miRNA-5119 regulates immune checkpoints in dendritic cells to enhance breast cancer immunotherapy

2020 ◽  
Vol 69 (6) ◽  
pp. 951-967 ◽  
Author(s):  
Meng Zhang ◽  
Yanmei Shi ◽  
Yujuan Zhang ◽  
Yifan Wang ◽  
Faizah Alotaibi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dendritic Cells ◽  
Cancer Immunotherapy ◽  
Immune Checkpoints

scholarly journals Molecular and Clinical Characterization of LAG3 in Breast Cancer Through 2994 Samples

2020 ◽  
Author(s):  
Qiang Liu ◽  
Yihang Qi ◽  
Jie Zhai ◽  
Xiangyi Kong ◽  
Xiangyu Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Immune Response ◽  
Cancer Immunotherapy ◽  
Cancer Patients ◽  
Immune Cell ◽  
Immune Checkpoints ◽  
Cell Populations ◽  
Potential Biomarker ◽  
The Impact

Abstract Background Despite the promising impact of cancer immunotherapy targeting CTLA4 and PD1/PDL1, a large number of cancer patients fail to respond. LAG3 (Lymphocyte Activating 3), also named CD233, is a protein Coding gene served as alternative inhibitory receptors to be targeted in the clinic. The impact of LAG3 on immune cell populations and co-regulation of immune response in breast cancer remained largely unknown. Methods To characterize the role of LAG3 in breast cancer, we investigated transcriptome data and associated clinical information derived from a total of 2994 breast cancer patients. Results We observed that LAG3 was closely correlated with major molecular and clinical characteristics, and was more likely to be enriched in higher malignant subtype, suggesting LAG3 was a potential biomarker of triple-negative breast cancer. Furthermore, we estimated the landscape of relationship between LAG3 and ten types of cell populations in breast cancer. Gene ontology analysis revealed LAG3 were strongly correlated with immune response and inflammatory activities. We investigated the correlation pattern between LAG3 and immune modulators in pan-cancer, especially the synergistic role of LAG3 with other immune checkpoints members in breast cancer. Conclusions LAG3 expression was closely related to malignancy of breast cancer and might serve as a potential biomarker; LAG3 might plays an important role in regulating tumor immune microenvironment, not only T cells, but also other immune cells. More importantly, LAG3 might synergize with CTLA4, PD1/ PDL1 and other immune checkpoints, thereby lending more evidences to combination cancer immunotherapy by targeting LAG3, PD1/PDL1, and CTLA4 together.

scholarly journals Targeting dendritic cells in situ for breast cancer immunotherapy

2012 ◽  
Vol 1 (8) ◽  
pp. 1398-1400 ◽  
Author(s):  
Bei Wang
Keyword(s):  
Breast Cancer ◽  
Dendritic Cells ◽  
Cancer Immunotherapy

scholarly journals Molecular and Clinical Characterization of LAG3 in Breast Cancer Through 2994 Samples

2021 ◽  
Vol 12 ◽  
Author(s):  
Qiang Liu ◽  
Yihang Qi ◽  
Jie Zhai ◽  
Xiangyi Kong ◽  
Xiangyu Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Immunotherapy ◽  
Cancer Patients ◽  
Immune Cell ◽  
Immune Checkpoints ◽  
Cell Populations ◽  
Breast Cancer Patients ◽  
Correlation Pattern ◽  
Potential Biomarker

Despite the promising impact of cancer immunotherapy targeting CTLA4 and PD1/PDL1, numerous cancer patients fail to respond. LAG3 (Lymphocyte Activating 3), also named CD233, serves as an alternative inhibitory receptor to be targeted in the clinic. The impacts of LAG3 on immune cell populations and coregulation of immune responses in breast cancer remain largely unknown. To characterize the role of LAG3 in breast cancer, we investigated transcriptome data and associated clinical information derived from 2,994 breast cancer patients. We estimated the landscape of the relationship between LAG3 and 10 types of cell populations of breast cancer. We investigated the correlation pattern between LAG3 and immune modulators in pancancer, particularly the synergistic role of LAG3 with other immune checkpoint members in breast cancer. LAG3 expression was closely related to the malignancy of breast cancer and may serve as a potential biomarker. LAG3 may play an important role in regulating the tumor immune microenvironment of T cells and other immune cells. More important, LAG3 may synergize with CTLA4, PD1/PDL1, and other immune checkpoints, thereby contributing more evidence to improve combination cancer immunotherapy by simultaneously targeting LAG3, PD1/PDL1, and CTLA4.

scholarly journals TIGIT-related transcriptome profile and its association with tumor immune microenvironment in breast cancer

2021 ◽  
Vol 41 (3) ◽  
Author(s):  
Qin Zhang ◽  
Chaowei Gao ◽  
Jianqiang Shao ◽  
Zunyi Wang
Keyword(s):  
Breast Cancer ◽  
Immune Responses ◽  
Cancer Immunotherapy ◽  
Large Scale ◽  
Immune Cell ◽  
Molecular Taxonomy ◽  
The Cancer Genome Atlas ◽  
Immune Checkpoints ◽  
Breast Cancer Patients ◽  
Transcriptome Profile

