Tyler Jacks

Tyler Jacks

David H. Koch Professor of Biology; Intramural Faculty, Koch Institute; Daniel K. Ludwig Scholar for Cancer Research

Tyler Jacks is interested in the genetic events contributing to the development of cancer, and his group has created a series of mouse strains engineered to carry mutations in genes known to be involved in human cancers.

617-253-0262

Phone

76-453

Office

tjacks@mit.edu

Email

Koch Institute for Integrative Cancer Research

Location

Lab Website
Judy Teixeira

Assistant

617-253-0263

Assistant Phone

Education

  • PhD, 1988, University of California, San Francisco
  • SB, 1983, Biology, Harvard University

Research Summary

Dr. Jacks’ research has focused on developing new methods for the construction and characterization of genetically engineered mouse models or GEMMs of human cancer, and recently has moved into the burgeoning area of tumor immunology to understand the interactions between the immune system and cancer.  His group has produced GEMMs with constitutive and conditional mutations in several tumor suppressor genes, oncogenes, and genes involved in oxidative stress, DNA repair and epigenetic control of gene expression. These GEMMS have been used to examine the mechanism of tumor initiation and progression, to uncover the molecular, genetic and biochemical relationship to the human diseases, as tools to study response and resistance to chemotherapy, and to explore methods in molecular imaging and early detection of cancer.

Awards

  • AACR Princess Takamatsu Memorial Lectureship, 2020
  • Massachusetts Institute of Technology, James R Killian Jr Faculty Achievement Award, 2015
  • Sergio Lombroso Award in Cancer Research, 2015
  • American Academy of Arts and Sciences, Fellow, 2012
  • National Academy of Sciences, Member, 2009
  • Institute of Medicine of the National Academies, Member, 2009
  • Paul Marks Prize for Cancer Research, 2005
  • Howard Hughes Medical Institute, HHMI Investigator, 1994

Recent Publications

  1. Mismatch repair deficiency is not sufficient to elicit tumor immunogenicity. Westcott, PMK, Muyas, F, Hauck, H, Smith, OC, Sacks, NJ, Ely, ZA, Jaeger, AM, Rideout, WM 3rd, Zhang, D, Bhutkar, A et al.. 2023. Nat Genet 55, 1686-1695.
    doi: 10.1038/s41588-023-01499-4PMID:37709863
  2. A prime editor mouse to model a broad spectrum of somatic mutations in vivo. Ely, ZA, Mathey-Andrews, N, Naranjo, S, Gould, SI, Mercer, KL, Newby, GA, Cabana, CM, Rideout, WM 3rd, Jaramillo, GC, Khirallah, JM et al.. 2023. Nat Biotechnol , .
    doi: 10.1038/s41587-023-01783-yPMID:37169967
  3. Modeling diverse genetic subtypes of lung adenocarcinoma with a next-generation alveolar type 2 organoid platform. Naranjo, S, Cabana, CM, LaFave, LM, Romero, R, Shanahan, SL, Bhutkar, A, Westcott, PMK, Schenkel, JM, Ghosh, A, Liao, LZ et al.. 2022. Genes Dev 36, 936-949.
    doi: 10.1101/gad.349659.122PMID:36175034
  4. Deciphering the immunopeptidome in vivo reveals new tumour antigens. Jaeger, AM, Stopfer, LE, Ahn, R, Sanders, EA, Sandel, DA, Freed-Pastor, WA, Rideout, WM 3rd, Naranjo, S, Fessenden, T, Nguyen, KB et al.. 2022. Nature 607, 149-155.
    doi: 10.1038/s41586-022-04839-2PMID:35705813
  5. Low neoantigen expression and poor T-cell priming underlie early immune escape in colorectal cancer. Westcott, PMK, Sacks, NJ, Schenkel, JM, Ely, ZA, Smith, O, Hauck, H, Jaeger, AM, Zhang, D, Backlund, CM, Beytagh, MC et al.. 2021. Nat Cancer 2, 1071-1085.
    doi: 10.1038/s43018-021-00247-zPMID:34738089
  6. Smarca4 Inactivation Promotes Lineage-Specific Transformation and Early Metastatic Features in the Lung. Concepcion, CP, Ma, S, LaFave, LM, Bhutkar, A, Liu, M, DeAngelo, LP, Kim, JY, Del Priore, I, Schoenfeld, AJ, Miller, M et al.. 2022. Cancer Discov 12, 562-585.
    doi: 10.1158/2159-8290.CD-21-0248PMID:34561242
  7. Antigen dominance hierarchies shape TCF1+ progenitor CD8 T cell phenotypes in tumors. Burger, ML, Cruz, AM, Crossland, GE, Gaglia, G, Ritch, CC, Blatt, SE, Bhutkar, A, Canner, D, Kienka, T, Tavana, SZ et al.. 2021. Cell 184, 4996-5014.e26.
    doi: 10.1016/j.cell.2021.08.020PMID:34534464
  8. Conventional type I dendritic cells maintain a reservoir of proliferative tumor-antigen specific TCF-1+ CD8+ T cells in tumor-draining lymph nodes. Schenkel, JM, Herbst, RH, Canner, D, Li, A, Hillman, M, Shanahan, SL, Gibbons, G, Smith, OC, Kim, JY, Westcott, P et al.. 2021. Immunity 54, 2338-2353.e6.
    doi: 10.1016/j.immuni.2021.08.026PMID:34534439
  9. The CD155/TIGIT axis promotes and maintains immune evasion in neoantigen-expressing pancreatic cancer. Freed-Pastor, WA, Lambert, LJ, Ely, ZA, Pattada, NB, Bhutkar, A, Eng, G, Mercer, KL, Garcia, AP, Lin, L, Rideout, WM 3rd et al.. 2021. Cancer Cell 39, 1342-1360.e14.
    doi: 10.1016/j.ccell.2021.07.007PMID:34358448
  10. Mitochondrial apoptotic priming is a key determinant of cell fate upon p53 restoration. Sánchez-Rivera, FJ, Ryan, J, Soto-Feliciano, YM, Clare Beytagh, M, Xuan, L, Feldser, DM, Hemann, MT, Zamudio, J, Dimitrova, N, Letai, A et al.. 2021. Proc Natl Acad Sci U S A 118, .
    doi: 10.1073/pnas.2019740118PMID:34074758
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Photo credit: Alisha Siegel