Search

Your search keyword '"Rashmi Srivastava"' showing total 10 results
Start Over Author "Rashmi Srivastava" Publisher american association for cancer research (aacr)
10 results on '"Rashmi Srivastava"'

2. Supplementary Table from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma

Author

Qianghu Wang, Tao Jiang, Roel G.W. Verhaak, Yongping You, Hongbing Shen, Zhibin Hu, Siyuan Zheng, Baoli Hu, Sali Lv, Xu Qian, Xiuxing Wang, Lang Hu, Fan Lin, Ruohan Zhang, Bin Huang, Yuan Liang, Yun Cai, Tingting Zhang, Rashmi Srivastava, Han Zou, Xiangwei Xiao, Yinan Jiang, Apeng Chen, Kening Li, Jie Li, Ziyu Wang, Quanzhong Liu, Xiaoguang Qiu, Wei Zhang, Rui-Chao Chai, Yuxin Du, Fengqi Zhou, Fan Wu, Min Wu, Mengyan Zhu, Liangyu Li, Zheng Zhao, Junxia Zhang, Wei Wu, and Lingxiang Wu

Abstract

Supplementary Table from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma

Published
2023
Full Text
View/download PDF

3. Data from IRF1 Inhibits Antitumor Immunity through the Upregulation of PD-L1 in the Tumor Cell

Author

Saumendra N. Sarkar, Greg M. Delgoffe, Christopher J. Bakkenist, Hassane M. Zarour, Veit Hornung, Stephen H. Thorne, Pooja Karukonda, Joe-Marc Chauvin, Yiyang Wang, Ashley V. Menk, Chandra Nath Roy, Rashmi Srivastava, Frank P. Vendetti, Nicole E. Scharping, Weizhou Hou, and Lulu Shao

Abstract

Multiple studies have associated the transcription factor IRF1 with tumor-suppressive activities. Here, we report an opposite tumor cell–intrinsic function of IRF1 in promoting tumor growth. IRF1-deficient tumor cells showed reduced tumor growth in MC38 and CT26 colon carcinoma and B16 melanoma mouse models. This reduction in tumor growth was dependent on host CD8+ T cells. Detailed profiling of tumor-infiltrating leukocytes did not show changes in the various T-cell and myeloid cell populations. However, CD8+ T cells that had infiltrated IRF1-deficieint tumors in vivo exhibited enhanced cytotoxicity. IRF1-deficient tumor cells lost the ability to upregulate PD-L1 expression in vitro and in vivo and were more susceptible to T-cell–mediated killing. Induced expression of PD-L1 in IRF1-deficient tumor cells restored tumor growth. These results indicate differential activity of IRF1 in tumor escape.

Published
2023
Full Text
View/download PDF

5. Supplementary Data from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma

Author

Qianghu Wang, Tao Jiang, Roel G.W. Verhaak, Yongping You, Hongbing Shen, Zhibin Hu, Siyuan Zheng, Baoli Hu, Sali Lv, Xu Qian, Xiuxing Wang, Lang Hu, Fan Lin, Ruohan Zhang, Bin Huang, Yuan Liang, Yun Cai, Tingting Zhang, Rashmi Srivastava, Han Zou, Xiangwei Xiao, Yinan Jiang, Apeng Chen, Kening Li, Jie Li, Ziyu Wang, Quanzhong Liu, Xiaoguang Qiu, Wei Zhang, Rui-Chao Chai, Yuxin Du, Fengqi Zhou, Fan Wu, Min Wu, Mengyan Zhu, Liangyu Li, Zheng Zhao, Junxia Zhang, Wei Wu, and Lingxiang Wu

Abstract

Supplementary Data from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma

Published
2023
Full Text
View/download PDF

6. Supplementary Figure from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma

Author

Qianghu Wang, Tao Jiang, Roel G.W. Verhaak, Yongping You, Hongbing Shen, Zhibin Hu, Siyuan Zheng, Baoli Hu, Sali Lv, Xu Qian, Xiuxing Wang, Lang Hu, Fan Lin, Ruohan Zhang, Bin Huang, Yuan Liang, Yun Cai, Tingting Zhang, Rashmi Srivastava, Han Zou, Xiangwei Xiao, Yinan Jiang, Apeng Chen, Kening Li, Jie Li, Ziyu Wang, Quanzhong Liu, Xiaoguang Qiu, Wei Zhang, Rui-Chao Chai, Yuxin Du, Fengqi Zhou, Fan Wu, Min Wu, Mengyan Zhu, Liangyu Li, Zheng Zhao, Junxia Zhang, Wei Wu, and Lingxiang Wu

