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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Ethnic differences and functional analysis of MET mutations in lung cancer.
PMID 19723643 · PMC2767337 · Clinical cancer research : an official journal of the American Association for Cancer Research · 2009 · 8 claims · 7 setups
MET mutations identified in lung tumors are predominantly germline rather than somatic
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Has reproduction · 67
Research and experimental verification on the mechanisms of cellular senescence in triple-negative breast cancer.
PMID 38435998 · PMC10909353 · PeerJ · 2024 · 8 claims · 8 setups
TNBC can be classified into three molecular subtypes (clusters 1, 2, 3) based on cellular senescence-related pathways, with distinct prognoses (cluster 1 best, then 2, then 3).
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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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Full-text index only
Functional restoration of BRCA2 protein by secondary BRCA2 mutations in BRCA2-mutated ovarian carcinoma.
PMID 19654294 · PMC2754824 · Cancer research · 2009 · 8 claims · 7 setups
Secondary BRCA2 mutations restore BRCA2 protein/reading frame and thereby cause acquired platinum and PARP inhibitor resistance in BRCA2-mutated ovarian carcinoma
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Disruption of the EGFR E884-R958 ion pair conserved in the human kinome differentially alters signaling and inhibitor sensitivity.
PMID 19015641 · PMC2633425 · Oncogene · 2009 · 8 claims · 8 setups
E884K works in concert with L858R in-cis, in a dominant fashion, to differentially alter EGFR downstream signaling and inhibitor sensitivity in an inhibitor-specific manner