Programmed cell death (PCD) has been proven to play a fundamental role in the development and metastasis of malignant tumors. Malignant tumor cells constantly overcome various forms of cell death and achieve further development.
PCD includes pyroptosis, ferroptosis, cuproptosis, necrotic apoptosis, etc. Studies have shown that pyroptosis can stimulate M1 polarization of macrophages, lead to the maturation of dendritic cells (DC) and activate CD8+cytotoxic T lymphocytes (CTL). The immune response caused by pyroptosis can transform the "cold" tumor microenvironment (TME) of immunosuppression into immunogenic "hot" TME, which can not only inhibit the growth of primary pancreatic cancer but also attack distant tumors. In addition, Ferroptosis is a unique targeted immunosuppressive mechanism of PMN MDSCs in the TME, which can limit tumor progression through pharmacological regulation. However, few studies have systematically investigated the differences in the regulation of the immune microenvironment by multiple PCDs. And there are still many malignant tumors that have not been thoroughly studied.
Given the pivotal roles of programmed cell death in the tumor immune microenvironment, we systematically evaluated the diversity of programmed cell death and its nonnegligible role in various malignant tumors. In addition, we explore how programmed cell death regulates the reshaping of tumor immune microenvironment across many types of cancers and gain insight into the mechanisms.
We welcome authors to contribute Original Research articles as well as Review articles that focus on the topic of tumor immunotherapy and metabolic dysfunction. Potential subtopics include, but are not limited to:
(1) Exploring the diversity and uniqueness of programmed cell death in TME.
(2) What influence will different programmed cell death modes have on the immune microenvironment and its mechanism?
(3) Whether programmed cell death in the tumor microenvironment is associated with immunotherapy response?
(4) How to use programmed cell death to enhance antitumor immune responses?
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 the scope for this section and will not be accepted as part of this Research Topic.
Programmed cell death (PCD) has been proven to play a fundamental role in the development and metastasis of malignant tumors. Malignant tumor cells constantly overcome various forms of cell death and achieve further development.
PCD includes pyroptosis, ferroptosis, cuproptosis, necrotic apoptosis, etc. Studies have shown that pyroptosis can stimulate M1 polarization of macrophages, lead to the maturation of dendritic cells (DC) and activate CD8+cytotoxic T lymphocytes (CTL). The immune response caused by pyroptosis can transform the "cold" tumor microenvironment (TME) of immunosuppression into immunogenic "hot" TME, which can not only inhibit the growth of primary pancreatic cancer but also attack distant tumors. In addition, Ferroptosis is a unique targeted immunosuppressive mechanism of PMN MDSCs in the TME, which can limit tumor progression through pharmacological regulation. However, few studies have systematically investigated the differences in the regulation of the immune microenvironment by multiple PCDs. And there are still many malignant tumors that have not been thoroughly studied.
Given the pivotal roles of programmed cell death in the tumor immune microenvironment, we systematically evaluated the diversity of programmed cell death and its nonnegligible role in various malignant tumors. In addition, we explore how programmed cell death regulates the reshaping of tumor immune microenvironment across many types of cancers and gain insight into the mechanisms.
We welcome authors to contribute Original Research articles as well as Review articles that focus on the topic of tumor immunotherapy and metabolic dysfunction. Potential subtopics include, but are not limited to:
(1) Exploring the diversity and uniqueness of programmed cell death in TME.
(2) What influence will different programmed cell death modes have on the immune microenvironment and its mechanism?
(3) Whether programmed cell death in the tumor microenvironment is associated with immunotherapy response?
(4) How to use programmed cell death to enhance antitumor immune responses?
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 the scope for this section and will not be accepted as part of this Research Topic.
