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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MSI test to distinguish between HNPCC and other predisposing syndromes -- of value in tailored surveillance.
PMID 15528791 · PMC3839337 · Disease markers · 2004 · 8 claims · 5 setups
MSI (or immunohistochemistry) testing applied to a pre-selected patient with a family history or early-onset colorectal cancer can distinguish HNPCC from unknown non-HNPCC colorectal cancer syndromes.
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Pharmacogenomics of gemcitabine: can genetic studies lead to tailor-made therapy?
PMID 17595663 · PMC2360307 · British journal of cancer · 2007 · 8 claims · 14 setups
A SNP in the cytidine deaminase (CDA) gene (208G>A, haplotype *3) decreases gemcitabine clearance, increases Cmax/AUC, and increases neutropenia risk when gemcitabine is combined with platinum drugs or 5-FU
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Development of a fluorescent multiplex assay for detection of MSI-High tumors.
PMID 15528789 · PMC3839403 · Disease markers · 2004 · 8 claims · 7 setups
Mononucleotide markers are the most sensitive and specific microsatellite marker type for detecting MSI-H tumors with MMR defects
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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.
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25th Annual San Antonio Breast Cancer Symposium, San Antonio, Texas, USA, 10-14 December 2002 Update on preclinical and translational research.
PMID 12631391 · PMC154153 · Breast cancer research : BCR · 2003 · 8 claims · 8 setups
Growth factor signalling (EGF/HER-2/MAPK, AKT) phosphorylates the oestrogen receptor and drives development of endocrine-resistant breast cancer