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Gyungyub Gong - One of the best experts on this subject based on the ideXlab platform.
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predictive value of Tertiary Lymphoid Structures assessed by high endothelial venule counts in the neoadjuvant setting of triple negative breast cancer
Cancer Research and Treatment, 2017Co-Authors: In Hye Song, In Ah Park, Won Seon Bang, Hye Seon Park, Suk Young Park, Gyungyub GongAbstract:PURPOSE: The Tertiary Lymphoid Structure (TLS) is an important source of tumor-infiltrating lymphocytes (TILs), which have a strong prognostic and predictive value in triple-negative breast cancer (TNBC). A previous study reported that the levels of CXCL13 mRNA expression were associated with TLSs, but measuring the gene expression is challenging in routine practice. Therefore, this study evaluated the MECA79-positive high endothelial venule (HEV) densities and their association with the histopathologically assessed TLSs in biopsy samples. In addition, the relationship of TLSs with the CXCL13 transcript levels and clinical outcomes were examined. MATERIALS AND METHODS: A total of 108 TNBC patients treated with neoadjuvant chemotherapy (NAC) were studied. The amounts of TILs and TLSs were measured histopathologically using hematoxylin and eosin-stained slides. The HEV densities and TIL subpopulations were measured by immunohistochemistry for MECA79, CD3, CD8, and CD20. CXCL13mRNA expression levels using a NanoString assay (NanoString Technologies). RESULTS: The mean number of HEVs in pre-NAC biopsies was 12 (range, 0 to 72). The amounts of TILs and TLSs, HEV density, and CXCL13 expression showed robust correlations with each other. A lower pre-NAC clinical T stage, higher TIL and TLS levels, a higher HEV density, CD20-positive cell density, and CXCL13 expression were significant predictors of a pathologic complete response (pCR). Higher CD8-positive cell density and levels of CXCL13 expression were significantly associated with a better disease-free survival rate. CONCLUSION: MECA79-positive HEV density in pre-NAC biopsies is an objective and quantitative surrogate marker of TLS and might be a valuable tool for predicting pCR of TNBC in routine pathology practice.
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abstract p3 07 56 predictive value of Tertiary Lymphoid Structure assessed by high endothelial venule count in neoadjuvant setting of triple negative breast cancer
Cancer Research, 2016Co-Authors: In Hye Song, Ia Park, Jong Han Yu, Gyungyub GongAbstract:Background Tertiary Lymphoid Structure (TLS) is an ectopic lymph node-like Structure characterized by Lymphoid aggregation with high endothelial venules (HEVs), and is an important source of tumor-infiltrating lymphocytes (TILs). TILs have a strong prognostic and predictive significance, particularly in triple-negative breast cancer (TNBC). We previously analyzed expression of immune-related genes in pre-neoadjuvant chemotherapy (NAC) biopsy samples using NanoString assay and showed that gene expression of follicular helper T cell marker CXCL13 , which is closely associated with TLSs, was an independent predictive factor for pathologic complete remission (pCR) in TNBC. However, measuring gene expression of biopsy sample is not easy to perform in daily pathology practice. Therefore, we evaluated TLSs by assessing hematoxylin and eosin (HE San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P3-07-56.
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Prognostic Significance of Tumor-Infiltrating Lymphocytes and the Tertiary Lymphoid Structures in HER2-Positive Breast Cancer Treated With Adjuvant Trastuzumab.
