Whitney Henry

Whitney Henry

Assistant Professor of Biology; Intramural Faculty, Koch Institute

Whitney Henry studies ferroptosis in human health and disease with a focus on cancer.

76-561

Office

wshenry@mit.edu

Email

Koch Institute for Integrative Cancer Research

Location

Lab Website
Jamie Rothman

Assistant

617-258-6635

Assistant Phone

Education

  • Graduate: PhD, 2016, Harvard University
  • Undergraduate: BS, 2010, Biology, Grambling State University

Research Summary

Ferroptosis is an iron-dependent form of cell death with profound implications in human health and disease. In the context of cancer, the use of ferroptosis inducers to target subpopulations of highly metastatic and therapy-resistant cancer cells has garnered much excitement over the last few years. However, to gain a comprehensive understanding of the full therapeutic potential of ferroptosis, our research focuses on (i) uncovering the molecular factors affecting ferroptosis susceptibility, (ii) studying its impact on the tumor microenvironment, and (iii) developing innovative ways to modulate ferroptosis resistance in vivo. We employ a multidisciplinary approach, combining functional genomics, metabolomics, bioengineering, and a range of in vitro and in vivo models to advance our understanding in this domain and to translate our findings into effective therapies.

Awards

  • The Margaret and Herman Sokol Postdoctoral Award, 2022
  • Ludwig Center at MIT Postdoctoral Fellowship, 2022
  • Jane Coffin Childs Memorial Fund Postdoctoral Fellowship, 2017
  • HHMI International Predoctoral Research Fellowship, 2013

Key Publications

  1. MMD collaborates with ACSL4 and MBOAT7 to promote polyunsaturated phosphatidylinositol remodeling and susceptibility to ferroptosis. Phadnis, VV, Snider, J, Varadharajan, V, Ramachandiran, I, Deik, AA, Lai, ZW, Kunchok, T, Eaton, EN, Sebastiany, C, Lyakisheva, A et al.. 2023. Cell Rep 42, 113023.
    doi: 10.1016/j.celrep.2023.113023PMID:37691145
  2. Plasticity of ether lipids promotes ferroptosis susceptibility and evasion. Zou, Y, Henry, WS, Ricq, EL, Graham, ET, Phadnis, VV, Maretich, P, Paradkar, S, Boehnke, N, Deik, AA, Reinhardt, F et al.. 2020. Nature 585, 603-608.
    doi: 10.1038/s41586-020-2732-8PMID:32939090

Recent Publications

  1. Advancing cancer research. Taabazuing, CY, Henry, WS, Oliphant, MUJ, Lawrence, SS. 2024. Trends Pharmacol Sci 45, 943-949.
    doi: 10.1016/j.tips.2024.10.004PMID:39477739
  2. Zeb1 mediates EMT/plasticity-associated ferroptosis sensitivity in cancer cells by regulating lipogenic enzyme expression and phospholipid composition. Schwab, A, Rao, Z, Zhang, J, Gollowitzer, A, Siebenkäs, K, Bindel, N, D'Avanzo, E, van Roey, R, Hajjaj, Y, Özel, E et al.. 2024. Nat Cell Biol 26, 1470-1481.
    doi: 10.1038/s41556-024-01464-1PMID:39009641
  3. ATF3 characterizes aggressive drug-tolerant persister cells in HGSOC. Böpple, K, Oren, Y, Henry, WS, Dong, M, Weller, S, Thiel, J, Kleih, M, Gaißler, A, Zipperer, D, Kopp, HG et al.. 2024. Cell Death Dis 15, 290.
    doi: 10.1038/s41419-024-06674-xPMID:38658567
  4. Lipidomes define immune cell identity. Levental, KR, Henry, WS. 2024. Nat Cell Biol 26, 516-518.
    doi: 10.1038/s41556-024-01398-8PMID:38589530
  5. Ether lipids influence cancer cell fate by modulating iron uptake. Henry, WS, Müller, S, Yang, JS, Innes-Gold, S, Das, S, Reinhardt, F, Sigmund, K, Phadnis, VV, Wan, Z, Eaton, E et al.. 2024. bioRxiv , .
    doi: 10.1101/2024.03.20.585922PMID:38562716
  6. MMD collaborates with ACSL4 and MBOAT7 to promote polyunsaturated phosphatidylinositol remodeling and susceptibility to ferroptosis. Phadnis, VV, Snider, J, Varadharajan, V, Ramachandiran, I, Deik, AA, Lai, ZW, Kunchok, T, Eaton, EN, Sebastiany, C, Lyakisheva, A et al.. 2023. Cell Rep 42, 113023.
    doi: 10.1016/j.celrep.2023.113023PMID:37691145
  7. Plasticity of ether lipids promotes ferroptosis susceptibility and evasion. Zou, Y, Henry, WS, Ricq, EL, Graham, ET, Phadnis, VV, Maretich, P, Paradkar, S, Boehnke, N, Deik, AA, Reinhardt, F et al.. 2020. Nature 585, 603-608.
    doi: 10.1038/s41586-020-2732-8PMID:32939090
  8. Pentraxin-3 is a PI3K signaling target that promotes stem cell-like traits in basal-like breast cancers. Thomas, C, Henry, W, Cuiffo, BG, Collmann, AY, Marangoni, E, Benhamo, V, Bhasin, MK, Fan, C, Fuhrmann, L, Baldwin, AS et al.. 2017. Sci Signal 10, .
    doi: 10.1126/scisignal.aah4674PMID:28223411
  9. Aspirin Suppresses Growth in PI3K-Mutant Breast Cancer by Activating AMPK and Inhibiting mTORC1 Signaling. Henry, WS, Laszewski, T, Tsang, T, Beca, F, Beck, AH, McAllister, SS, Toker, A. 2017. Cancer Res 77, 790-801.
    doi: 10.1158/0008-5472.CAN-16-2400PMID:27940576
  10. LINC00520 is induced by Src, STAT3, and PI3K and plays a functional role in breast cancer. Henry, WS, Hendrickson, DG, Beca, F, Glass, B, Lindahl-Allen, M, He, L, Ji, Z, Struhl, K, Beck, AH, Rinn, JL et al.. 2016. Oncotarget 7, 81981-81994.
    doi: 10.18632/oncotarget.11962PMID:27626181