Publications by authors named "Sarah E Ferrara"

The immature and dysfunctional vascular network within solid tumors poses a substantial obstacle to immunotherapy because it creates a hypoxic tumor microenvironment that actively limits immune cell infiltration. The molecular basis underpinning this vascular dysfunction is not fully understood. Using genome-scale receptor array technology, we showed here that insulin-like growth factor binding protein 7 (IGFBP7) interacts with its receptor CD93, and we subsequently demonstrated that this interaction contributes to abnormal tumor vasculature.

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  • * Researchers identified a protein called mediator of DNA damage checkpoint 1 (MDC1) that acts as a novel ER coregulator in ILC, influencing cell proliferation and tamoxifen resistance when its expression is suppressed.
  • * The study suggests that MDC1's role in ILC differs from its traditional tumor suppressor function in DNA damage response, indicating it may help regulate estrogen-related activities specific to ILC and offers potential targets for overcoming treatment resistance.
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  • Research is focused on overcoming resistance to radiation therapy (RT) combined with immunotherapy in head and neck squamous cell carcinoma (HNSCC) using mouse models to understand the tumor microenvironment's response to treatment.
  • Findings reveal that targeting traditional immunosuppressive myeloids is ineffective; instead, a combination of RT, Treg depletion, and anti-CD137 agonism enhances dendritic cell activation and reprograms Tregs, leading to a strong CD8 T cell response.
  • Successfully increasing RT dosage and combining it with specific treatments results in tumor eradication, while high Treg levels in human oral squamous cell carcinoma are linked to quicker tumor recurrence, emphasizing the need to manipulate
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  • Rearrangements during transfection occur in a small percentage (1-2%) of lung adenocarcinomas and are now targeted by tyrosine kinase inhibitors; researchers developed three new cancer cell lines (CUTO22, CUTO32, CUTO42) to explore RET signaling and therapy responses.
  • Sensitivity tests revealed CUTO22 and CUTO42 to be responsive to multiple RET inhibitors, while CUTO32 showed over ten times resistance and exhibited different regulation of the AKT pathway compared to the others.
  • Drug screening identified CUTO32 as sensitive to Polo-like kinase 1 and Aurora kinase A inhibitors, and the effectiveness of RET inhibitor BLU-667 was demonstrated in CUTO42 tumors but less so
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Protein Kinase C-δ (PKCδ), regulates a broad group of biological functions and disease processes, including well-defined roles in immune function, cell survival and apoptosis. PKCδ primarily regulates apoptosis in normal tissues and non-transformed cells, and genetic disruption of the PRKCD gene in mice is protective in many diseases and tissue damage models. However pro-survival/pro-proliferative functions have also been described in some transformed cells and in mouse models of cancer.

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In a substantial fraction of cancers promoter (TERTp) mutations drive expression of the catalytic subunit of telomerase, contributing to their proliferative immortality. We conducted a pan-cancer analysis of cell lines and find a TERTp mutation expression signature dominated by epithelial-to-mesenchymal transition and MAPK signaling. These data indicate that TERTp mutants are likely to generate distinctive tumor microenvironments and intercellular interactions.

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