ArticleeLife2019
Mutationally-activated PI3'-kinase-α promotes de-differentiation of lung tumors initiated by the BRAF
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- Tumor-enriched circRNA TAFCR1 drives cancer progression and metastasis by disrupting UBE1-dependent TRIM21-mediated CD44 ubiquitination.Biomarker research · 2026Article
- BRAFbioRxiv : the preprint server for biology · 2025Article
- Preclinical Modeling of Pathway-Targeted Therapy of Human Lung Cancer in the Mouse.Cold Spring Harbor perspectives in medicine · 2024Review
- Oncogenic context shapes the fitness landscape of tumor suppression.Nature communications · 2023Article
- Tissue specificity of oncogenic BRAF targeted to lung and thyroid through a shared lineage factor.iScience · 2023Article
- Novel Therapeutic Approaches Targeting Post-Translational Modifications in Lung Cancer.Pharmaceutics · 2023Review
- Identification of tumor-suppressor genes in lung squamous cell carcinoma through integrated bioinformatics analyses.Oncology research · 2023Article
- Transposon Mutagenesis Reveals RBMS3 Silencing as a Promoter of Malignant Progression of BRAFV600E-Driven Lung Tumorigenesis.Cancer research · 2022Article
- Decrypting a path based approach for identifying the interplay between PI3K and GSK3 signaling cascade from the perspective of cancer.Genes & diseases · 2022Review
- Combinatorial Inactivation of Tumor Suppressors Efficiently Initiates Lung Adenocarcinoma with Therapeutic Vulnerabilities.Cancer research · 2022Article
- From targeted therapy to a novel way: Immunogenic cell death in lung cancer.Frontiers in medicine · 2022Review
- A role for club cells in smoking-associated lung adenocarcinoma.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Positive correlation between transcriptomic stemness and PI3K/AKT/mTOR signaling scores in breast cancer, and a counterintuitive relationship with PIK3CA genotype.PLoS genetics · 2021Article
- PI3K in stemness regulation: from development to cancer.Biochemical Society transactions · 2020Review
- Mutationally-activated PI3'-kinase-α promotes de-differentiation of lung tumors initiated by the BRAFeLife · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Human lung adenocarcinoma exhibits a propensity for de-differentiation, complicating diagnosis and treatment, and predicting poorer patient survival. In genetically engineered mouse models of lung cancer, expression of the BRAF
Indexed as
Identifiers
What Socratic 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 Socratic graph.