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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Identification of transformation-related pathways in a breast epithelial cell model using a ribonomics approach.
PMID 18829526 · PMC2692251 · Cancer research · 2008 · 7 claims · 6 setups
Global association of HuR and AUF1 with target mRNAs changes substantially and largely reciprocally between MCT-1-transformed and nontransformed MCF10A cells
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Has reproduction · 85
PDGFRA defines the mesenchymal stem cell Kaposi's sarcoma progenitors by enabling KSHV oncogenesis in an angiogenic environment.
PMID 31881074 · PMC6980685 · PLoS pathogens · 2019 · 8 claims · 8 setups
PDGFRA(+)/SCA-1(+) bone marrow-derived MSCs (Pα(+)S MSCs) are KS spindle-cell progenitors
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Has reproduction · 10
FOXM1 inhibitor, RCM‑1, enhances venetoclax mediated apoptosis through downregulation of ATP2B4 in rhabdomyosarcoma.
PMID 41789627 · PMC12987556 · International journal of oncology · 2026 · 8 claims · 8 setups
Combination therapy of RCM-1 and venetoclax inhibits RMS tumor growth more efficiently than venetoclax alone in an animal model by decreasing proliferation and inducing apoptosis
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Frequent somatic mutations of GNAQ in uveal melanoma and blue naevi.
PMID 19078957 · PMC2696133 · Nature · 2009 · 8 claims · 8 setups
GNAQ is frequently somatically mutated in blue nevi (83%) and uveal melanoma (46%)
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Has reproduction · 92
Synergism between IL7R and CXCR4 drives BCR-ABL induced transformation in Philadelphia chromosome-positive acute lymphoblastic leukemia.
PMID 32581241 · PMC7314847 · Nature communications · 2020 · 8 claims · 8 setups
IL7R interacts/colocalizes with CXCR4 on the cell surface, recruiting BCR-ABL1 and JAK kinases into close proximity to form a platform for transformation
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C-terminal mutants of apolipoprotein L-I efficiently kill both Trypanosoma brucei brucei and Trypanosoma brucei rhodesiense.
PMID 19997494 · PMC2778949 · PLoS pathogens · 2009 · 8 claims · 8 setups
The C-terminal helix of apoL1 is entirely responsible for its interaction with SRA