The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins

Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from ov...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Li, Zheng [verfasserIn] Block, Matthew S. Vierkant, Robert A. Fogarty, Zachary C. Winham, Stacey J. Visscher, Daniel W. Kalli, Kimberly R. Wang, Chen Goode, Ellen L.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Epithelial ovarian cancer Toll-like receptor four (TLR4) Myeloid differentiation primary response gene eighty-eight (MyD88) Endogenous ligands NF-κB signaling pathway

Anmerkung:	© International Society of Oncology and BioMarkers (ISOBM) 2016

Übergeordnetes Werk:	Enthalten in: Tumor biology - Amsterdam : IOS Press, 1987, 37(2016), 10 vom: 26. Juli, Seite 13279-13286
Übergeordnetes Werk:	volume:37 ; year:2016 ; number:10 ; day:26 ; month:07 ; pages:13279-13286

Links:	Volltext

DOI / URN:	10.1007/s13277-016-5163-2

Katalog-ID:	SPR03116367X

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allfields	10.1007/s13277-016-5163-2 doi (DE-627)SPR03116367X (SPR)s13277-016-5163-2-e DE-627 ger DE-627 rakwb eng Li, Zheng verfasserin aut The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2016 Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. Epithelial ovarian cancer (dpeaa)DE-He213 Toll-like receptor four (TLR4) (dpeaa)DE-He213 Myeloid differentiation primary response gene eighty-eight (MyD88) (dpeaa)DE-He213 Endogenous ligands (dpeaa)DE-He213 NF-κB signaling pathway (dpeaa)DE-He213 Block, Matthew S. aut Vierkant, Robert A. aut Fogarty, Zachary C. aut Winham, Stacey J. aut Visscher, Daniel W. aut Kalli, Kimberly R. aut Wang, Chen aut Goode, Ellen L. aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 37(2016), 10 vom: 26. Juli, Seite 13279-13286 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:37 year:2016 number:10 day:26 month:07 pages:13279-13286 https://dx.doi.org/10.1007/s13277-016-5163-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 37 2016 10 26 07 13279-13286
spelling	10.1007/s13277-016-5163-2 doi (DE-627)SPR03116367X (SPR)s13277-016-5163-2-e DE-627 ger DE-627 rakwb eng Li, Zheng verfasserin aut The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2016 Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. Epithelial ovarian cancer (dpeaa)DE-He213 Toll-like receptor four (TLR4) (dpeaa)DE-He213 Myeloid differentiation primary response gene eighty-eight (MyD88) (dpeaa)DE-He213 Endogenous ligands (dpeaa)DE-He213 NF-κB signaling pathway (dpeaa)DE-He213 Block, Matthew S. aut Vierkant, Robert A. aut Fogarty, Zachary C. aut Winham, Stacey J. aut Visscher, Daniel W. aut Kalli, Kimberly R. aut Wang, Chen aut Goode, Ellen L. aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 37(2016), 10 vom: 26. Juli, Seite 13279-13286 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:37 year:2016 number:10 day:26 month:07 pages:13279-13286 https://dx.doi.org/10.1007/s13277-016-5163-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 37 2016 10 26 07 13279-13286
allfields_unstemmed	10.1007/s13277-016-5163-2 doi (DE-627)SPR03116367X (SPR)s13277-016-5163-2-e DE-627 ger DE-627 rakwb eng Li, Zheng verfasserin aut The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2016 Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. Epithelial ovarian cancer (dpeaa)DE-He213 Toll-like receptor four (TLR4) (dpeaa)DE-He213 Myeloid differentiation primary response gene eighty-eight (MyD88) (dpeaa)DE-He213 Endogenous ligands (dpeaa)DE-He213 NF-κB signaling pathway (dpeaa)DE-He213 Block, Matthew S. aut Vierkant, Robert A. aut Fogarty, Zachary C. aut Winham, Stacey J. aut Visscher, Daniel W. aut Kalli, Kimberly R. aut Wang, Chen aut Goode, Ellen L. aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 37(2016), 10 vom: 26. Juli, Seite 13279-13286 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:37 year:2016 number:10 day:26 month:07 pages:13279-13286 https://dx.doi.org/10.1007/s13277-016-5163-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 37 2016 10 26 07 13279-13286
allfieldsGer	10.1007/s13277-016-5163-2 doi (DE-627)SPR03116367X (SPR)s13277-016-5163-2-e DE-627 ger DE-627 rakwb eng Li, Zheng verfasserin aut The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2016 Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. Epithelial ovarian cancer (dpeaa)DE-He213 Toll-like receptor four (TLR4) (dpeaa)DE-He213 Myeloid differentiation primary response gene eighty-eight (MyD88) (dpeaa)DE-He213 Endogenous ligands (dpeaa)DE-He213 NF-κB signaling pathway (dpeaa)DE-He213 Block, Matthew S. aut Vierkant, Robert A. aut Fogarty, Zachary C. aut Winham, Stacey J. aut Visscher, Daniel W. aut Kalli, Kimberly R. aut Wang, Chen aut Goode, Ellen L. aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 37(2016), 10 vom: 26. Juli, Seite 13279-13286 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:37 year:2016 number:10 day:26 month:07 pages:13279-13286 https://dx.doi.org/10.1007/s13277-016-5163-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 37 2016 10 26 07 13279-13286
