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models of chronic inflammatory diseases

The Bradford Laboratory focuses on how breast cancer cells and tumor-associated macrophages (TAMs) communicate via the nuclear factor-kappaB (NF-κB) pathway to promote cancer progression. NF-κB is a family of five transcription factors (RelA/p65, RelB, p50, p52, c-Rel) that form different dimers to regulate target gene expression in diverse biological functions, including, normal immune function, synaptic plasticity, and even memory. Aberrant NF-κB activity is associated with autoimmune diseases, and importantly, cancer. NF-κB is known to be up-regulated in breast cancer subtypes that also have high numbers of infiltrating macrophages, the TAMs. TAMs are found in many types of cancer and can compose upwards of half of total invasive breast cancer tumor mass, which is associated with poor prognosis. The basal and claudinlow subtypes of breast cancer are very aggressive and difficult to treat; interestingly, these subtypes are also associated with high macrophage infiltration. Recent microarray data indicate that NF-κBdependent target genes are strongly up-regulated in basal-like and claudin-low breast cancers, which could be due to the large numbers of infiltrating macrophages. This finding along with the fact that NFκB can also regulate tumor-initiating cells (cancer stem cells) makes the issue of uncovering the role NFκB communication between TAMs and breast cancer cells very important. The Bradford Laboratory is also collaborating with Dr. Ali Arbab (GRU Cancer Center). Together, they are studying NF-κB signaling in tumor-associated macrophages and the pathway’s influence on angiogenesis and cancer stem cell phenotypes in glioblastoma.