STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior
Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activati...
Ausführliche Beschreibung
Autor*in: |
Okabe, Naota [verfasserIn] Fujiwara, Masachika [verfasserIn] Tachibana, Keisei [verfasserIn] Tanaka, Ryota [verfasserIn] Kondo, Haruhiko [verfasserIn] Kamma, Hiroshi [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2021 |
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Anmerkung: |
© The Japanese Association for Thoracic Surgery 2021 |
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Übergeordnetes Werk: |
Enthalten in: The Japanese journal of thoracic and cardiovascular surgery - Tōkyō : Springer Japan, 1998, 69(2021), 11 vom: 01. Juni, Seite 1482-1491 |
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Übergeordnetes Werk: |
volume:69 ; year:2021 ; number:11 ; day:01 ; month:06 ; pages:1482-1491 |
Links: |
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DOI / URN: |
10.1007/s11748-021-01655-9 |
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Katalog-ID: |
SPR045232504 |
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520 | |a Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. | ||
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10.1007/s11748-021-01655-9 doi (DE-627)SPR045232504 (SPR)s11748-021-01655-9-e DE-627 ger DE-627 rakwb eng 610 ASE Okabe, Naota verfasserin aut STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2021 Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. Thymic epithelial tumors (dpeaa)DE-He213 JAK/STAT pathway (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Cyclin D1 (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Fujiwara, Masachika verfasserin aut Tachibana, Keisei verfasserin aut Tanaka, Ryota verfasserin aut Kondo, Haruhiko verfasserin aut Kamma, Hiroshi verfasserin aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 69(2021), 11 vom: 01. Juni, Seite 1482-1491 (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:69 year:2021 number:11 day:01 month:06 pages:1482-1491 https://dx.doi.org/10.1007/s11748-021-01655-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 69 2021 11 01 06 1482-1491 |
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10.1007/s11748-021-01655-9 doi (DE-627)SPR045232504 (SPR)s11748-021-01655-9-e DE-627 ger DE-627 rakwb eng 610 ASE Okabe, Naota verfasserin aut STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2021 Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. Thymic epithelial tumors (dpeaa)DE-He213 JAK/STAT pathway (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Cyclin D1 (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Fujiwara, Masachika verfasserin aut Tachibana, Keisei verfasserin aut Tanaka, Ryota verfasserin aut Kondo, Haruhiko verfasserin aut Kamma, Hiroshi verfasserin aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 69(2021), 11 vom: 01. Juni, Seite 1482-1491 (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:69 year:2021 number:11 day:01 month:06 pages:1482-1491 https://dx.doi.org/10.1007/s11748-021-01655-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 69 2021 11 01 06 1482-1491 |
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10.1007/s11748-021-01655-9 doi (DE-627)SPR045232504 (SPR)s11748-021-01655-9-e DE-627 ger DE-627 rakwb eng 610 ASE Okabe, Naota verfasserin aut STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2021 Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. Thymic epithelial tumors (dpeaa)DE-He213 JAK/STAT pathway (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Cyclin D1 (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Fujiwara, Masachika verfasserin aut Tachibana, Keisei verfasserin aut Tanaka, Ryota verfasserin aut Kondo, Haruhiko verfasserin aut Kamma, Hiroshi verfasserin aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 69(2021), 11 vom: 01. Juni, Seite 1482-1491 (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:69 year:2021 number:11 day:01 month:06 pages:1482-1491 https://dx.doi.org/10.1007/s11748-021-01655-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 69 2021 11 01 06 1482-1491 |
allfieldsGer |
10.1007/s11748-021-01655-9 doi (DE-627)SPR045232504 (SPR)s11748-021-01655-9-e DE-627 ger DE-627 rakwb eng 610 ASE Okabe, Naota verfasserin aut STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2021 Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. Thymic epithelial tumors (dpeaa)DE-He213 JAK/STAT pathway (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Cyclin D1 (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Fujiwara, Masachika verfasserin aut Tachibana, Keisei verfasserin aut Tanaka, Ryota verfasserin aut Kondo, Haruhiko verfasserin aut Kamma, Hiroshi verfasserin aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 69(2021), 11 vom: 01. Juni, Seite 1482-1491 (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:69 year:2021 number:11 day:01 month:06 pages:1482-1491 https://dx.doi.org/10.1007/s11748-021-01655-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 69 2021 11 01 06 1482-1491 |
