In recent years, there have been considerable achievements in cancer immunotherapy based on immune checkpoint inhibitors (ICIs). However, many cancer patients respond poorly or even non-responsively to ICIs, in part due to the lack of tumor-infiltrating lymphocytes (TILs), which greatly limits the application of ICIs. Transforming these immune "cold" tumors into "hot" tumors that may respond to ICIs is an unsolved problem in cancer immunotherapy. Some cell death patterns also exhibit immunogenicity and can enhance the body's anticancer immunity. Programmed cell death (PCD), including apoptosis, autophagy, pyroptosis, necroptosis, and ferroptosis, has been reported to play an important role in the clearance of abnormal cells in homeostasis and is considered a promising cancer treatment strategy. Recently, several studies have shown crosstalk between different cell death mechanisms and antitumor immunity. Induction of pyroptosis, ferroptosis, and necroptosis combined with ICI showed synergistically enhanced antitumor activity, even in ICI-resistant tumors. As various cell deaths progress, many antigens, cytokines, and chemokines are released from cancer cells into the extracellular milieu, and these agonists effectively initiate and amplify immune responses. Therefore, an in-depth understanding of the molecular mechanisms of different tumor cell death modes and the interaction of these cell death modes with anti-tumor immunity is of great significance for improving anti-tumor immunity.
The purpose of this research topic is to deeply study the role of each PCD in tumor immune regulation; to explore the biological function, expression regulation and activation mechanism of PCD cell death mediators in tumors, so as to find more efficient immunotherapy targets. We hope to improve the efficacy of immunotherapy by promoting the death of cancer cells and helping "cold" tumors become "hot" tumors.
In this research topic, we welcome researchers to submit perspectives, original articles, reviews, comments and letters on the topic. Including but not limited to the following topics:
(1) The role of programmed cell death in mediating tumor microenvironment heterogeneity
(2) Drugs targeting cell death pathways (small molecules, peptides, nano-drugs, gene therapy, etc.)
(3) Identification of multiple biomarkers associated with programmed cell death for cancer diagnosis and prognosis
(4) Correlation between tumor cell death mode and immune cell infiltration
(5) Combination therapy of cell death inducers and tumor immunity
(6) Interactions between different types of programmed cell death in cancer
(7) Influence of tumor cell death mode on cancer microenvironment and immunotherapy
(8) The role of immunogenic cell death in tumor immunity
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this Research Topic and will not be accepted as part of this Research Topic.
In recent years, there have been considerable achievements in cancer immunotherapy based on immune checkpoint inhibitors (ICIs). However, many cancer patients respond poorly or even non-responsively to ICIs, in part due to the lack of tumor-infiltrating lymphocytes (TILs), which greatly limits the application of ICIs. Transforming these immune "cold" tumors into "hot" tumors that may respond to ICIs is an unsolved problem in cancer immunotherapy. Some cell death patterns also exhibit immunogenicity and can enhance the body's anticancer immunity. Programmed cell death (PCD), including apoptosis, autophagy, pyroptosis, necroptosis, and ferroptosis, has been reported to play an important role in the clearance of abnormal cells in homeostasis and is considered a promising cancer treatment strategy. Recently, several studies have shown crosstalk between different cell death mechanisms and antitumor immunity. Induction of pyroptosis, ferroptosis, and necroptosis combined with ICI showed synergistically enhanced antitumor activity, even in ICI-resistant tumors. As various cell deaths progress, many antigens, cytokines, and chemokines are released from cancer cells into the extracellular milieu, and these agonists effectively initiate and amplify immune responses. Therefore, an in-depth understanding of the molecular mechanisms of different tumor cell death modes and the interaction of these cell death modes with anti-tumor immunity is of great significance for improving anti-tumor immunity.
The purpose of this research topic is to deeply study the role of each PCD in tumor immune regulation; to explore the biological function, expression regulation and activation mechanism of PCD cell death mediators in tumors, so as to find more efficient immunotherapy targets. We hope to improve the efficacy of immunotherapy by promoting the death of cancer cells and helping "cold" tumors become "hot" tumors.
In this research topic, we welcome researchers to submit perspectives, original articles, reviews, comments and letters on the topic. Including but not limited to the following topics:
(1) The role of programmed cell death in mediating tumor microenvironment heterogeneity
(2) Drugs targeting cell death pathways (small molecules, peptides, nano-drugs, gene therapy, etc.)
(3) Identification of multiple biomarkers associated with programmed cell death for cancer diagnosis and prognosis
(4) Correlation between tumor cell death mode and immune cell infiltration
(5) Combination therapy of cell death inducers and tumor immunity
(6) Interactions between different types of programmed cell death in cancer
(7) Influence of tumor cell death mode on cancer microenvironment and immunotherapy
(8) The role of immunogenic cell death in tumor immunity
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this Research Topic and will not be accepted as part of this Research Topic.
