Hanne Lind

Hanne Lind has been active in cancer research since 2013, and has studied tumor immunology since 2017. She graduated from the University of Michigan’s Cellular and Molecular Biology Department with an Honor’s research BS degree in 2017 from researching the TGF-beta signaling pathway in triple-negative breast cancer. She was a Postbaccalaureate intramural research fellow at the Center for Immuno-Oncology in the National Cancer Institute under the mentorship of Dr. Claudia Palena, Ph.D. from 2017-2019, then continued as a staff scientist in the same lab. During this time, Hanne studied CXCR1/CXCR2 signaling in head and neck squamous cell carcinoma (HNSCC) and led the project, discovering the multiplied benefit of CXCR1/CXCR2 inhibition with docetaxel.

Hanne has worked with Dr. Wang since 2021, studying the mechanism of resistance to radiation and immune checkpoint inhibitor combination therapy, specifically how downregulation of MHC class I expression prevents immunoregulation of HNSCC tumors.

Peer-Review Publications

Hanne T. Lind, Spencer C. Hall, Alexander A. Strait, Jack B. Goon, John D. Aleman, Samantha M.Y. Chen, Sana D. Karam, Christian D. Young, Jing H. Wang, Xiao-Jing Wang. MHC class I upregulation contributes to the therapeutic response to radiotherapy in combination with anti-PD-L1/anti-TGF-β in squamous cell carcinomas with enhanced CD8 T cell memory-driven response. Cancer Letters. 608:217347 (2024)

Horn, L.A. & Lind, H., et al. Inhibition of the chemokine receptors CXCR1 and CXCR2 synergizes with docetaxel for effective tumor control and remodeling of the immune microenvironment of HPV-negative head and neck cancer models. J Exp Clin Cancer Res 43, 318 (2024).

O’Neill KI, Kuo LW, MW Williams, Lind H, Crump LY, Hammond NG, Spoelstra NS, Caino CM, Richer JK. NPC1 confers metabolic flexability in triple-negative breast cancer. Cancers. 2022 Jul; 14(14):3543

Horn LA, Riskin J, Hempel HA, Fousek K, Lind H, McCampbell KM, Maeda DY, Zebala JA, Su Z, Schlom J, Palena C. Simultaneous inhibition of CXCR1/2, TGF-β, and PD-L1 remodels the tumor and its microenvironment to drive antitumor immunity. Journal for ImmunoTherapy of Cancer. 2020 Mar;8(1):e000326.

Lind H, Gameiro SR, Jochems C, Donahue RN, Strauss J, Gulley JL, Palena C, Schlom J. Dual targeting of TGF-β and PD-L1 via a bifunctional anti-PD-L1/TGF-βRII agent: status of preclinical and clinical advances. Journal for ImmunoTherapy of Cancer. 2020;8:e000433.

Thomas AL, Lind H, Hong H, Donic D, Oppat K, Rosenthal E, Guo A, Thomas A, Hamden R, Jeruss JS. Inhibition of CDK-mediated Smad3 phosphorylation reduces the Pin1-Smad3 interaction and aggressiveness of triple negative breast cancer cells. Cell Cycle 2017; 16 (15): 145-1464

Barton VN, D’Amato NC, Gordon MA, Lind HT, Spoelstra NS, Babbs BL, Heinz RE, Elias A, Jedlicka J, Jacobsen BM, and Richer JK. Multiple Molecular Subtypes of Triple-Negative Breast Cancer Critically Rely on Androgen Receptor and Respond to Enzalutamide In Vivo. Molecular Cancer Therapeutics 2015; 14 (3): 769-778

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