jennifer bradford

Associate Professor of Biological Sciences

  • Member of the Cancer Immunology, Inflammation and Tolerance Program, Georgia Cancer Center
  • Member of the Graduate School

Office: Science Hall C2020
Phone: (706) 667-4575
Email: jebradford@augusta.edu

Classes Taught at Augusta University
  • BIOL 1101L: Fundamentals of Biology Laboratory

  • BIOL 1107: Principles of Biology I

  • BIOL 1107L: Principles of Biology I Laboratory

  • BIOL 3200: Genetics 

  • BIOL 4780/BIOL 6780: Molecular Carcinogenesis

  • BIOL 6170: Biomolecular Techniques

Research Related Courses
  • CURS 2990/3990/4990: Undergraduate Research
  • HONR 4000: Honors Thesis
  • BIOL 4990: Undergraduate Research for Major Elective
  • BIOL 6980: Research Proposal Development
  • BIOL 6990: Biological Research
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

Awards:
  • College of Science and Mathematics Excellence in Research Award (Spring 2019)
  • CURS Undergraduate Mentor Award (Spring 2019)
  • Augusta University “Favorite Faculty” Recipient (Spring 2017)
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.

Glioblastoma
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. 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. More recent work focuses on production and characterization of a conditional and inducible microglial NF-κB knockout model. This model will be used to investigate the role of microglial NF-κB signaling in GBM tumor growth and resistance to treatment.

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.

Research Funding:
  • NIH Academic Research Enhancement Award (R15) (2019-2022)
  • American Cancer Society Internal Research Grant (2017-2018)
  • Pilot Study Research Program Award (PSRP) (2017-2018)
  • Center for Undergraduate Research Summer Scholars Program (2016-2021)
  • Summerville-Cancer Center Collaborative Research Award (2015-2016)
Publications:

Piranlioglu R, Bradford J, Arbab A. Targeting tumor microenvironment-associated cells to reverse therapy resistance. In: Cancer Sensitizing Agents for ChemotherapyLondon, UK: Elsevier; 2021. Chapter 7; p.115-144.

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

#Designates undergraduate researchers

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. Review.

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 U.S.A. 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.