allfieldsSound	10.1007/s13277-016-5163-2 doi (DE-627)SPR03116367X (SPR)s13277-016-5163-2-e DE-627 ger DE-627 rakwb eng Li, Zheng verfasserin aut The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © International Society of Oncology and BioMarkers (ISOBM) 2016 Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. Epithelial ovarian cancer (dpeaa)DE-He213 Toll-like receptor four (TLR4) (dpeaa)DE-He213 Myeloid differentiation primary response gene eighty-eight (MyD88) (dpeaa)DE-He213 Endogenous ligands (dpeaa)DE-He213 NF-κB signaling pathway (dpeaa)DE-He213 Block, Matthew S. aut Vierkant, Robert A. aut Fogarty, Zachary C. aut Winham, Stacey J. aut Visscher, Daniel W. aut Kalli, Kimberly R. aut Wang, Chen aut Goode, Ellen L. aut Enthalten in Tumor biology Amsterdam : IOS Press, 1987 37(2016), 10 vom: 26. Juli, Seite 13279-13286 (DE-627)300897855 (DE-600)1483579-4 1423-0380 nnns volume:37 year:2016 number:10 day:26 month:07 pages:13279-13286 https://dx.doi.org/10.1007/s13277-016-5163-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_22 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_63 GBV_ILN_95 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_370 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 AR 37 2016 10 26 07 13279-13286
language	English
source	Enthalten in Tumor biology 37(2016), 10 vom: 26. Juli, Seite 13279-13286 volume:37 year:2016 number:10 day:26 month:07 pages:13279-13286
sourceStr	Enthalten in Tumor biology 37(2016), 10 vom: 26. Juli, Seite 13279-13286 volume:37 year:2016 number:10 day:26 month:07 pages:13279-13286
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Epithelial ovarian cancer Toll-like receptor four (TLR4) Myeloid differentiation primary response gene eighty-eight (MyD88) Endogenous ligands NF-κB signaling pathway
isfreeaccess_bool	false
container_title	Tumor biology
authorswithroles_txt_mv	Li, Zheng @@aut@@ Block, Matthew S. @@aut@@ Vierkant, Robert A. @@aut@@ Fogarty, Zachary C. @@aut@@ Winham, Stacey J. @@aut@@ Visscher, Daniel W. @@aut@@ Kalli, Kimberly R. @@aut@@ Wang, Chen @@aut@@ Goode, Ellen L. @@aut@@
publishDateDaySort_date	2016-07-26T00:00:00Z
hierarchy_top_id	300897855
id	SPR03116367X
language_de	englisch
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author	Li, Zheng
spellingShingle	Li, Zheng misc Epithelial ovarian cancer misc Toll-like receptor four (TLR4) misc Myeloid differentiation primary response gene eighty-eight (MyD88) misc Endogenous ligands misc NF-κB signaling pathway The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins
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topic_title	The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins Epithelial ovarian cancer (dpeaa)DE-He213 Toll-like receptor four (TLR4) (dpeaa)DE-He213 Myeloid differentiation primary response gene eighty-eight (MyD88) (dpeaa)DE-He213 Endogenous ligands (dpeaa)DE-He213 NF-κB signaling pathway (dpeaa)DE-He213
topic	misc Epithelial ovarian cancer misc Toll-like receptor four (TLR4) misc Myeloid differentiation primary response gene eighty-eight (MyD88) misc Endogenous ligands misc NF-κB signaling pathway
topic_unstemmed	misc Epithelial ovarian cancer misc Toll-like receptor four (TLR4) misc Myeloid differentiation primary response gene eighty-eight (MyD88) misc Endogenous ligands misc NF-κB signaling pathway
topic_browse	misc Epithelial ovarian cancer misc Toll-like receptor four (TLR4) misc Myeloid differentiation primary response gene eighty-eight (MyD88) misc Endogenous ligands misc NF-κB signaling pathway
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title	The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins
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title_full	The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins
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author_browse	Li, Zheng Block, Matthew S. Vierkant, Robert A. Fogarty, Zachary C. Winham, Stacey J. Visscher, Daniel W. Kalli, Kimberly R. Wang, Chen Goode, Ellen L.
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title_sort	inflammatory microenvironment in epithelial ovarian cancer: a role for tlr4 and myd88 and related proteins
title_auth	The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins
abstract	Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. © International Society of Oncology and BioMarkers (ISOBM) 2016
abstractGer	Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. © International Society of Oncology and BioMarkers (ISOBM) 2016
abstract_unstemmed	Abstract The tumor-associated inflammatory microenvironment may play a pivotal role in epithelial ovarian cancer (EOC) carcinogenesis and outcomes, but a detailed profile in patient-derived tumors is needed. Here, we investigated the expression of TLR4- and MyD88-associated markers in tumors from over 500 EOC patients using immunohistochemical staining. We demonstrate that high expression of TLR4 and MyD88 predicts poorer overall survival in patients with EOC; most likely, this is due to their association with serous histology and features of high tumor burden and aggressiveness, including stage, grade, and ascites at surgery. Combined TLR4 and MyD88 expression appears to serve as an independent risk factor for shortened survival time, even after covariate adjustment (both moderate HR 1.1 [95 % CI 0.7–1.8], both strong HR 2.1 [95 % CI 1.1–3.8], both weak as referent; p = 0.027). We reveal that in EOC tissues with elevated expression of both TLR4 and MyD88 and activated NF-κB signaling pathway, expression of hsp60, hsp70, beta 2 defensin, and HMGB1 are also enriched. In total, these results suggest that activation of TLR4/MyD88/NF-κB signaling by endogenous ligands may contribute to an inflammatory microenvironment that drives a more aggressive phenotype with poorer clinical outcome in EOC patients. © International Society of Oncology and BioMarkers (ISOBM) 2016
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title_short	The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins
url	https://dx.doi.org/10.1007/s13277-016-5163-2
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The inflammatory microenvironment in epithelial ovarian cancer: a role for TLR4 and MyD88 and related proteins

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