Jacqueline Lees

Jacqueline Lees

Virginia and D.K. Ludwig Professor for Cancer Research

Jacqueline Lees develops mouse and zebrafish models, identifying the molecular pathways leading to tumor formation.

617-252-1972

Phone

76-261C

Office

jalees@mit.edu

Email

Koch Institute for Integrative Cancer Research

Location

Lab Website
Paul Thompson

Assistant

617-258-0480

Assistant Phone

Education

  • PhD, 1990, University of London
  • BSc, 1986, Biochemistry, University of York

Research Summary

We identify the proteins and pathways involved in tumorigenicity — establishing their mechanism of action in both normal and tumor cells. To do so, we use a combination of molecular and cellular analyses, mutant mouse models and genetic screens in zebrafish.

Recent Publications

  1. The PRMT5-splicing axis is a critical oncogenic vulnerability that regulates detained intron splicing. Fowler, CE, O'Hearn, NA, Salus, GJ, Singh, A, Boutz, PL, Lees, JA. 2024. bioRxiv , .
    doi: 10.1101/2024.12.17.628905PMID:39763796
  2. BMI1 is required for melanocyte stem cell maintenance and hair pigmentation. Wilson, MM, Danielian, PS, Salus, G, Ferretti, R, Whittaker, CA, Lees, JA. 2023. Pigment Cell Melanoma Res 36, 399-406.
    doi: 10.1111/pcmr.13088PMID:37132544
  3. MITF deficiency and oncogenic GNAQ each promote proliferation programs in zebrafish melanocyte lineage cells. Phelps, GB, Amsterdam, A, Hagen, HR, García, NZ, Lees, JA. 2022. Pigment Cell Melanoma Res 35, 539-547.
    doi: 10.1111/pcmr.13057PMID:35869673
  4. MITF deficiency accelerates GNAQ-driven uveal melanoma. Phelps, GB, Hagen, HR, Amsterdam, A, Lees, JA. 2022. Proc Natl Acad Sci U S A 119, e2107006119.
    doi: 10.1073/pnas.2107006119PMID:35512098
  5. Acquired resistance to PRMT5 inhibition induces concomitant collateral sensitivity to paclitaxel. Mueller, HS, Fowler, CE, Dalin, S, Moiso, E, Udomlumleart, T, Garg, S, Hemann, MT, Lees, JA. 2021. Proc Natl Acad Sci U S A 118, .
    doi: 10.1073/pnas.2024055118PMID:34408017
  6. E2F4's cytoplasmic role in multiciliogenesis is mediated via an N-terminal domain that binds two components of the centriole replication machinery, Deup1 and SAS6. Hazan, R, Mori, M, Danielian, PS, Guen, VJ, Rubin, SM, Cardoso, WV, Lees, JA. 2021. Mol Biol Cell 32, ar1.
    doi: 10.1091/mbc.E21-01-0039PMID:34260288
  7. The Rb tumor suppressor regulates epithelial cell migration and polarity. Parisi, T, Balsamo, M, Gertler, F, Lees, JA. 2018. Mol Carcinog 57, 1640-1650.
    doi: 10.1002/mc.22886PMID:30084175
  8. Uveal melanoma driver mutations in GNAQ/11 yield numerous changes in melanocyte biology. Perez, DE, Henle, AM, Amsterdam, A, Hagen, HR, Lees, JA. 2018. Pigment Cell Melanoma Res 31, 604-613.
    doi: 10.1111/pcmr.12700PMID:29570931
  9. EMT programs promote basal mammary stem cell and tumor-initiating cell stemness by inducing primary ciliogenesis and Hedgehog signaling. Guen, VJ, Chavarria, TE, Kröger, C, Ye, X, Weinberg, RA, Lees, JA. 2017. Proc Natl Acad Sci U S A 114, E10532-E10539.
    doi: 10.1073/pnas.1711534114PMID:29158396
  10. Coordinated Splicing of Regulatory Detained Introns within Oncogenic Transcripts Creates an Exploitable Vulnerability in Malignant Glioma. Braun, CJ, Stanciu, M, Boutz, PL, Patterson, JC, Calligaris, D, Higuchi, F, Neupane, R, Fenoglio, S, Cahill, DP, Wakimoto, H et al.. 2017. Cancer Cell 32, 411-426.e11.
    doi: 10.1016/j.ccell.2017.08.018PMID:28966034
More Publications
Photo courtesy of the MIT Koch Institute for Integrative Cancer Research

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