The compression of brain tissue by a tumour mass is believed to be a major cause of the clinical symptoms seen in patients with brain cancer. However, the biological consequences of these physical stresses on brain tissue are unknown. Here, via imaging studies in patients and by using mouse models of human brain tumours, we show that a subgroup of primary and metastatic brain tumours, classified as nodular on the basis of their growth pattern, exert solid stress on the surrounding brain tissue, causing a decrease in local vascular perfusion as well as neuronal death and impaired function. We demonstrate a causal link between solid stress and neurological dysfunction by applying and removing cerebral compression, which respectively mimic the mechanics of tumour growth and of surgical resection. We also show that, in mice, treatment with lithium reduces solid-stress-induced neuronal death and improves motor coordination. Our findings indicate that brain-tumour-generated solid stress impairs neurological function in patients, and that lithium as a therapeutic intervention could counter these effects.

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Data availability

The authors declare that all data supporting the findings of this study are available within the paper and its Supplementary Information. Raw RNA-Seq data from this study have been deposited in the NCBI Sequence Read Archive (SRA) under submission ID SUB4405185 and BioProject ID PRJNA486395.

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We thank A. Ivinson (UK Dementia Research Institute), M. A. Moskowitz and M. J. Whalen (MGH) for critical discussion and insightful suggestions; S. Roberge, M. Duquette, C. Smith and E. L. Jones (MGH) for technical support, H. Wakimoto (MGH) for the MGG8 cell line and O. Rapalino (MGH) for help with the pre-operative clinical study. This work was supported by the National Cancer Institute (NCI; P01-CA080124, P50-CA165962, R01-CA129371, R01-CA208205, U01-CA 224348), NCI Outstanding Investigator Award (R35-CA197743), the Lustgarten Foundation, the Ludwig Center at Harvard, the National Foundation for Cancer Research and the Gates Foundation (R.K.J), R01-HL128168 (to J.W.B., T.P.P. and L.L.M.), DP2OD008780 (T.P.P.), R01CA214913 (T.P.P.), P41EB015903 (Center for Biomedical OCT Research and Translation), NIH/NINDS P30NS045776 (EM facility core) and P30-CA14051 from NCI (Koch Institute Genomics core). This work was also supported in part by the Susan G. Komen Foundation Fellowship PDF14301739, Fondation ARC pour la recherche sur le cancer and the INSERM-CNRS ATIP-Avenir grant (G.S.), NCI F32-CA216944-01 (H.T.N.), the European Research Council (ERC) under the European Union’s Horizon 2020 (grant agreement no. 758657), the South-Eastern Norway Regional Health Authority grants 2017073, 2016102 and 2013069, the Research Council of Norway grants 261984 and ES435705, the Norwegian Cancer Society grants 6817564 and 3434180 (K.E.E.), F31HL126449 from the National Heart, Lung, and Blood Institute at the NIH (M.D.), SolidarImmun fellowship (J.K.), Feodor-Lynen Postdoctoral Fellowship from Alexander von Humboldt Foundation (M.G.) and Deutsche Forschungsgemeinschaft AS422-2/1 (V.A.).

Author information

Author notes

  1. These authors contributed equally: Giorgio Seano, Hadi T. Nia, Kyrre E. Emblem


  1. Edwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

    • Giorgio Seano
    • , Hadi T. Nia
    • , Meenal Datta
    • , Jun Ren
    • , Shanmugarajan Krishnan
    • , Jonas Kloepper
    • , William W. Ho
    • , Mitrajit Ghosh
    • , Vasileios Askoxylakis
    • , Gino B. Ferraro
    • , Lars Riedemann
    • , Dai Fukumura
    • , Peigen Huang
    • , Timothy P. Padera
    • , Lance L. Munn
    •  & Rakesh K. Jain
  2. Institut Curie Research Center, PSL Research University, Inserm U1021, CNRS UMR3347, Orsay, France

