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).

• A big circuit model.

  PMID 12940284 · PMC1316925 · Environmental health perspectives · 2003 · 8 claims · 8 setups

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  In early prostate carcinogenesis, apoptosis signals are primarily suppressed rather than growth rate being increased.

  prostate blood model genes microarray proteomic gene

• 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

  Has reproduction · 10

  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

  rms injected muscle cck-8 caspase subcutaneous

• Lysine 63-polyubiquitination guards against translesion synthesis-induced mutations.

  PMID 16789823 · PMC1513265 · PLoS genetics · 2006 · 8 claims · 8 setups

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  K63-polyubiquitin chain formation protects human cells against translesion synthesis-induced mutations by promoting error-free recovery of blocked replication forks.

  a549 western proliferation clonogenic

• RAS mutations affect tumor necrosis factor-induced apoptosis in colon carcinoma cells via ERK-modulatory negative and positive feedback circuits along with non-ERK pathway effects.

  PMID 19789336 · PMC2927135 · Cancer research · 2009 · 8 claims · 8 setups

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  K-RAS and N-RAS mutation status differentially determine the level of TNFα-induced apoptosis in an isogenic colon carcinoma cell panel

  isogenic same conditioned dld-1 flow luminex immunoblot

• Expression of neurofibromin 1 in colorectal cancer and cetuximab resistance.

  PMID 34779495 · PMC8611403 · Oncology reports · 2022 · 7 claims · 8 setups

  Has reproduction · 73

  NF1 is highly expressed in cetuximab-sensitive colorectal cancer cell lines (NCI-H508, Caco2) but weakly expressed in cetuximab-resistant lines (KM12C, SW480)

  crc cetuximab-sensitive nf1 cetuximab-resistant western sirna dapi

• Gli1-expressing stromal cells are highly reparative precursors of long-lived chondroprogenitors in the fetal murine limb.

  PMID 41253754 · PMC12627582 · Nature communications · 2025 · 7 claims · 8 setups

  Has reproduction · 10

  Fetal Gli1+ cells (including cells outside the cartilage) are the precursors of postnatal long-lived chondroprogenitors and give rise to most growth-plate chondrocytes juvenile/adult.

  fetal left-cart-p21moe growth gli1creer single-nuclei bulk cre-based

• Fingerprinting cancer development.

  PMID 14694892 · PMC1241638 · Environmental health perspectives · 2003 · 8 claims · 6 setups

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  Protein microarrays can detect phosphoprotein fingerprints that identify early-stage cancer or monitor drug toxicity.

  prostate blood model genes microarray proteomic gene

• Mathematical models in mammalian cell biology.

  PMID 18638360 · PMC2530880 · Genome biology · 2008 · 8 claims · 8 setups

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  A point mutation in the circadian Per2 gene causes familial advanced sleep phase syndrome (FASPS) via a phosphorylation defect that alters PER2 stability and subcellular localization.

  culture skin hela mammalian live-cell confocal phosphoprotein

• CHD5, a tumor suppressor gene deleted from 1p36.31 in neuroblastomas.

  PMID 18577749 · PMC2483574 · Journal of the National Cancer Institute · 2008 · 7 claims · 8 setups

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  CHD5 promoter is highly methylated in neuroblastoma cell lines with 1p deletion and absent CHD5 expression (NLF, IMR5)

  neuroblastoma nlf athymic methylation-specific quantitative soft

• An oncogenomics-based in vivo RNAi screen identifies tumor suppressors in liver cancer.

  PMID 19012953 · PMC2990916 · Cell · 2008 · 7 claims · 8 setups

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  shRNA pools targeting genes recurrently deleted in human HCC accelerate hepatocarcinogenesis in vivo, whereas randomly selected shRNA pools do not.

  hepatocellular p53 genomic hepatoma array-based pooled shrna