Supplementary Materials

Supplementary Material for:

Stress hormones promote EGFR inhibitor resistance in NSCLC: Implications for combinations with β-blockers

Monique B. Nilsson, Huiying Sun, Lixia Diao, Pan Tong, Diane Liu, Lerong Li, Youhong Fan, Alissa Poteete, Seung-Oe Lim, Kathryn Howells, Vincent Haddad, Daniel Gomez, Hai Tran, Guillermo Armaiz Pena, Lecia V. Sequist, James C. Yang, Jing Wang, Edward S. Kim, Roy S. Herbst, J. Jack Lee, Waun Ki Hong, Ignacio Wistuba, Mien-Chie Hung, Anil K. Sood, John V. Heymach*

*Corresponding author. Email: jheymach{at}

Published 8 November 2017, Sci. Transl. Med. 9, eaao4307 (2017)
DOI: 10.1126/scitranslmed.aao4307

This PDF file includes:

  • Fig. S1. Frequency of T790M EGFR secondary mutations in erlotinib-resistant cells.
  • Fig. S2. Resistance of HCC827 ER and HCC4006 ER cells to EGFR TKIs.
  • Fig. S3. ADRB expression and EGFR status in NSCLC cell lines.
  • Fig. S4. Induction of IL-6 after β-AR activation.
  • Fig. S5. Differential effects of β2-AR signaling on EGFR mutant and wild-type cells.
  • Fig. S6. Stress hormone–induced effects on LKB1, PKC, and CREB.
  • Fig. S7. Effect of EGFR inhibition on β-AR–induced p-LKB1, p-CREB, and IL-6.
  • Fig. S8. Effect of β-AR signaling on NF-κB activity.
  • Fig. S9. Effect of chronic stress on IL-6 expression and MVD in NSCLC xenografts.
  • Fig. S10. The effects of stress hormones on EGFR inhibitor resistance in NSCLC.
  • Table S1. PFS and OS of NSCLC patients with high or low IL-6 treated with erlotinib.
  • Table S2. Smoking status of patients with high or low circulating IL-6 in the ZEST trial.
  • Table S3. Lung cancer cell lines used in ADRB gene expression analysis.

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