Trial reportMolecular & cellular proteomics : MCP2015
Activating PIK3CA Mutations Induce an Epidermal Growth Factor Receptor (EGFR)/Extracellular Signal-regulated Kinase (ERK) Paracrine Signaling Axis in Basal-like Breast Cancer.
Trial report in Molecular & cellular proteomics : MCP, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- (Phospho)proteomic Profiling Reveals Mutation-Specific Adaptive Signaling to PI3Kα Inhibition inJournal of proteome research · 2026Article
- Article
- A pooled Cell Painting CRISPR screening platform enables de novo inference of gene function by self-supervised deep learning.Nature communications · 2025Article
- Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025Review
- The PIK3CA gene and its pivotal role in tumor tropism of triple-negative breast cancer.Translational oncology · 2024Review
- Obesity-driven changes in breast tissue exhibit a pro-angiogenic extracellular matrix signature.Matrix biology plus · 2024Article
- Genomic dissection and mutation-specific target discovery for breast cancer PIK3CA hotspot mutations.BMC genomics · 2024Article
- Article
- Amphiregulin Exerts Proangiogenic Effects in Developing Murine Lungs.Antioxidants (Basel, Switzerland) · 2024Article
- Genomic dissection and mutation-specific target discovery for breast cancerbioRxiv : the preprint server for biology · 2024Article
- Extracellular vesicles from human breast cancer-resistant cells promote acquired drug resistance and pro-inflammatory macrophage response.Frontiers in immunology · 2024Article
- Article
- The role of peroxidasin in solid cancer progression.Biochemical Society transactions · 2023Review
- Automatic detection of spatio-temporal signaling patterns in cell collectives.The Journal of cell biology · 2023Article
- The molecular landscape of breast mucoepidermoid carcinoma.Cancer medicine · 2023Article
- Prolactin and endocrine therapy resistance in breast cancer: The next potential hope for breast cancer treatment.Journal of cellular and molecular medicine · 2021Review
- Emerging Importance of Tyrosine Kinase Inhibitors against Cancer: Quo Vadis to Cure?International journal of molecular sciences · 2021Review
- Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Cisplatin inhibits the proliferation of Saos-2 osteosarcoma cells via the miR-376c/TGFA pathway.Bosnian journal of basic medical sciences · 2021Article
- Hierarchical tumor heterogeneity mediated by cell contact between distinct genetic subclones.The Journal of clinical investigation · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors at 9 institutions in 2 countries.
Funding
Abstract
Mutations in PIK3CA, the gene encoding the p110α catalytic subunit of phosphoinositide 3-kinase (PI3K) have been shown to transform human mammary epithelial cells (MECs). These mutations are present in all breast cancer subtypes, including basal-like breast cancer (BLBC). Using liquid chromatography-tandem mass spectrometry (LC-MS/MS), we identified 72 protein expression changes in human basal-like MECs with knock-in E545K or H1047R PIK3CA mutations versus isogenic MECs with wild-type PIK3CA. Several of these were secreted proteins, cell surface receptors or ECM interacting molecules and were required for growth of PIK3CA mutant cells as well as adjacent cells with wild-type PIK3CA. The proteins identified by MS were enriched among human BLBC cell lines and pointed to a PI3K-dependent amphiregulin/EGFR/ERK signaling axis that is activated in BLBC. Proteins induced by PIK3CA mutations correlated with EGFR signaling and reduced relapse-free survival in BLBC. Treatment with EGFR inhibitors reduced growth of PIK3CA mutant BLBC cell lines and murine mammary tumors driven by a PIK3CA mutant transgene, all together suggesting that PIK3CA mutations promote tumor growth in part by inducing protein changes that activate EGFR.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.