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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Inactivation of O6-methylguanine-DNA methyltransferase by promoter CpG island hypermethylation in gastric cancers.
PMID 12085181 · PMC2375420 · British journal of cancer · 2002 · 6 claims · 8 setups
Loss of MGMT expression in gastric carcinomas frequently results from promoter CpG island hypermethylation.
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Has reproduction · 100
Differential Gene Expression and Methylation Analysis of Melanoma in TCGA Database to Further Study the Expression Pattern of KYNU in Melanoma.
PMID 35893303 · PMC9329910 · Journal of personalized medicine · 2022 · 8 claims · 8 setups
Oncogenes MITF, KIT, CDH1, NRAS, AKT1, EGFR, TP53, and CDK4 are elevated while tumor suppressors PTEN, cAMP, and BCL2 are reduced in melanoma
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Aberrations of the p14(ARF) and p16(INK4a) genes in renal cell carcinomas.
PMID 11749694 · PMC5926680 · Japanese journal of cancer research : Gann · 2001 · 7 claims · 6 setups
Homozygous co-deletion of p14ARF and p16INK4a is frequent in RCC cell lines (5 of 6 lines)
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Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis.
PMID 11161385 · PMC2363700 · British journal of cancer · 2001 · 8 claims · 6 setups
PDC shows frequent alterations of K-ras, p53, p16 and DPC4, confirming these as the core molecular fingerprint of ductal cancer
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Genetic and epigenetic changes in primary metastatic and nonmetastatic colorectal cancer.
PMID 16969349 · PMC2360724 · British journal of cancer · 2006 · 8 claims · 8 setups
K-Ras codon 12 mutations are significantly associated with metastatic (M+) CRC
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Alterations in candidate genes PHF2, FANCC, PTCH1 and XPA at chromosomal 9q22.3 region: pathological significance in early- and late-onset breast carcinoma.
PMID 18990233 · PMC2633285 · Molecular cancer · 2008 · 8 claims · 5 setups
PHF2, FANCC and PTCH1 show high frequency of alterations (deletion/methylation) compared to XPA in both early- and late-onset breast carcinoma groups
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Molecular tumor profiling: translating genomic insights into clinical advances.
PMID 15287965 · PMC507868 · Genome biology · 2004 · 8 claims · 8 setups
Gene-expression profiling can distinguish BRCA1- and BRCA2-linked breast tumors from sporadic breast tumors with similar hormone-receptor status
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The field of tissue injury in the lung and airway.
PMID 19138985 · PMC2705781 · Cancer prevention research (Philadelphia, Pa.) · 2008 · 8 claims · 8 setups
Field cancerization and the field of injury reflect molecular changes (genomic, epigenomic, transcriptomic, proteomic) present in histologically normal-appearing tissue distant from and independent of a tumor, throughout the carcinogen-exposed respiratory epithelium
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MSH6 missense mutations are often associated with no or low cancer susceptibility.
PMID 15354210 · PMC2409912 · British journal of cancer · 2004 · 7 claims · 8 setups
Most MSH6 missense changes found in MSI-positive tumours are likely clinically innocent or of low cancer-susceptibility significance
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A review on the molecular diagnostics of Lynch syndrome: a central role for the pathology laboratory.
PMID 19929944 · PMC3837620 · Journal of cellular and molecular medicine · 2010 · 8 claims · 7 setups
Lynch syndrome is caused by germline mutations in the mismatch repair genes MLH1, MSH2, MSH6 or PMS2
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Has reproduction · 59
The motor neuron m6A repertoire governs neuronal homeostasis and FTO inhibition mitigates ALS symptom manifestation.
PMID 40307231 · PMC12043976 · Nature communications · 2025 · 8 claims · 8 setups
m6A hypomethylation (not hypermethylation) is consistently associated with ALS across patient iPSC-MNs, postmortem tissue, and independent transcriptomic datasets
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The role of MYH and microsatellite instability in the development of sporadic colorectal cancer.
PMID 17031395 · PMC2360566 · British journal of cancer · 2006 · 8 claims · 8 setups
MYH-associated colorectal cancers can develop through either a chromosomal instability pathway or a microsatellite instability (MSI) pathway, contradicting the assumption that these are mutually exclusive.