American journal of clinical pathology, 2015Co-Authors: Hee Jin Lee, In Hye Song, Joo Young Kim, In Ah Park, Jin-hee Ahn, Gyungyub GongAbstract:Objectives: Tumor-infiltrating lymphocytes (TILs) have prognostic significance in breast cancer. The Tertiary Lymphoid Structure (TLS) is related to the influx of TILs, and expression of major histocompatibility complex (MHC) I in tumor cells is necessary for the effective action of TILs. Methods: We retrospectively evaluated the relationship of TILs and TLS and the expression of MHC I in 447 HER2-positive breast cancers treated with chemotherapy and 1 year of trastuzumab. Results: TILs were more abundant in hormone receptor (HR)−/HER2+ tumors than in HR+/HER2+ tumors. HR−/HER2+ breast cancers with abundant TILs showed a higher histologic grade, the absence of lymphovascular invasion, the presence of peritumoral lymphocytic infiltration, moderate to abundant TLSs in adjacent tissue, and stronger HLA-ABC and HLA-A expression. Abundant TILs and the absence of lymphovascular invasion were found to be good, independent prognostic factors for disease-free survival in patients with HR−/HER2+ breast cancer. The level of TILs was not associated with the patients’ prognosis in HR+ tumors. Conclusions: Abundant TILs are an independent prognostic factor in HR−/HER2+ breast cancers. Evaluation of TILs in HR−/HER2+ breast cancers may provide valuable information regarding the prognosis of patients treated using adjuvant chemotherapy and trastuzumab.
Masanobu Oshima - One of the best experts on this subject based on the ideXlab platform.
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hyperactive gp130 stat3 driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International Journal of Cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu OshimaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.
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Hyperactive gp130/STAT3‐driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International journal of cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu Oshima, Awen Gallimore, Kimberley D'costaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.
Hugh Gao - One of the best experts on this subject based on the ideXlab platform.
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hyperactive gp130 stat3 driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International Journal of Cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu OshimaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.
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Hyperactive gp130/STAT3‐driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International journal of cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu Oshima, Awen Gallimore, Kimberley D'costaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.
Alison C. West - One of the best experts on this subject based on the ideXlab platform.
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hyperactive gp130 stat3 driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International Journal of Cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu OshimaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.
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Hyperactive gp130/STAT3‐driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International journal of cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu Oshima, Awen Gallimore, Kimberley D'costaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.
Jesse J. Balic - One of the best experts on this subject based on the ideXlab platform.
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hyperactive gp130 stat3 driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International Journal of Cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu OshimaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.
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Hyperactive gp130/STAT3‐driven gastric tumourigenesis promotes submucosal Tertiary Lymphoid Structure development
International journal of cancer, 2018Co-Authors: David Hill, Hugh Gao, Jesse J. Balic, Alison C. West, Hiroko Oshima, Louise Mcleod, Masanobu Oshima, Awen Gallimore, Kimberley D'costaAbstract:Tertiary Lymphoid Structures (TLSs) display phenotypic and functional characteristics of secondary Lymphoid organs, and often develop in tissues affected by chronic inflammation, as well as in certain inflammation-associated cancers where they are prognostic of improved patient survival. However, the mechanisms that govern the development of tumour-associated TLSs remain ill-defined. Here, we observed tumour-associated TLSs in a preclinical mouse model (gp130F/F ) of gastric cancer, where tumourigenesis is dependent on hyperactive STAT3 signalling through the common IL-6 family signalling receptor, gp130. Gastric tumourigenesis was associated with the development of B and T cell-rich submucosal Lymphoid aggregates, containing CD21+ cellular networks and high endothelial venules. Temporally, TLS formation coincided with the development of gastric adenomas and induction of homeostatic chemokines including Cxcl13, Ccl19 and Ccl21. Reflecting the requirement of gp130-driven STAT3 signalling for gastric tumourigenesis, submucosal TLS development was also STAT3-dependent, but independent of the cytokine IL-17 which has been linked with Lymphoid neogenesis in chronic inflammation and autoimmunity. Interestingly, upregulated Lymphoid chemokine expression and TLS formation were also observed in a chronic gastritis model induced by Helicobacter felis infection. Tumour-associated TLSs were also observed in patients with intestinal-type gastric cancer, and a gene signature linked with TLS development in gp130F/F mice was associated with advanced clinical disease, but was not prognostic of patient survival. Collectively, our in vivo data reveal that hyperactive gp130-STAT3 signalling closely links gastric tumourigenesis with Lymphoid neogenesis, and while a TLS gene signature was associated with advanced gastric cancer in patients, it did not indicate a favourable prognosis.