About this Research Topic
This Research Topic is the second volume in this series, "Community Series in Title". Please see volume I here.
The canonical Notch pathway is based on a conserved signal transduction machinery that, in mammals, begins with the interaction between receptors (Notch-1 to -4) and ligands (Jagged-1 and -2 or Delta-like (Dll)-1, -3 and -4), physiologically expressed on neighboring cells. Then, sequential cleavages result in the release of the Notch intracellular domain that translocates into the nucleus, interacts with the DNA binding protein CSL/RBP-Jk, and promotes the transcription of target genes. The activation of Notch signaling influences the biology of many cell types, including cells of the immune system, through the control of crucial biological processes, such as survival, proliferation, differentiation, and tissue homeostasis. The outcome of Notch signaling is highly context-dependent due to the many levels of regulation involved. Not surprisingly, the aberrant modulation of the Notch pathway, either positive or negative, is involved in the development of different types of solid tumors and hematologic malignancies where the role of Notch can be either oncogenic or tumor suppressive.
In the past, many efforts have focused on the dissection of the role of Notch in tumor onset and progression. More recently, accumulating evidence suggests a pivotal role of Notch signaling in the cross-talk between tumor cells and the microenvironment. However, the effects of Notch signaling on tumor immune responses and immune surveillance remain underexplored. The interactions between Notch, tumor cells, the tumor environment, and the immune system may influence the progression and the outcome of neoplastic processes and likely represent new targets of tailored cancer therapies.
This Research Topic will focus on the description of the mechanisms through which the modulation of Notch signaling in tumor cells and/or components of the tumor environment may impact on the behavior of cell subsets involved in the adaptive and innate immune response, and subsequently, on their responses against the tumor, either favoring or limiting cancer cell growth and expansion.
We welcome the submission of Original Research and Review articles that cover, but are not limited, to the following topics:
1. Notch and effector T cell response in cancer
2. Notch and MDSC response in cancer
3. Notch and regulatory T cell response in cancer
4. Notch and B cell response in cancer
5. Notch and NK cell response in cancer
6. Notch and myeloid cell subset response in cancer
7. Notch and Innate Lymphoid Cells (ILC) in cancer
8. Notch, chemokines, and cancer
9. Notch and non-coding RNAs in cancer
10. Notch, inflammation and cancer
11. Notch and nutrition in cancer
12. Notch and metabolism in cancer
13. Notch and cancer immunotherapies
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
The canonical Notch pathway is based on a conserved signal transduction machinery that, in mammals, begins with the interaction between receptors (Notch-1 to -4) and ligands (Jagged-1 and -2 or Delta-like (Dll)-1, -3 and -4), physiologically expressed on neighboring cells. Then, sequential cleavages result in the release of the Notch intracellular domain that translocates into the nucleus, interacts with the DNA binding protein CSL/RBP-Jk, and promotes the transcription of target genes. The activation of Notch signaling influences the biology of many cell types, including cells of the immune system, through the control of crucial biological processes, such as survival, proliferation, differentiation, and tissue homeostasis. The outcome of Notch signaling is highly context-dependent due to the many levels of regulation involved. Not surprisingly, the aberrant modulation of the Notch pathway, either positive or negative, is involved in the development of different types of solid tumors and hematologic malignancies where the role of Notch can be either oncogenic or tumor suppressive.
In the past, many efforts have focused on the dissection of the role of Notch in tumor onset and progression. More recently, accumulating evidence suggests a pivotal role of Notch signaling in the cross-talk between tumor cells and the microenvironment. However, the effects of Notch signaling on tumor immune responses and immune surveillance remain underexplored. The interactions between Notch, tumor cells, the tumor environment, and the immune system may influence the progression and the outcome of neoplastic processes and likely represent new targets of tailored cancer therapies.
This Research Topic will focus on the description of the mechanisms through which the modulation of Notch signaling in tumor cells and/or components of the tumor environment may impact on the behavior of cell subsets involved in the adaptive and innate immune response, and subsequently, on their responses against the tumor, either favoring or limiting cancer cell growth and expansion.
We welcome the submission of Original Research and Review articles that cover, but are not limited, to the following topics:
1. Notch and effector T cell response in cancer
2. Notch and MDSC response in cancer
3. Notch and regulatory T cell response in cancer
4. Notch and B cell response in cancer
5. Notch and NK cell response in cancer
6. Notch and myeloid cell subset response in cancer
7. Notch and Innate Lymphoid Cells (ILC) in cancer
8. Notch, chemokines, and cancer
9. Notch and non-coding RNAs in cancer
10. Notch, inflammation and cancer
11. Notch and nutrition in cancer
12. Notch and metabolism in cancer
13. Notch and cancer immunotherapies
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Keywords: Notch signaling, Tumor immunology, Immune surveillance, Tumor microenvironment, Cancer immunotherapy
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
