Francisco J. Sánchez-Rivera

Francisco J. Sánchez-Rivera

Assistant Professor of Biology; Intramural Faculty, Koch Institute

Francisco J. Sánchez-Rivera aims to understand how genetic variation shapes normal physiology and disease, with a focus on cancer.

617-715-3389

Phone

76-361A

Office

fsr@mit.edu

Email

Koch Institute for Integrative Cancer Research

Location

Jamie Rothman

Assistant

Education

  • PhD, 2016, Biology, MIT
  • BS, 2008, Microbiology, University of Puerto Rico at Mayagüez

Research Summary

The overarching goal of the Sánchez-Rivera laboratory is to elucidate the cellular and molecular mechanisms by which genetic variation shapes normal physiology and disease, particularly in the context of cancer. To do so, we develop and apply genome engineering technologies, genetically-engineered mouse models (GEMMs), and single cell lineage tracing and omics approaches to obtain comprehensive biological pictures of disease evolution at single cell resolution. By doing so, we hope to produce actionable discoveries that could pave the way for better therapeutic strategies to treat cancer and other diseases.

Awards

  • V Foundation Award, 2022
  • Hanna H. Gray Fellowship, Howard Hughes Medical Institute, 2018-2026
  • GMTEC Postdoctoral Researcher Innovation Grant, Memorial Sloan Kettering Cancer Center, 2020-2022
  • 100 inspiring Hispanic/Latinx scientists in America, Cell Mentor/Cell Press, 2020

Key Publications

  1. High throughput evaluation of genetic variants with prime editing sensor libraries. Gould, S.I, Wuest, A.N., Dong, K., Johnson, G.A., Hsu, A., Narendra, V.K., Levine, S.S., Liu, D.R., and Sanchez-Rivera, F.J. 2023. bioRxiv.
    doi: https://doi.org/10.1101/2022.10.26.513842

Recent Publications

  1. Solid tumor growth depends on an intricate equilibrium of malignant cell states. Torborg, SR, Grbovic-Huezo, O, Singhal, A, Holm, M, Wu, K, Han, X, Ho, YJ, Haglund, C, Mitchell, MJ, Lowe, SW et al.. 2023. bioRxiv , .
    doi: 10.1101/2023.12.30.573100PMID:38234855
  2. Somatic mouse models of gastric cancer reveal genotype-specific features of metastatic disease. Leibold, J, Tsanov, KM, Amor, C, Ho, YJ, Sánchez-Rivera, FJ, Feucht, J, Baslan, T, Chen, HA, Tian, S, Simon, J et al.. 2024. Nat Cancer , .
    doi: 10.1038/s43018-023-00686-wPMID:38177458
  3. Metabolic reprogramming by histone deacetylase inhibition preferentially targets NRF2-activated tumors. Karagiannis, D, Wu, W, Li, A, Hayashi, M, Chen, X, Yip, M, Mangipudy, V, Xu, X, Sánchez-Rivera, FJ, Soto-Feliciano, YM et al.. 2024. Cell Rep 43, 113629.
    doi: 10.1016/j.celrep.2023.113629PMID:38165806
  4. Aberrant gene activation in synovial sarcoma relies on SSX specificity and increased PRC1.1 stability. Benabdallah, NS, Dalal, V, Scott, RW, Marcous, F, Sotiriou, A, Kommoss, FKF, Pejkovska, A, Gaspar, L, Wagner, L, Sánchez-Rivera, FJ et al.. 2023. Nat Struct Mol Biol 30, 1640-1652.
    doi: 10.1038/s41594-023-01096-3PMID:37735617
  5. Generation of precision preclinical cancer models using regulated in vivo base editing. Katti, A, Vega-Pérez, A, Foronda, M, Zimmerman, J, Zafra, MP, Granowsky, E, Goswami, S, Gardner, EE, Diaz, BJ, Simon, JM et al.. 2023. Nat Biotechnol , .
    doi: 10.1038/s41587-023-01900-xPMID:37563300
  6. How CRISPR Is Revolutionizing the Generation of New Models for Cancer Research. Sánchez Rivera, FJ, Dow, LE. 2023. Cold Spring Harb Perspect Med , .
    doi: 10.1101/cshperspect.a041384PMID:37487630
  7. Context-defined cancer co-dependency mapping identifies a functional interplay between PRC2 and MLL-MEN1 complex in lymphoma. Chen, X, Li, Y, Zhu, F, Xu, X, Estrella, B, Pazos, MA 2nd, McGuire, JT, Karagiannis, D, Sahu, V, Mustafokulov, M et al.. 2023. Nat Commun 14, 4259.
    doi: 10.1038/s41467-023-39990-5PMID:37460547
  8. 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
  9. Metabolic Reprogramming by Histone Deacetylase Inhibition Selectively Targets NRF2-activated tumors. Karagiannis, D, Wu, W, Li, A, Hayashi, M, Chen, X, Yip, M, Mangipudy, V, Xu, X, Sánchez-Rivera, FJ, Soto-Feliciano, YM et al.. 2023. bioRxiv , .
    doi: 10.1101/2023.04.24.538118PMID:37162970
  10. STING inhibits the reactivation of dormant metastasis in lung adenocarcinoma. Hu, J, Sánchez-Rivera, FJ, Wang, Z, Johnson, GN, Ho, YJ, Ganesh, K, Umeda, S, Gan, S, Mujal, AM, Delconte, RB et al.. 2023. Nature 616, 806-813.
    doi: 10.1038/s41586-023-05880-5PMID:36991128
  11. High throughput evaluation of genetic variants with prime editing sensor libraries. Gould, S.I, Wuest, A.N., Dong, K., Johnson, G.A., Hsu, A., Narendra, V.K., Levine, S.S., Liu, D.R., and Sanchez-Rivera, F.J. 2023. bioRxiv.
    doi: https://doi.org/10.1101/2022.10.26.513842
More Publications

Multimedia

 

 

Photo credit: Adam Lerner