    • Giorgio Seano
  3. The Department of Diagnostic Physics, Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway

    • Kyrre E. Emblem
  4. Department of Chemical and Biological Engineering, Tufts University, Medford, MA, USA

    • Meenal Datta
  5. Department of Radiology, UT Southwestern Medical Center, Dallas, TX, USA

    • Marco C. Pinho
  6. Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA

    • William W. Ho
  7. Stephen E. and Catherine Pappas Center for Neuro-Oncology, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

    • Elizabeth R. Gerstner
    •  & Tracy T. Batchelor
  8. Department of Neuro-Oncology, Dana-Farber/Brigham and Women’s Cancer Center, Harvard Medical School, Boston, MA, USA

    • Patrick Y. Wen
  9. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA

    • Nancy U. Lin
  10. Center for Biomedical Engineering, Departments of Mechanical, Electrical and Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA

    • Alan J. Grodzinsky
  11. Department of Biomedical Engineering, Bucknell University, Lewisburg, PA, USA

    • James W. Baish


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G.S., H.T.N. and K.E.E. conceived the project and wrote the manuscript; G.S. conducted most of the experiments, performed data analysis and generated most of the experimental mice; H.T.N. designed and developed the in vivo compression device and conducted the biomedical engineering experiments; K.E.E. designed the patient stratification method and analysed the perfusion MRIs; J.K., L.R. and V.A. performed OCT intravital angiography experiments on multiple models; M.D., J.R., S.K. and M.G. assisted with histological analyses, preclinical models and pharmacological treatments; M.C.P. blindly classified the clinical cohorts using the VASARI features; W.W.H. analysed RNA-Seq results; G.B.F. provided expertise on the neuroscience parts of the manuscript; E.R.G., T.T.B., P.Y.W. and N.U.L. provided MRI images and patients’ characteristics from clinical trials; A.J.G., D.F., P.H., J.W.B., T.P.P. and L.L.M. contributed to discussions on crucial aspects of the project and drafted the manuscript; R.K.J. supervised the project and provided guidance on experimental design, data interpretation and writing of the manuscript.

Competing interests

R.K.J. received an honorarium from AMGEN and consultant fees from Pfizer, Ophthotech, Merck, SPARC, SynDevRx and XTuit. R.K.J. owns equity in Enlight, Ophthotech and SynDevRx, and serves on the Boards of Trustees of Tekla Healthcare Investors, Tekla Life Sciences Investors, the Tekla Healthcare Opportunities Fund and the Tekla World Healthcare Fund. No reagents or funding from these companies was used in these studies. K.E.E. has intellectual properties with NordicNeuroLab AS, Bergen, Norway.

Corresponding author

Correspondence to Rakesh K. Jain.

Supplementary information

  1. Supplementary Information

    Supplementary Tables 1–5, Supplementary Figures 1–11, Supplementary Video Legends 1–7 and Supplementary References 1–38.

  2. Reporting Summary

  3. Supplementary Dataset 1

    RNA-Seq of compressed/released lithium-treated cortexes.

  4. Supplementary Video 1

    Illustration of the mathematical model to estimate the tumour-induced solid stress in the normal brain.

  5. Supplementary Video 2

    Representative longitudinal MRI of archetypal post-surgery patients with a nodular GBM tumour.

  6. Supplementary Video 3

    Representative longitudinal MRI of archetypal post-surgery patients with an infiltrative GBM tumour.

  7. Supplementary Video 4

    OCT longitudinal intravital angiography of the nodular GBM U87 mouse model.

  8. Supplementary Video 5

    OCT longitudinal intravital angiography of the nodular BC BT474 mouse model.

  9. Supplementary Video 6

    Representative Rotarod test (index of motor coordination and balance) in a mouse with no compression.

  10. Supplementary Video 7

    OCT longitudinal intravital angiography of the decompression phase in the compression apparatus model.

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