Supplementary Materials

Supplementary Material for:

Afatinib restrains K-RAS–driven lung tumorigenesis

Herwig P. Moll, Klemens Pranz, Monica Musteanu, Beatrice Grabner, Natascha Hruschka, Julian Mohrherr, Petra Aigner, Patricia Stiedl, Luka Brcic, Viktoria Laszlo, Daniel Schramek, Richard Moriggl, Robert Eferl, Judit Moldvay, Katalin Dezso, Pedro P. Lopez-Casas, Dagmar Stoiber, Manuel Hidalgo, Josef Penninger, Maria Sibilia, Balázs Győrffy, Mariano Barbacid, Balázs Dome, Helmut Popper, Emilio Casanova*

*Corresponding author. Email: emilio.casanova{at}meduniwien.ac.at

Published 20 June 2018, Sci. Transl. Med. 10, eaao2301 (2018)
DOI: 10.1126/scitranslmed.aao2301

This PDF file includes:

  • Materials and Methods
  • Fig. S1. K-RAS–mutated lung ACs display increased ERBB expression profile.
  • Fig. S2. K-RAS–mutated lung ACs exhibit activated EGFR.
  • Fig. S3. Genetic EGFR ablation in K-RAS–mutated lung AC reduces tumor growth.
  • Fig. S4. Genetic EGFR ablation in K-RAS–mutated lung AC cells reduces tumor growth.
  • Fig. S5. Inhibition of EGFR signaling down-regulates mutated K-RAS activity.
  • Fig. S6. Afatinib reduces growth of K-RAS–mutant lung AC in vitro.
  • Fig. S7. Afatinib reduces K-RAS–mediated tumorigenesis in vivo.
  • Fig. S8. ERBB family members mediate resistance to EGFR inhibition, which can be blocked by afatinib.
  • Table S4. List of genotyping primers.
  • Table S5. List of primers for quantitative PCR analysis.
  • References (4451)

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Other Supplementary Material for this manuscript includes the following:

  • Table S1. Alveolar_KRAS_up gene set (provided as an Excel file).
  • Table S2. KRAS_NSCLC_up gene set (provided as an Excel file).
  • Table S3. Primary data shown in the figures (provided as an Excel file).

[Download Tables S1 to S3]