jennifer bradford

Classes taught at Augusta University
  • BIOL 1107: Principles of Biology I
  • BIOL 4780: Molecular Carcinogenesis
  • BIOL 3200: Genetics 
  • BIOL 1107: Lab
Educational / Career Background:
  • Postdoctoral Fellow at the Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC

  • PhD. Biological and Biomedical Sciences; Program in Genetics and Molecular Biology, Emory University, Atlanta, GA

  • B.S. Biology, Minor in Classical Studies, Virginia Tech, Blacksburg, VA

Interesting Fact:
  • I have been fly fishing since I was 11 years old, and even worked at Orvis during college teaching people about the sport. If I’m not in the lab or working on lectures you might just find me on a mountain trout stream.

Research Interests:

Our lab focuses on the interactions between cancer cells and macrophages via the nuclear factor-kappaB (NF-κB) signaling pathway. 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.

Our lab’s research efforts in the area of NF-κB signaling in glioblastoma (GBM) are part of a collaboration with Dr. Ali Arbab’s lab (Georgia Cancer Center). We have been using various models to determine the role of myeloid NF-κB on GBM growth. We have found that stimulation of GBM cell lines with bone marrow derived macrophage conditioned media from control cells, but not from cells lacking p65 (a canonical transcription factor), elevates GBM NF-κB signaling, and increases stem cell properties. Recently, we have identified that conditional deletion of canonical NF-κB signaling in myeloid cells inhibits syngeneic GBM growth, decreases CD45 infiltration into tumors, and positively influences CD8+ T cell proliferation. These data suggest that canonical NF-κB signaling has an anti-inflammatory role and is required for macrophage polarization, immune suppression, and GBM growth. Combining a NF-κB signaling inhibitor with standard therapy could improve anti-tumor immunity in GBM.

Breast Cancer
Our lab also has an interest in stromal macrophage NF-κB signaling in breast cancer. NF-κB is known to be up-regulated in breast cancer subtypes that also have high numbers of infiltrating macrophages, which are called tumor associated macrophages (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 claudin-low subtypes of breast cancer are very aggressive, difficult to treat, and interestingly, these subtypes are also associated with high macrophage infiltration. Microarray data indicate that NF-κB-dependent target genes are strongly upregulated 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 NF-κB can also regulate tumor stem cells makes the issue of uncovering the role NF-κB communication between TAMs and breast cancer cells very important.


American Cancer Society Internal Research Grant (2017-2018)

Pilot Study Research Program Award (PSRP) (2017-2018)

Center for Undergraduate Research Summer Scholars Program (2016, 2017 and 2018)

Augusta University “Favorite Faculty” Recipient (Spring 2017)

Summerville-Cancer Center Collaborative Research Award (2015-2016)


Bhagelu Achyut*, Kartik Angara, Meenu Jain, Thaiz Borin, Mohammad Rashid, Asm Iskander, Roxan Ara, Ravindra Kolhe, Shelby Howard#, Natasha Venugopal#, Paulo Rodriguez, Jennifer Bradford*, and Ali Arbab*.  Canonical NF-κB signaling in myeloid cells is required for the glioblastoma growth. Scientific Reports.  2017 Oct 23;7(1):13754.
*Designates co-corresponding authors
# indicates undergraduate researcher

Sierra RA, Trillo-Tinoco J, Mohamed E, Yu L, Achyut BR, Arbab A, Bradford JW, Osborne BA, Miele L, Rodriguez PC. Anti-Jagged immunotherapy inhibits MDSCs and overcomes tumor-induced tolerance. Cancer Research. 2017 Oct 15;77(20):5628-5638.
**A figure from this manuscript was chosen for this issue’s cover**

Bradford, JW, Baldwin, AS. IKK/Nuclear factor-kappaB and Oncogenesis: Roles in Tumor Initiating Cells and in the Tumor Microenvironment. 2014. Advances in Cancer Research. 121:125-145.

Kendellen, MF*, Bradford, JW*, Lawrence, CL, Clark, KS, Baldwin, AS. Canonical and Non-Canonical NF-κB Signaling Promotes the Function of Basal-Like Breast Cancer Tumor-Initiating Cells. 2013. Oncogene. 33(10):1297-305.      * indicates co-first authors

Bradford J, Shin JY, Roberts M, Wang CE, Sheng G, Li S, Li XJ. Mutant huntingtin in glial cells exacerbates neurological symptoms of Huntington disease mice. 2010. Journal of Biological Chemistry. 285(14):10653-10661.

Bradford JW, Li S, Li XJ. Polyglutamine toxicity in non-neuronal cells. 2010. Cell Research. 20(4):400-407.

Bradford J, Shin JY, Roberts M, Wang CE, Li XJ, Li S. Expression of mutant huntingtin in mouse brain astrocytes causes age-dependent neurological symptoms. 2009. PNAS. 106(52):22480-22485.

Xin ZT, Beauchamp AD, Calado RT, Bradford JW, Regal JA, Shenoy A, Liang Y, Lansdorp PM, Young NS, Ly H. Functional characterization of natural telomerase mutations found in patients with hematologic disorders. 2007. Blood. 109(2):524-32.