Publications by authors named "Aaron G Baugh"
Myeloid Derived Suppressor Cells (MDSCs) support breast cancer growth via immune suppression and non-immunological mechanisms. Although 15% of patients with breast cancer will develop brain metastasis, there is scant understanding of MDSCs' contribution within the breast-to-brain metastatic microenvironment. Utilizing co-culture models mimicking a tumor-neuron-immune microenvironment and patient tissue arrays, we identified serotonergic receptor, HTR2B, on MDSCs to upregulate pNF-κB and suppress T cell proliferation, resulting in enhanced tumor growth.
View Article and Find Full Text PDFArticle Synopsis
- Metastatic disease, a major cause of death in advanced breast cancer, involves tumor cells spreading from their original site to distant organs, highlighting the importance of studying these processes.
- Researchers have developed a new murine breast tumor cell line, NT2.5-LM, that shows a much faster spread of metastases after implantation, making it a valuable tool for understanding cancer progression and treatment.
- The NT2.5-LM cell line displays characteristics of enhanced metastatic potential, responds well to HER2-targeted therapies, and offers advantages over previous models, enabling better exploration of therapeutic strategies and mechanisms of metastasis.
Article Synopsis
- Researchers have developed a new murine (mouse) breast tumor cell line called NT2.5-LM, which models aggressively spreading breast cancer that can spontaneously metastasize to various organs.
- This model shows quick tumor spread within weeks, demonstrating distant metastases in the lungs, bones, spleen, colon, and liver, making it useful for studying how cancer spreads.
- The NT2.5-LM model also reveals changes in cancer cell properties associated with increased metastatic potential, allowing for more effective testing of new cancer treatments targeting widespread metastases.
Therapeutic combinations to alter immunosuppressive, solid tumor microenvironments (TME), such as in breast cancer, are essential to improve responses to immune checkpoint inhibitors (ICI). Entinostat, an oral histone deacetylase inhibitor, has been shown to improve responses to ICIs in various tumor models with immunosuppressive TMEs. The precise and comprehensive alterations to the TME induced by entinostat remain unknown.
View Article and Find Full Text PDF