Publications by authors named "Amber E de Groot"

Article Synopsis
  • TIGIT is an inhibitory receptor that competes with CD226 on immune cells, and targeting it may improve anti-tumor immunity, especially in exhausted CD8+ T cells and regulatory T cells.
  • Combining different types of anti-TIGIT antibodies (Fc-enabled and Fc-silent) with another treatment showed varied effects on tumors: Fc-enabled antibodies reduced regulatory T cell numbers, while Fc-silent antibodies did not deplete these cells but enhanced the activity of tumor-specific CD8+ T cells.
  • The study highlights that Fc-silent anti-TIGIT antibodies can drive antitumor responses by activating exhausted T cells without affecting regulatory T cells, indicating their potential for cancer therapy.
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  • The prostate cancer tumor microenvironment (TME) contains various cell types, including macrophages that can be M1-like (anti-tumor) or M2-like (pro-tumor), with M2 macrophages playing a key role in efferocytosis, the process of engulfing dying cells.
  • Research suggests that targeting MerTK, a receptor involved in efferocytosis, may hinder tumor growth and enhance anti-tumor immune responses.
  • Initial findings from experiments show that M2 macrophages have a higher capacity for efferocytosis of prostate cancer cells and that inhibiting MerTK reduces this process, promoting a shift toward a more anti-tumor immune profile in a mouse model.
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  • Tumor-associated macrophages (TAMs) are key components in the tumor microenvironment, often promoting tumor growth and metastasis through a pro-tumor M2-like phenotype.
  • Treatment with Dupilumab, an IL-4 receptor alpha antagonist, reduces M2 macrophage characteristics in human ex vivo models by altering cell surface markers and gene expression.
  • In animal studies, targeting IL-4R alpha significantly decreases M2-like markers on TAMs, suggesting it could be a promising therapeutic strategy in cancer treatment.
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  • Tumor-associated macrophages (TAMs) are important in prostate cancer and common orthotopic models do not accurately represent the tumor microenvironment.
  • Genetically engineered mouse models, specifically Hi-Myc and TRAMP, have been studied to understand TAM characteristics and their role in tumor progression.
  • The Hi-Myc model shows a higher density of TAMs and is suggested to better reflect human prostate cancer, making it a more suitable option for developing novel therapies targeting the TME.
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  • Solid tumors trigger an immune response, but this response often aids tumor growth instead of fighting it, mainly due to the presence of tumor-associated macrophages (TAMs).
  • RP-182 is a synthetic compound that targets the mannose receptor on M2-like macrophages, reprogramming them from supporting tumors to an antitumor M1-like phenotype, which boosts immune activity.
  • In various murine cancer models, RP-182 showed success in slowing tumor growth and enhancing survival, especially when used alongside traditional therapies, while also increasing the phagocytosis of cancer cells by the reprogrammed TAMs.
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Article Synopsis
  • The progression of cancer is influenced by both malignant cell growth and the behavior of the tumor microenvironment (TME), particularly tumor-associated macrophages (TAMs).
  • Depending on their polarization, TAMs can either promote (M2) or inhibit (M1) tumor growth, with epigenetic regulation playing a critical role in this process.
  • The review discusses current knowledge on key epigenetic enzymes and their potential as pharmacologic modulators to selectively target M2 macrophages in cancer treatment.
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  • Cancers are complex ecosystems made up of various cell types and noncellular components, including a crucial part called the tumour stroma.
  • Most cancer treatments focus solely on killing cancer cells, but the tumour stroma can help cancer cells resist these therapies, complicating treatment outcomes.
  • Combining treatments that target both cancer cells and the tumour stroma could lead to more effective therapies and better results for patients.
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  • Metastasis occurs when cancer cells spread from the original tumor to other parts of the body, which can lead to severe complications.
  • Current research primarily emphasizes the interaction between metastatic cells ("seeds") and their new environments ("soil"), but the conditions within the original tumor’s environment have received less attention.
  • Understanding the selective pressures within the primary tumor that lead to the development of aggressive metastatic cells is crucial for advancing our knowledge of prostate cancer metastasis.
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  • A new method called "Glyco-seek" allows for the non-destructive analysis of O-GlcNAcylated proteins using a combination of labeling, proximity ligation, and quantitative PCR.
  • This technique offers extremely high sensitivity, enabling the detection of very low amounts (attomoles) of glycoproteins in cellular samples.
  • Glyco-seek can operate alongside traditional assays to measure both O-GlcNAcylation levels and total protein amounts, providing a comprehensive view of protein modifications without the need for complex isolation processes.
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  • Developing reagents to detect glycosylated proteins poses challenges, but cyclooctyne-aptamer conjugates offer a promising solution.
  • These conjugates target and bind to specific glycans on a protein in live cells, allowing for precise detection.
  • The study shows these aptamer conjugates can successfully identify different glycosylation forms using techniques like mass spectrometry and Western blotting, indicating their potential for broader research applications in cell biology.
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