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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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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Glioblastoma subclasses can be defined by activity among signal transduction pathways and associated genomic alterations.
PMID 19915670 · PMC2771920 · PloS one · 2009 · 8 claims · 6 setups
Proteomic analysis of glioma samples reveals three signaling subclasses of GBM associated with predominant EGFR activation, PDGFR activation, or loss of NF1
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Different molecular patterns in glioblastoma multiforme subtypes upon recurrence.
PMID 19644652 · PMC2811648 · Journal of neuro-oncology · 2010 · 7 claims · 5 setups
Type 1 GBM (p53 mutation, no EGFR amplification) and type 2 GBM (EGFR amplification, no p53 mutation) conserve their original molecular pattern at relapse.
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Has reproduction · 73
Integrated multiomic analysis reveals disulfidptosis subtypes in glioblastoma: implications for immunotherapy, targeted therapy, and chemotherapy.
PMID 38504986 · PMC10950096 · Frontiers in immunology · 2024 · 8 claims · 8 setups
Consensus clustering on 32 disulfidptosis-associated genes stratifies GBM patients into two subtypes, DRGcluster A and B, with distinct survival outcomes.
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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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Has reproduction · 62
Specific Marker Gene Analysis for Primary Central Nervous System Lymphoma Based on Methylation Difference and Development of Detection Primers.
PMID 41097902 · PMC12528802 · Brain and behavior · 2025 · 6 claims · 6 setups
RHEB promoter hypermethylation is a PCNSL-specific biomarker distinguishing PCNSL from other CNS diseases.
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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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An integrated genomic analysis of human glioblastoma multiforme.
PMID 18772396 · PMC2820389 · Science (New York, N.Y.) · 2008 · 8 claims · 7 setups
IDH1 is recurrently mutated at its active site (R132) in 12% of GBM patients, a previously unrecognized alteration in GBM.
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Has reproduction
Immunoregulatory Roles of Tumor-Originated Pericytes Identified by Single-Cell Analysis in Glioblastoma.
PMID 41001759 · PMC12713092 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025 · 6 claims · 8 setups
Human primary GBMs contain both tumor-originated pericytes (T-PCs) and normal-originated pericytes (N-PCs) with distinctive cell-intrinsic features.
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Has reproduction · 64
Spatial-reprogramming derived GPNMB(+) macrophages interact with COL6A3(+) fibroblasts to enhance vascular fibrosis in glioblastoma.
PMID 41174767 · PMC12577258 · Genome medicine · 2025 · 7 claims · 8 setups
A distinct subset of COL6A3+ tumor-associated fibroblasts (TAFs) with matrix-fibroblast characteristics exists in GBM and is significantly enriched in non-responders to neoadjuvant combination therapy.
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Has reproduction · 100
Proneural-mesenchymal antagonism dominates the patterns of phenotypic heterogeneity in glioblastoma.
PMID 38433919 · PMC10905000 · iScience · 2024 · 8 claims · 8 setups
The four proposed GBM molecular subtypes (Proneural, Neural, Classical, Mesenchymal / NPC-like, OPC-like, AC-like, MES-like) are not mutually exclusive or independent of one another
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Has reproduction · 86
RNASEQR--a streamlined and accurate RNA-seq sequence analysis program.
PMID 22199257 · PMC3315322 · Nucleic acids research · 2012 · 8 claims · 7 setups
RNASEQR is a new RNA-seq mapper/aligner that combines a BWT-based (Bowtie) transcriptomic/genomic alignment with hash-based BLAT local alignment in three sequential steps: transcriptome mapping, novel exon detection, and anchor-and-align novel splice junction identification.
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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.
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Has reproduction
Fast, accurate, and racially unbiased pan-cancer tumor-only variant calling with tabular machine learning.
PMID 36611079 · PMC9825621 · NPJ precision oncology · 2023 · 7 claims · 8 setups
Tabular ML classifiers (TabNet, XGBoost, LightGBM) trained on tumor-only-derived features achieve state-of-the-art somatic vs germline classification, with AUC>94% on TCGA holdout and AUC>85% on metastatic melanoma.
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Has reproduction · 79
The relationship between PLOD1 expression level and glioma prognosis investigated using public databases.
PMID 34040895 · PMC8127981 · PeerJ · 2021 · 8 claims · 8 setups
PLOD1 mRNA expression is significantly higher in glioma tissue than in normal brain tissue
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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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Has reproduction · 59
Application of Machine Learning in Predicting Hepatic Metastasis or Primary Site in Gastroenteropancreatic Neuroendocrine Tumors.
PMID 37887568 · PMC10605255 · Current oncology (Toronto, Ont.) · 2023 · 8 claims · 7 setups
Multi-gene random forest models classify primary tumor vs. liver metastasis samples with 100% accuracy in training/test cohorts and >90% accuracy in an independent validation cohort