Publications by authors named "Kayla Myers Chen"
Introduction: Solid cancers Myeloid cells are prevalent in solid cancers, but they frequently exhibit an anti-inflammatory pro-tumor phenotype that contribute to the immunosuppressive tumor microenvironment (TME), which hinders the effectiveness of cancer immunotherapies. Myeloid cells' natural ability of tumor trafficking makes engineered myeloid cell therapy an intriguing approach to tackle the challenges posed by solid cancers, including tumor infiltration, tumor cell heterogenicity and the immunosuppressive TME. One such engineering approach is to target the checkpoint molecule PD-L1, which is often upregulated by solid cancers to evade immune responses.
View Article and Find Full Text PDFArticle Synopsis
- 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.