A Pan-Cancer Proteogenomic Atlas of PI3K/AKT/mTOR Pathway Alterations
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Summary Molecular alterations involving PI3K/AKT/mTOR pathway (including mutation, copy number, protein, or RNA) were examined across 11219 human cancers representing 32 major types. Within specific mutated genes, frequency, mutation hotspot residues, in silico predictions, and functional assays were all informative in distinguishing the subset of genetic variants more likely to have functional relevance. Multiple oncogenic pathways including PI3K/AKT/mTOR converged on similar sets of downstream transcriptional targets. In addition to mutation, structural variations and partial copy losses involving PTEN and STK11 showed evidence for having functional relevance. A substantial fraction of cancers showed high mTOR pathway activity without an associated canonical genetic or genomic alteration, including cancers harboring IDH1 or VHL mutations, suggesting multiple mechanisms for pathway activation.
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E545K at exon 9 and H1047R at exon 20 are prevalent in cancers.
“In particular, the occurrence of E545K at exon 9 and H1047R at exon 20 is prevalent in cancers, and these mutations can constitutively activate PI3K signaling32,33.”
From Mechanisms of KRAS inhibitor resistance in KRAS-mutant colorectal cancer harboring Her2 amplification and aberrant KRAS localization (2025) · cites this paper as [32]
The Results section identifies E545 and H1047 as among the most frequently mutated PIK3CA positions in cancers. Our copy does not specify that the prevalent substitutions are E545K and H1047R, or identify those positions as being in exons 9 and 20. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPIK3CA E545K and H1047R mutations can constitutively activate PI3K signaling.
“In particular, the occurrence of E545K at exon 9 and H1047R at exon 20 is prevalent in cancers, and these mutations can constitutively activate PI3K signaling32,33.”
From Mechanisms of KRAS inhibitor resistance in KRAS-mutant colorectal cancer harboring Her2 amplification and aberrant KRAS localization (2025) · cites this paper as [32]
The Introduction (page unavailable) identifies E545 and H1047 as PIK3CA mutation hotspots that activate the PI3K kinase. The Results section on recurrently mutated residues (page unavailable) reports high activity for mutants at those sites, but the available text does not specify E545K or H1047R or establish that their activation is constitutive. (LLM, conf=0.82)
Experimental — accuracy not yet measured
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- Authors
- Zhang, Y., Kwok-Shing Ng, P., Kucherlapati, M., Chen, F., Liu, Y., Tsang, Y. H., de Velasco, G., Jeong, K. J., Akbani, R., Hadjipanayis, A., Pantazi, A., Bristow, C. A., Lee, E., Mahadeshwar, H. S., Tang, J., Zhang, J., Yang, L., Seth, S., Lee, S., Ren, X., Song, X., Sun, H., Seidman, J., Luquette, L. J., Xi, R., Chin, L., Protopopov, A., Westbrook, T. F., Shelley, C. S., Choueiri, T. K., Ittmann, M., Van Waes, C., Weinstein, J. N., Liang, H., Henske, E. P., Godwin, A. K., Park, P. J., Kucherlapati, R., Scott, K. L., Mills, G. B., Kwiatkowski, D. J., & Creighton, C. J.
- Affiliations
- Baylor College of Medicine (US)
- Brigham and Women's Hospital (US)
- The University of Texas MD Anderson Cancer Center (US)
- Harvard University (US)
- Broad Institute (US)
- University of Wisconsin–Madison (US)
- Dana-Farber Cancer Institute (US)
- University of Kansas Medical Center (US)
- Corresponding author
- Mills, Gordon B.
- Kwiatkowski, David J.
- Creighton, Chad J.
- ORCID
- Zhang, Yiqun
- Kucherlapati, Melanie
- Chen, Fengju
- Liu, Yuexin
- Tsang, Yiu Huen
- Jeong, Kang Jin
- Akbani, Rehan
- Hadjipanayis, Angela
- Pantazi, Angeliki
- Bristow, Christopher A.
- Lee, Eunjung
- Zhang, Jianhua
- Yang, Lixing
- Seth, Sahil
- Lee, Semin
- Song, Xingzhi
- Seidman, Jonathan
- Luquette, Lovelace J.
- Xi, Ruibin
- Protopopov, Alexei
- Westbrook, Thomas F.
- Shelley, Carl Simon
- Choueiri, Toni K.
- Ittmann, Michael
- Weinstein, John N.
- Liang, Han
- Henske, Elizabeth P.
- Godwin, Andrew K.
- Park, Peter J.
- Mills, Gordon B.
- Kwiatkowski, David J.
- Creighton, Chad J.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2017-06
- Volume
- 31
- Issue
- 6
- Pages
- 820-832.e3
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC5502825
- OpenAlex
- W2616761213
- Semantic Scholar
- 1ca50d3272a9c1aa38b714579d66b2dff0588a2d
- Cited by
- 626
- References
- 45
- Citations by year
- 2026: 29 · 2025: 59 · 2024: 84 · 2023: 83 · 2022: 80 · 2021: 84 · 2020: 93 · 2019: 61 · 2018: 44 · 2017: 7
- FWCI
- 23.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Scholarworks@UNIST (Ulsan National Institute of Science and Technology) (submittedVersion)
- Funders
- Cancer Prevention and Research Institute of Texas (RP120713 C2, 5P50CA098258, 5U01CA168394)
- NIH (U24CA143883, 2P50CA101942-11A1, 1R21CA191687, 5P01CA120964, CA175486, CA209851, P30CA125123)
- Cancer Center (P30CA016672)
- Abbvie
- Adelson Medical Research Foundation
- AstraZeneca
- Breast Cancer Research Foundation
- Critical Outcomes Technology
- Horizon Diagnostics
- Illumina
- Ionis
- Karus Therapeutics
- Komen Research Foundation
- Nanostring
- Pfizer
- Takeda/Millennium Pharmaceuticals
- Tesaro
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- PI3K/AKT/mTOR pathway, somatic mutations, copy number alterations, PTEN, STK11, structural variants, IDH1 mutation, VHL mutation, mutational hotspots
- MeSH terms
- Proteogenomics, Humans, Mutation, Neoplasms, Signal Transduction, Survival Analysis, Phosphatidylinositol 3-Kinases, Gene Expression Profiling, Databases, Genetic, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases
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