Supplementary Materials

Supplementary Material for:

Anti-VEGF therapy induces ECM remodeling and mechanical barriers to therapy in colorectal cancer liver metastases

Nuh N. Rahbari, Dmitriy Kedrin, Joao Incio, Hao Liu, William W. Ho, Hadi T. Nia, Christina M. Edrich, Keehoon Jung, Julien Daubriac, Ivy Chen, Takahiro Heishi, John D. Martin, Yuhui Huang, Nir Maimon, Christoph Reissfelder, Jurgen Weitz, Yves Boucher, Jeffrey W. Clark, Alan J. Grodzinsky, Dan G. Duda, Rakesh K. Jain*, Dai Fukumura*

*Corresponding author. Email: dai{at}steele.mgh.harvard.edu (D.F.); jain{at}steele.mgh.harvard.edu (R.K.J.)

Published 12 October 2016, Sci. Transl. Med. 8, 360ra135 (2016)
DOI: 10.1126/scitranslmed.aaf5219

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Expression of HA is increased in CRC liver metastases compared to liver parenchyma.
  • Fig. S2. DNA content in murine CRC liver metastases is decreased after anti-VEGF therapy.
  • Fig. S3. CD44 expression is increased in liver metastases after anti-VEGF therapy.
  • Fig. S4. Bevacizumab increases sGAG expression in human CRC liver metastases.
  • Fig. S5. Anti-VEGF therapy does not alter ECM expression in healthy liver parenchyma.
  • Fig. S6. Anti-VEGF therapy results in recruitment of MDSCs into CT26 liver metastases.
  • Fig. S7. Anti-VEGF therapy does not alter IM and neutrophil counts in the bone marrow.
  • Fig. S8. Agtr1a knockout does not alter anti-VEGF–induced tumor stiffness and expression of noncollagenous matrix.
  • Fig. S9. Anti-VEGF therapy does not increase TGF-β1 expression in CRC liver metastases.
  • Fig. S10. Microvessel density is decreased, and hypoxia is increased in CT26 liver metastases after anti-VEGF therapy.
  • Fig. S11. Treatment with PEG-HAse lowers HA content in SL4 liver metastases.
  • Table S1. Clinicopathologic data of patients with CRC liver metastases.
  • Reference (78)

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