Experiments
Searchable full-text extractions: founding hypothesis, core claims, experimental setups, key results and statistics — pulled out of each paper as structure. Search a cell line, an assay or an entity (e.g. HUH7) and find every paper that worked with it. This corpus stands on its own: most entries carry no reproduction assessment (yet).
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Comprehensive genomic characterization defines human glioblastoma genes and core pathways.
PMID 18772890 · PMC2671642 · Nature · 2008 · 8 claims · 5 setups
NF1 is a genuine human glioblastoma suppressor gene, inactivated by mutation, deletion, or expression loss in at least 23% of GBM samples
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Has reproduction · 100
Computational modeling demonstrates that glioblastoma cells can survive spatial environmental challenges through exploratory adaptation.
PMID 31836713 · PMC6911112 · Nature communications · 2019 · 8 claims · 6 setups
Stochastic exploration of the gene-regulatory network structure confers enhanced adaptive capacity, enabling GBM cells to converge to new target phenotypes in novel environments.
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Has reproduction · 89
Inference of Subpathway Activity Profiles Reveals Metabolism Abnormal Subpathway Regions in Glioblastoma Multiforme.
PMID 33072547 · PMC7533644 · Frontiers in oncology · 2020 · 7 claims · 8 setups
A metabolic subpathway activity score matrix method combining the k-clique algorithm and GSVA can accurately identify disease-related metabolic abnormal subpathways in GBM
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Cancer-specific high-throughput annotation of somatic mutations: computational prediction of driver missense mutations.
PMID 19654296 · PMC2763410 · Cancer research · 2009 · 7 claims · 7 setups
CHASM, a Random Forest-based computational method, was developed to identify and prioritize missense mutations likely to be functional drivers of tumor cell proliferation.
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iTRAQ-based proteomics profiling reveals increased metabolic activity and cellular cross-talk in angiogenic compared with invasive glioblastoma phenotype.
PMID 19674965 · PMC2773724 · Molecular & cellular proteomics : MCP · 2009 · 6 claims · 5 setups
Serial transplantation of human GBM xenografts in nude rats converts an initially highly infiltrative, non-angiogenic phenotype into a highly angiogenic phenotype over 4-6 generations.