The relationship between host immunity and gynecologic cancer is one of the most studied topics. At the present stage, it has been confirmed that gynecologic cancer development is supported by multiple non-tumor cells and soluble mediators, namely the tumor microenvironment (TME). In the TME, tumor-infiltrating lymphocytes (TILs) act as guardians, which can recognize and kill tumor cells. Moreover, the TME contains cancer-associated fibroblasts (CAFs), angiogenic cells (AVCs), endothelial cells, chemokines, growth factors, and antibodies. It has been validated that the dysregulated TME contributes to gynecologic cancer initiation and progression, as well as treatment resistance. Gynecologic cancer cells and other components in the TME could generate large numbers of immunomodulatory signals that can negatively (inhibitors) or positively (activators) affect the functions of immune cells. Therefore, the TME could switch the immunity from antitumor to pro-tumor mode according to the TME composition. Components in the TME, such as TGF-ß, are associated with poor outcomes of cervical cancer patients. Also, treatment strategies targeting the TME components, including regulatory T cells, MDSC, and TGF-ß have exhibited potent antitumor activity in the preclinical and clinical studies. Exploring the predictive and therapeutic values of the TME is meaningful for gynecologic cancer treatment.
This Research Topic will focus on the clinical significance of the TME components (such as tumor-infiltrating immune cells, cytokine, chemokines, and CAFs) for gynecologic cancer patients. Besides, due to the development of omics techniques, including single-cell RNA sequencing and bioinformatics, we could effectively reveal the changes in the TME during gynecologic cancer development. Omics-based predictive model or identifying the chemopathological features of the TME is helpful to risk classification for gynecologic cancer patients. Additionally, targeted strategies manipulating the TME are promising to restore antitumor immune response and overcome treatment resistance. In the era of immunotherapy, TME-targeted therapies, such as agents targeting monocyte or macrophage populations, might have synergistic effects with anti-PD-1/PD-L1 antibodies.
We welcome submissions of Original Research, Clinical Trials, Literature Reviews, Systematic Reviews, Short Reports, and Comments, on the subtopics of the following, but are not limited to:
? Prognostic significance of the TME components, such as tumor-infiltrating immune cells, cytokines, chemokines, and CAFs for gynecologic cancer patients.
? Omics-based or bioinformatics-involved model predicts the prognosis or treatment response of gynecologic cancer patients. Additional experiments are essential to validate the conclusion from public databases.
? Advances of TME-targeted therapies such as TGF-ß inhibitor, VEGF blockade, CXCR1/2 antagonist, CD40 agonist, CCR2 antagonist, and CSF1R inhibitor in gynecologic cancer.
? Single-cell RNA sequencing reveals the changes in the TME during gynecologic cancer development.
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.
The relationship between host immunity and gynecologic cancer is one of the most studied topics. At the present stage, it has been confirmed that gynecologic cancer development is supported by multiple non-tumor cells and soluble mediators, namely the tumor microenvironment (TME). In the TME, tumor-infiltrating lymphocytes (TILs) act as guardians, which can recognize and kill tumor cells. Moreover, the TME contains cancer-associated fibroblasts (CAFs), angiogenic cells (AVCs), endothelial cells, chemokines, growth factors, and antibodies. It has been validated that the dysregulated TME contributes to gynecologic cancer initiation and progression, as well as treatment resistance. Gynecologic cancer cells and other components in the TME could generate large numbers of immunomodulatory signals that can negatively (inhibitors) or positively (activators) affect the functions of immune cells. Therefore, the TME could switch the immunity from antitumor to pro-tumor mode according to the TME composition. Components in the TME, such as TGF-ß, are associated with poor outcomes of cervical cancer patients. Also, treatment strategies targeting the TME components, including regulatory T cells, MDSC, and TGF-ß have exhibited potent antitumor activity in the preclinical and clinical studies. Exploring the predictive and therapeutic values of the TME is meaningful for gynecologic cancer treatment.
This Research Topic will focus on the clinical significance of the TME components (such as tumor-infiltrating immune cells, cytokine, chemokines, and CAFs) for gynecologic cancer patients. Besides, due to the development of omics techniques, including single-cell RNA sequencing and bioinformatics, we could effectively reveal the changes in the TME during gynecologic cancer development. Omics-based predictive model or identifying the chemopathological features of the TME is helpful to risk classification for gynecologic cancer patients. Additionally, targeted strategies manipulating the TME are promising to restore antitumor immune response and overcome treatment resistance. In the era of immunotherapy, TME-targeted therapies, such as agents targeting monocyte or macrophage populations, might have synergistic effects with anti-PD-1/PD-L1 antibodies.
We welcome submissions of Original Research, Clinical Trials, Literature Reviews, Systematic Reviews, Short Reports, and Comments, on the subtopics of the following, but are not limited to:
? Prognostic significance of the TME components, such as tumor-infiltrating immune cells, cytokines, chemokines, and CAFs for gynecologic cancer patients.
? Omics-based or bioinformatics-involved model predicts the prognosis or treatment response of gynecologic cancer patients. Additional experiments are essential to validate the conclusion from public databases.
? Advances of TME-targeted therapies such as TGF-ß inhibitor, VEGF blockade, CXCR1/2 antagonist, CD40 agonist, CCR2 antagonist, and CSF1R inhibitor in gynecologic cancer.
? Single-cell RNA sequencing reveals the changes in the TME during gynecologic cancer development.
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.