allfieldsSound |
10.1007/s11748-021-01655-9 doi (DE-627)SPR045232504 (SPR)s11748-021-01655-9-e DE-627 ger DE-627 rakwb eng 610 ASE Okabe, Naota verfasserin aut STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2021 Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. Thymic epithelial tumors (dpeaa)DE-He213 JAK/STAT pathway (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Cyclin D1 (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 Fujiwara, Masachika verfasserin aut Tachibana, Keisei verfasserin aut Tanaka, Ryota verfasserin aut Kondo, Haruhiko verfasserin aut Kamma, Hiroshi verfasserin aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 69(2021), 11 vom: 01. Juni, Seite 1482-1491 (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:69 year:2021 number:11 day:01 month:06 pages:1482-1491 https://dx.doi.org/10.1007/s11748-021-01655-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 69 2021 11 01 06 1482-1491 |
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Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. 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610 ASE STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior Thymic epithelial tumors (dpeaa)DE-He213 JAK/STAT pathway (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Cyclin D1 (dpeaa)DE-He213 JAK3 (dpeaa)DE-He213 |
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stat3 activation in thymic epithelial tumors: correlation with cyclin d1, jak3, and clinical behavior |
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STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior |
abstract |
Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. © The Japanese Association for Thoracic Surgery 2021 |
abstractGer |
Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. © The Japanese Association for Thoracic Surgery 2021 |
abstract_unstemmed |
Objectives Thymic epithelial tumors are the most common adult mediastinal tumors; however, their growth mechanism remains relatively unknown. Among the JAK/STAT pathway-related proteins, which control various intracellular events, STAT3 is deeply involved in cell proliferation. Constitutive activation of STAT3 and the resulting overexpression of cyclin D1 have been confirmed in various tumors, but have not been thoroughly investigated in thymic epithelial tumors. In this study, we immunohistochemically examined STAT3 activation, cyclin D1 expression, and JAK3 activation in thymic epithelial tumors and statistically analyzed their correlation with clinicopathological features. Methods Formalin-fixed paraffin-embedded specimens of 94 thymic epithelial tumors surgically resected at Kyorin University Hospital between 2005 and 2018 were included in this study. pSTAT3, cyclin D1, and pJAK3 were immunohistochemically examined, and the correlation with histology, Masaoka stage, and survival time was statistically analyzed. Results Cyclin D1 was found to be significantly overexpressed in the STAT3-activated group. This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. STAT3 activation, cyclin D1 overexpression, and JAK3 activation are biomarker candidates that indicate clinically poor prognosis. © The Japanese Association for Thoracic Surgery 2021 |
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STAT3 activation in thymic epithelial tumors: correlation with cyclin D1, JAK3, and clinical behavior |
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Fujiwara, Masachika Tachibana, Keisei Tanaka, Ryota Kondo, Haruhiko Kamma, Hiroshi |
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This phenomenon was associated with histology and Masaoka stage. JAK3 was also activated in thymic epithelial tumors; however, JAK3 and STAT3 activation were not always correlated. Using survival time analysis, the STAT3-activated group, cyclin D1-expressed group, and JAK3-activated group had significantly lower progression-free survival times than those for both the non-activated and non-expressed groups. Conclusions STAT3 activation may promote cyclin D1 overexpression in thymic epithelial tumors, and intracellular signaling pathways other than JAK3 may be involved in STAT3 activation. 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