Publications by authors named "Anna Mistarz"

Article Synopsis
  • The study aimed to understand how inflammation within the perivascular tumor microenvironment (TME) influences the movement and effectiveness of T-cells in fighting ovarian tumors.
  • Researchers found that moderate inflammation, triggered by a specialized oncolytic virus, led to better T-cell activity and less immune suppression compared to weak or strong inflammation.
  • The results suggest that combining treatments could help T-cells better navigate the TME and improve their efficiency in combating cancer.
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Tumor antigen-driven responses to weakly immunogenic self-antigens and neoantigens directly affect treatment efficacy following immunotherapy. Using orthotopically grown SV40 T antigen ovarian carcinoma in antigen-naive wild-type or Tg transgenic mice expressing SV40 T antigen as a self-antigen, we investigated the impact of CXCR4-antagonist-armed oncolytic virotherapy on tumor progression and antitumor immunity. Immunostaining and single-cell RNA sequencing analyses of the peritoneal tumor microenvironment of untreated tumors in syngeneic wild-type mice revealed the presence of SV40 T antigen-specific CD8 T cells, a balanced M1/M2 transcriptomic signature of tumor-associated macrophages, and immunostimulatory cancer-associated fibroblasts.

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Objectives: Standard chemotherapy agents, including carboplatin, have known immunogenic properties. We sought to determine how carboplatin may influence lymphocyte trafficking to tumor sites.

Methods: Murine models of ovarian cancer were utilized to examine lymphocyte trafficking with common clinically used agents including carboplatin, anti-PD-1 antibody, or anti-VEGFR-2 antibody.

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We have demonstrated that oncolytic vaccinia virus synergizes with doxorubicin (DOX) in inducing immunogenic cell death in platinum-resistant ovarian cancer cells and increases survival in syngeneic and xenograft tumor models. However, the mechanisms underlying the virus- and doxorubicin-mediated cancer cell death remain unknown. In this study, we investigated the effect of the oncolytic virus and doxorubicin used alone or in combination on activation of the cytoplasmic transcription factor CREB3L1 (cyclic AMP [cAMP] response element-binding protein 3-like 1) in ovarian cancer cell lines and clinical specimens.

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Intratumoral dendritic cells play an important role in stimulating cytotoxic T cells and driving antitumor immunity. Using a metastatic ovarian tumor model in syngeneic mice, we explored whether therapy with a CXCR4 antagonist-armed oncolytic vaccinia virus activates endogenous CD103 dendritic cell responses associated with the induction of adaptive immunity against viral and tumor antigens. The overall goal of this study was to determine whether expansion of CD103 dendritic cells by the virally delivered CXCR4 antagonist augments overall survival and boosting with a tumor antigen peptide-based vaccine.

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Article Synopsis
  • - The study investigates MCPIP1, a protein linked to cell differentiation and tumor suppression, which is minimally understood in the context of cancer, specifically neuroblastoma, a common childhood cancer.
  • - Findings show that MCPIP1 is not expressed in primary neuroblastoma and enforcing its expression in neuroblastoma cells significantly reduces their growth and survival.
  • - The research reveals that overexpressed MCPIP1 decreases levels of the choline transporter (CTL1) and identifies microRNA-3613-3p as a key player, suggesting that MCPIP1 may regulate this microRNA, impacting choline transport in cancer cells.
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