Supplementary Materials

Supplementary Material for:

Targeted BMI1 inhibition impairs tumor growth in lung adenocarcinomas with low CEBPα expression

Kol Jia Yong, Daniela S. Basseres, Robert S. Welner, Wen Cai Zhang, Henry Yang, Benedict Yan, Meritxell Alberich-Jorda, Junyan Zhang, Lorena Lobo de Figueiredo- Pontes, Chiara Battelli, Christopher J. Hetherington, Min Ye, Hong Zhang, Giorgia Maroni, Karen O'Brien, Maria Cristina Magli, Alain C. Borczuk, Lyuba Varticovski, Olivier Kocher, Pu Zhang, Young-Choon Moon, Nadiya Sydorenko, Liangxian Cao, Thomas W. Davis, Bhavin M. Thakkar, Ross A. Soo, Atsushi Iwama, Bing Lim, Balazs Halmos, Donna Neuberg, Daniel G. Tenen,* Elena Levantini*

*Corresponding author. Email: elevanti{at}bidmc.harvard.edu (E.L.); csidgt{at}nus.edu.sg (D.G.T.)

Published 3 August 2016, Sci. Transl. Med. 8, 350ra104 (2016)
DOI: 10.1126/scitranslmed.aad6066

This PDF file includes:

  • Materials and Methods
  • Fig. S1. IHC data show BMI1 and C/EBPα expression in NSCLC patient subtypes.
  • Fig. S2. C/EBPα determines BMI1-related overall survival probability in NSCLC patients.
  • Fig. S3. C/EBPαLung-Δ mice develop pulmonary adenocarcinomas.
  • Fig. S4. Schematic representation shows generation of Bmi1-haploinsufficient C/EBPαLung-Δ mice and subcutaneous transplantation models.
  • Fig. S5. The BMI1 inhibitor molecule PTC-209 inhibits BMI1 and induces cell cycle arrest in vitro.
  • Table S1. Patient demographic and clinicopathological parameters for all NSCLC cases.
  • References (4450)

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