middle Aged Neoplasm Metastasis Neoplasm Staging NF-kappa B - genetics NF-kappa B - metabolism Phosphorylation Prednisone - therapeutic use Prognosis Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Signal Transduction STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Tumor Burden Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Vincristine - therapeutic use |
| Title | Clinical Implications of Phosphorylated STAT3 Expression in De Novo Diffuse Large B-cell Lymphoma |
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