Abstract

Supplementary Figure from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma

Published
2023
Full Text
View/download PDF

8. Data from Natural Coevolution of Tumor and Immunoenvironment in Glioblastoma

Author

Qianghu Wang, Tao Jiang, Roel G.W. Verhaak, Yongping You, Hongbing Shen, Zhibin Hu, Siyuan Zheng, Baoli Hu, Sali Lv, Xu Qian, Xiuxing Wang, Lang Hu, Fan Lin, Ruohan Zhang, Bin Huang, Yuan Liang, Yun Cai, Tingting Zhang, Rashmi Srivastava, Han Zou, Xiangwei Xiao, Yinan Jiang, Apeng Chen, Kening Li, Jie Li, Ziyu Wang, Quanzhong Liu, Xiaoguang Qiu, Wei Zhang, Rui-Chao Chai, Yuxin Du, Fengqi Zhou, Fan Wu, Min Wu, Mengyan Zhu, Liangyu Li, Zheng Zhao, Junxia Zhang, Wei Wu, and Lingxiang Wu

Abstract

Isocitrate dehydrogenase (IDH) wild-type glioblastoma (GBM) has a dismal prognosis. A better understanding of tumor evolution holds the key to developing more effective treatment. Here we study GBM's natural evolutionary trajectory by using rare multifocal samples. We sequenced 61,062 single cells from eight multifocal IDH wild-type primary GBMs and defined a natural evolution signature (NES) of the tumor. We show that the NES significantly associates with the activation of transcription factors that regulate brain development, including MYBL2 and FOSL2. Hypoxia is involved in inducing NES transition potentially via activation of the HIF1A–FOSL2 axis. High-NES tumor cells could recruit and polarize bone marrow–derived macrophages through activation of the FOSL2–ANXA1–FPR1/3 axis. These polarized macrophages can efficiently suppress T-cell activity and accelerate NES transition in tumor cells. Moreover, the polarized macrophages could upregulate CCL2 to induce tumor cell migration.Significance:GBM progression could be induced by hypoxia via the HIF1A–FOSL2 axis. Tumor-derived ANXA1 is associated with recruitment and polarization of bone marrow–derived macrophages to suppress the immunoenvironment. The polarized macrophages promote tumor cell NES transition and migration.This article is highlighted in the In This Issue feature, p. 2711

Published
2023
Full Text
View/download PDF

10. IRF1 Inhibits Antitumor Immunity through the Upregulation of PD-L1 in the Tumor Cell

Author

Saumendra N. Sarkar, Christopher J. Bakkenist, Hassane M. Zarour, Veit Hornung, rashmi Srivastava, Yiyang Wang, Weizhou Hou, Ashley V. Menk, Nicole E. Scharping, Lulu Shao, Joe-Marc Chauvin, Stephen H. Thorne, Pooja Karukonda, Chandra Nath Roy, Greg M. Delgoffe, and Frank P. Vendetti

Subjects
0301 basic medicine, Cancer Research, Myeloid, T-Lymphocytes, Immunology, Cell, Melanoma, Experimental, B7-H1 Antigen, Article, Immunomodulation, Mice, 03 medical and health sciences, Lymphocytes, Tumor-Infiltrating, 0302 clinical medicine, In vivo, Cell Line, Tumor, medicine, Animals, Humans, Mice, Knockout, Chemistry, Melanoma, medicine.disease, Gene Expression Regulation, Neoplastic, Disease Models, Animal, Cell Transformation, Neoplastic, 030104 developmental biology, medicine.anatomical_structure, IRF1, Tumor Escape, Cell culture, 030220 oncology & carcinogenesis, Disease Progression, Cancer research, Immunologic Memory, CD8, Interferon Regulatory Factor-1
Abstract

Multiple studies have associated the transcription factor IRF1 with tumor-suppressive activities. Here, we report an opposite tumor cell–intrinsic function of IRF1 in promoting tumor growth. IRF1-deficient tumor cells showed reduced tumor growth in MC38 and CT26 colon carcinoma and B16 melanoma mouse models. This reduction in tumor growth was dependent on host CD8+ T cells. Detailed profiling of tumor-infiltrating leukocytes did not show changes in the various T-cell and myeloid cell populations. However, CD8+ T cells that had infiltrated IRF1-deficieint tumors in vivo exhibited enhanced cytotoxicity. IRF1-deficient tumor cells lost the ability to upregulate PD-L1 expression in vitro and in vivo and were more susceptible to T-cell–mediated killing. Induced expression of PD-L1 in IRF1-deficient tumor cells restored tumor growth. These results indicate differential activity of IRF1 in tumor escape.

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results