Supplementary Materials

Supplementary Material for:

The brain microenvironment mediates resistance in luminal breast cancer to PI3K inhibition through HER3 activation

David P. Kodack, Vasileios Askoxylakis, Gino B. Ferraro, Qing Sheng, Mark Badeaux, Shom Goel, Xiaolong Qi, Ram Shankaraiah, Z. Alexander Cao, Rakesh R. Ramjiawan, Divya Bezwada, Bhushankumar Patel, Yongchul Song, Carlotta Costa, Kamila Naxerova, Christina S. F. Wong, Jonas Kloepper, Rita Das, Angela Tam, Jantima Tanboon, Dan G. Duda, C. Ryan Miller, Marni B. Siegel, Carey K. Anders, Melinda Sanders, Monica V. Estrada, Robert Schlegel, Carlos L. Arteaga, Elena Brachtel, Alan Huang, Dai Fukumura, Jeffrey A. Engelman,* Rakesh K. Jain* *

*Corresponding author. Email: jain{at}steele.mgh.harvard.edu (R.K.J.); jeffrey.engelman{at}novartis.com (J.A.E.)

Published 24 May 2017, Sci. Transl. Med. 9, eaal4682 (2017)
DOI: 10.1126/scitranslmed.aal4682

This PDF file includes:

  • Fig. S1. The blood Gluc activity is directly correlated with tumor volume for each tumor model.
  • Fig. S2. Liver BT474 tumors respond to buparlisib.
  • Fig. S3. Microenvironment-dependent regulation of BC cells alters FOXO3 activity.
  • Fig. S4. MDA-MB-361 brain lesions transiently respond to buparlisib.
  • Fig. S5. HER3 expression is increased in BMs from HER2-positive BC.
  • Fig. S6. Several NRG isoforms induce resistance to buparlisib.
  • Fig. S7. NRG-1 is expressed in MFP and brain lesions.
  • Table S1. Differential expression of HER3 in intracranial and extracranial lesions from unmatched patient clinical samples.
  • Table S2. List of recombinant human growth factors screened for their ability to induce resistance to buparlisib.

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