Department / Division
Medicine / Medicine - Oncology
Durham, NC 27710
Melanoma, cancer immunotherapy, Merkel cell carcinoma
My lab is interested in elucidating the molecular and cellular mechanisms involved in tumor-mediated immune suppression. Our overriding hypothesis is that tumor cells and/or their associated stromal elements elicit soluble factors to target local dendritic cell populations; thereby, interfering with their ability to generate an effective anti-tumor immune response. This work has both basic and translational significance in that it provides 1. insight into the little known signalling mechanisms and resulting biology of specific dendritic cell subsets such as the plasmacytoid dendritic cell within the tumor microenvironment, 2. novel soluble protein targets for therapeutic inhibition to improve immunotherapy efficacy, and 3. much needed putative dendritic cell-based predictive biomarkers for tumor immunotherapy patient selection as well as for the selection of patient-specific tumor immunotherapy strategies. We focus our efforts in the fields of melanoma and breast cancer.
We currently have the following ongoing projects in our lab:
1. Elucidation of the role of the type III TGF-beta receptor in modulating the anti-tumor immune response
2. Characterizing the role of Wnt/Beta-catenin-TGFbeta cooperative signaling in the generation of tolerogenic dendritic cells in the setting of melanoma
3. Determining the ability of soluble type I TGF-beta receptor inhibitors to augment the efficacy of CTLA-4 blockade in a transgenic murine melanoma model
4. Elucidation of a novel chemotherapy-induced BMP-CCL22-regulatory T cell axis and its role in the development of breast cancer recurrence
5. Identifying melanoma-draining lymph node dendritic cell-specific gene expression signatures as predictive biomarkers to tumor immunotherapy efficacy
This faculty member (or a member of their immediate family) has a working relationship (i.e. consulting, research, and/or educational services) with the companies listed below. These relations have been reported to the health system leadership and, when appropriate, management plans are in place to address potential conflicts.
Hanks, BA; Morse, MA. Pharmacological inhibition of TGFß as a strategy to augment the antitumor immune response. Current Opinion in Investigational Drugs. 2010;11:1342-1353. (2010) Abstract
Lapteva, N; Seethammagari, MR; Hanks, BA; Jiang, J; Levitt, JM; Slawin, KM; Spencer, DM. Enhanced activation of human dendritic cells by inducible CD40 and Toll-like receptor-4 ligation. Cancer Research. 2007;67:10528-10537. (2007) Abstract
Hanks, BA; Jiang, J; Singh, RA; Song, W; Barry, M; Huls, MH; Slawin, KM; Spencer, DM. Re-engineered CD40 receptor enables potent pharmacological activation of dendritic-cell cancer vaccines in vivo. Nature Medicine. 2005;11:130-137. (2005) Abstract