【がん研セミナー（７月１３日）のお知らせ「Deciphering the mechanisms regulating tumor microenvironment promoting cancer progression」千場 隆 博士（熊本大学国際先端医学研究機構（IRCMS）消化器がん生物学）】
2023年07月04日
がん研セミナー（７月１３日）のお知らせ
演題：Deciphering the mechanisms regulating tumor microenvironment promoting cancer progression
演者：千場 隆 博士（熊本大学国際先端医学研究機構（IRCMS）消化器がん生物学）
抄録：A tumor microenvironment (TME) is key for tumor progression. However, the molecular characteristics associated with the pro-tumor TME remain largely unknown. We have examined how the mitogen-activated protein kinase signaling and related pathways mediate the cell-cell cross-talk in immunosuppressive TME. We identified that a cluster with activated C-JUN N-terminal kinase (JNK)/JUN pathway in triple-negative breast cancer (TNBC) represents immunosuppressive TME status. We confirmed that JNK/JUN pathway-regulated CCL2 production from tumor-associated macrophages fosters an immunosuppressive TME by recruiting regulatory T cells (Tregs) to promote TNBC aggressiveness.
In addition, we examined the role of epidermal growth factor receptor (EGFR) in modulating TME in tiple-negative inflammatory breast cancer (TN-IBC). We analyzed patient samples in clinical trials and found that treatment with anti-EGFR antibody panitumumab converts the immunosuppressive TN-IBC TME to an immunoreactive status. Further examination revealed that EGFR/EGR1 pathway modulates the global expression of chemokines involved in the recruitment of immunosuppressive M2 macrophages and Tregs in TN-IBC tumors. This presentation will also discuss our future plans.
参考論文：
Semba T. et al. J Natl Cancer Inst 2022;114(1):97-108.
Wang X., Semba T. et al. Sci Adv 2022;8(50):eabn7983.
日時：２０２３年７月１３日（木） １１:４５ 〜 １２：４５
場所：吉田記念講堂
連絡先：野田 哲生
演題：Deciphering the mechanisms regulating tumor microenvironment promoting cancer progression
演者：千場 隆 博士（熊本大学国際先端医学研究機構（IRCMS）消化器がん生物学）
抄録：A tumor microenvironment (TME) is key for tumor progression. However, the molecular characteristics associated with the pro-tumor TME remain largely unknown. We have examined how the mitogen-activated protein kinase signaling and related pathways mediate the cell-cell cross-talk in immunosuppressive TME. We identified that a cluster with activated C-JUN N-terminal kinase (JNK)/JUN pathway in triple-negative breast cancer (TNBC) represents immunosuppressive TME status. We confirmed that JNK/JUN pathway-regulated CCL2 production from tumor-associated macrophages fosters an immunosuppressive TME by recruiting regulatory T cells (Tregs) to promote TNBC aggressiveness.
In addition, we examined the role of epidermal growth factor receptor (EGFR) in modulating TME in tiple-negative inflammatory breast cancer (TN-IBC). We analyzed patient samples in clinical trials and found that treatment with anti-EGFR antibody panitumumab converts the immunosuppressive TN-IBC TME to an immunoreactive status. Further examination revealed that EGFR/EGR1 pathway modulates the global expression of chemokines involved in the recruitment of immunosuppressive M2 macrophages and Tregs in TN-IBC tumors. This presentation will also discuss our future plans.
参考論文：
Semba T. et al. J Natl Cancer Inst 2022;114(1):97-108.
Wang X., Semba T. et al. Sci Adv 2022;8(50):eabn7983.
日時：２０２３年７月１３日（木） １１:４５ 〜 １２：４５
場所：吉田記念講堂
連絡先：野田 哲生
