Supplementary Materials

Supplementary Material for:

PIK3CA mutations enable targeting of a breast tumor dependency through mTOR-mediated MCL-1 translation

Grace R. Anderson, Suzanne E. Wardell, Merve Cakir, Lorin Crawford, Jim C. Leeds, Daniel P. Nussbaum, Pallavi S. Shankar, Ryan S. Soderquist, Elizabeth M. Stein, Jennifer P. Tingley, Peter S. Winter, Elizabeth K. Zieser-Misenheimer, Holly M. Alley, Alexander Yllanes, Victoria Haney, Kimberly L. Blackwell, Shannon J. McCall, Donald P. McDonnell, Kris C. Wood*

*Corresponding author. Email: kris.wood{at}duke.edu

Published 14 December 2016, Sci. Transl. Med. 8, 369ra175 (2016)
DOI: 10.1126/scitranslmed.aae0348

This PDF file includes:

  • Materials and methods
  • Fig. S1. Solid tumors can be sensitized to BH3 mimetics.
  • Fig. S2. Breast cancer cell lines were stratified by genotype and histological subtype.
  • Fig. S3. Direct inhibition of MCL-1 phenocopies PI3K pathway inhibition.
  • Fig. S4. MCL-1 is not regulated transcriptionally or posttranslationally by PI3K/mTOR.
  • Fig. S5. PIK3CA WT breast cancers respond to direct MCL-1 inhibition.
  • Fig. S6. MCL-1 and BCL-XL targeting has therapeutic potential.
  • Table S1. Molecular and histological characteristics of the breast cancer cell lines from fig. S2C.
  • Table S2. Sequences of shRNA clones.
  • Legend for Table S3
  • Table S4. Sequences of sgRNA clones.
  • Table S5. ER status, HER2 status, and PIK3CA mutation status (when available) of patient samples.
  • References (5157)

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Other Supplementary Material for this manuscript includes the following:

  • Table S3 (Microsoft Excel format). Raw tumor measurements for xenograft studies.