<p>The protein levels of Twist1 (A) and p53 (B) in tumor samples. Protein levels were determined by the quantification of western blot band intensity comparing to GAPDH bands as loading control.</p>
<p>A. Kaplan Meier curve comparing overall survival in mice treated with PBS Control, CARG-2020, VLV-IL-12, VLV-17R ECD, VLV-shRNA PD-L1, and VLV-GFP; p<0.0001. B. CARG-2020 but not VLV-IL-12 modulates the innate immune system. Peritoneal lavage from VLV-IL-12 and CARG-2020-treated mice (n=6) were analyzed by flow cytometry for macrophages using CD11b and CD206. VLV-IL-12 treatment is not able to increase the number of CD11blow/CD206- macrophages compared to CARG2020. Representative dot plots shown. Gating strategy is shown in Supp. Fig. 1. C. Decrease on Ly6C+/Ly6G+ MSC is observed only in the CARG2020 treated group but not in those treated with VLV-IL-12 group. Representative dot plots shown. Gating strategy is shown in Supp. Fig. 1.</p>
<p>A. Kaplan Meier curve comparing overall survival in mice treated with PBS Control, CARG-2020, VLV-IL-12, VLV-17R ECD, VLV-shRNA PD-L1, and VLV-GFP; p<0.0001. B. CARG-2020 but not VLV-IL-12 modulates the innate immune system. Peritoneal lavage from VLV-IL-12 and CARG-2020-treated mice (n=6) were analyzed by flow cytometry for macrophages using CD11b and CD206. VLV-IL-12 treatment is not able to increase the number of CD11blow/CD206- macrophages compared to CARG2020. Representative dot plots shown. Gating strategy is shown in Supp. Fig. 1. C. Decrease on Ly6C+/Ly6G+ MSC is observed only in the CARG2020 treated group but not in those treated with VLV-IL-12 group. Representative dot plots shown. Gating strategy is shown in Supp. Fig. 1.</p>
Ovarian and other peritoneal cancers have a strong tendency to metastasize into the surrounding adipose tissue. This study describes an effect of the adipose microenvironment on upregulation of sialic acid-containing glycans in ovarian cancer (OC). Heterogeneous populations of glycosylated OC tumors converged to a highly sialylated cell state that regulates tumorigenesis in an immune-dependent manner.
The association between chronic inflammation and cancer has long been observed. Furthermore, NF‐ κ B activation and the subsequent production of cytokines, chemokines, growth factors, and antiapoptotic proteins has been found to be involved in cancer progression and chemoresistance. However, the signals inducing NF‐ κ B in cancer cells are still not well understood. Here, we reviewed the association between chronic inflammation and cancer, the role of NF‐ κ B and its inhibitors as potential anticancer drugs, and Toll‐like receptors as possible signal initiators for NF‐ κ B activation and inflammation‐induced carcinogenesis and chemoresistance. Furthermore, we propose that, the stimulation of Toll‐like receptors by microbial components and/or endogenous ligands may represent the initial signal promoting a proinflammatory environment that will enhance tumor growth and chemoresistance.
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