Abstract Immune checkpoints are intensively investigated as targets in cancer immunotherapy. T-cell immunoreceptor with immunoglobulin (Ig) and ITIM domains (TIGIT) are recently emerging as a novel promising target in cancer immunotherapy. Herein, we systematically investigated TIGIT-related transcriptome profile and relevant clinical information derived from a total of 2994 breast cancer patients recorded in The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC). We uncovered the relationship between TIGIT and major molecular and clinical characteristics in breast cancer. More importantly, we depicted the landscape of associations between TIGIT and other immune cell populations. Gene ontology analyses and Gene Set Variation Analysis (GSVA) of genes correlated with TIGIT revealed that TIGIT were mainly involved in immune responses and inflammatory activities. In summary, TIGIT expression was tightly related to the aggressiveness of breast cancer; TIGIT might manipulate anti-tumor immune responses by impacting not only T cells but also other immune cells. To the best of our knowledge, this is by far the most comprehensive and largest study characterizing the molecular and clinical features of TIGIT in breast cancer through large-scale transcriptome data.

scholarly journals Beyond PD-1/PD-L1 Inhibition: What the Future Holds for Breast Cancer Immunotherapy

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 628 ◽  
Author(s):  
Sebastian Chrétien ◽  
Ioannis Zerdes ◽  
Jonas Bergh ◽  
Alexios Matikas ◽  
Theodoros Foukakis
Keyword(s):  
Breast Cancer ◽  
Cancer Immunotherapy ◽  
Cytotoxic T Lymphocyte ◽  
Immune Checkpoints ◽  
Cancer Subtypes ◽  
Host Interactions ◽  
Inhibitory Molecules ◽  
The Cost ◽  
Cell Death Protein ◽  
Triple Negative Subtype

Cancer immunotherapy has altered the management of human malignancies, improving outcomes in an expanding list of diseases. Breast cancer - presumably due to its perceived low immunogenicity - is a late addition to this list. Furthermore, most of the focus has been on the triple negative subtype because of its higher tumor mutational load and lymphocyte-enriched stroma, although emerging data show promise on the other breast cancer subtypes as well. To this point the clinical use of immunotherapy is limited to the inhibition of two immune checkpoints, Programmed Cell Death Protein 1 (PD-1) and Cytotoxic T-lymphocyte-associated Protein 4 (CTLA-4). Consistent with the complexity of the regulation of the tumor – host interactions and their lack of reliance on a single regulatory pathway, combinatory approaches have shown improved efficacy albeit at the cost of increased toxicity. Beyond those two checkpoints though, a large number of co-stimulatory or co-inhibitory molecules play major roles on tumor evasion from immunosurveillance. These molecules likely represent future targets of immunotherapy provided that the promise shown in early data is translated into improved patient survival in randomized trials. The biological role, prognostic and predictive implications regarding breast cancer and early clinical efforts on exploiting these immune-related therapeutic targets are herein reviewed.

scholarly journals Silencing IDO in dendritic cells: A novel approach to enhance cancer immunotherapy in a murine breast cancer model

2012 ◽  
Vol 132 (4) ◽  
pp. 967-977 ◽  
Author(s):  
Xiufen Zheng ◽  
James Koropatnick ◽  
Di Chen ◽  
Thomas Velenosi ◽  
Hong Ling ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dendritic Cells ◽  
Cancer Immunotherapy ◽  
Cancer Model ◽  
Novel Approach ◽  
Breast Cancer Model

scholarly journals Research Progresses in Immunological Checkpoint Inhibitors for Breast Cancer Immunotherapy

2021 ◽  
Vol 11 ◽  
Author(s):  
Wenxiang Zhang ◽  
Xiangyi Kong ◽  
Bolun Ai ◽  
Zhongzhao Wang ◽  
Xiangyu Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Immunotherapy ◽  
Immune Checkpoint ◽  
Immune Escape ◽  
Checkpoint Inhibitors ◽  
Immune Checkpoints ◽  
Tumor Immune Escape ◽  
Cell Death Protein

Tumor immune escape refers to the phenomenon in which tumor cells escape the recognition and attack of the body’s immune system through various mechanisms so that they can survive and proliferate in vivo. The imbalance of immune checkpoint protein expression is the primary mechanism for breast cancer to achieve immune escape. Cytotoxic T lymphocyte antigen 4 (CTLA4) and programmed cell death protein 1 (PD-1)/programmed cell death protein-ligand 1 (PD-L1) are critical immune checkpoints for breast cancer. Immune checkpoint inhibitors block the checkpoint and relieve its inhibition effect on immune cells, reactivate T-cells and destroy cancer cells and restore the body’s ability to resist tumors. At present, immunological checkpoint inhibitors have made significant progress in breast cancer immunotherapy, and it is expected to become a new treatment for breast cancer.

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