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).

• Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia.

  PMID 19039135 · PMC2746051 · Science (New York, N.Y.) · 2008 · 8 claims · 7 setups

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  Diagnosis and relapse ALL samples show different patterns of CNAs, with relapse-acquired abnormalities preferentially affecting cell cycle regulation and B-cell development genes

  matched bone leukemia diagnosis snp flow quantitative

• A genomic approach to improve prognosis and predict therapeutic response in chronic lymphocytic leukemia.

  PMID 19861443 · PMC2783430 · Clinical cancer research : an official journal of the American Association for Cancer Research · 2009 · 8 claims · 8 setups

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  A genomic signature derived from CLL patient leukemic cells significantly differentiates stable from progressive disease

  duke nci-60 mayo spanish gene cdna igvh

• Intrinsic suppression of type I interferon production underlies the therapeutic efficacy of IL-15-producing natural killer cells in B-cell acute lymphoblastic leukemia.

  PMID 37217248 · PMC10231005 · Journal for immunotherapy of cancer · 2023 · 8 claims · 8 setups

  Has reproduction · 76

  High expression of IFN-I signaling/response genes predicts favorable clinical outcome (longer relapse-free survival) in B-ALL patients

  cog b-all eμ-myc crispra relapse-free flow mass

• Downregulation of death-associated protein kinase 1 (DAPK1) in chronic lymphocytic leukemia.

  PMID 17540169 · PMC4647864 · Cell · 2007 · 8 claims · 13 setups

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  DAPK1 promoter is epigenetically silenced by DNA methylation in almost all sporadic CLL cases

  cd19+ leukemia raji jurkat quantitative cobra chromatin

• Proteomic and genetic approaches identify Syk as an AML target.

  PMID 19800574 · PMC2803063 · Cancer cell · 2009 · 8 claims · 8 setups

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  EGFR inhibitors (e.g., gefitinib) induce AML differentiation through a non-EGFR, off-target mechanism

  hl-60 aml molm-14 luciferase-labeled phospho-tyrosine kinome-wide secondary