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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Novel selection and genetic characterisation of an etoposide-resistant human leukaemic CCRF-CEM cell line.
PMID 8382508 · PMC1968246 · British journal of cancer · 1993 · 8 claims · 5 setups
CEM/VP-1 is 15-fold more resistant to etoposide than parental CCRF-CEM cells
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Activating mutations in ALK provide a therapeutic target in neuroblastoma.
PMID 18923525 · PMC2587486 · Nature · 2008 · 8 claims · 8 setups
Non-synonymous ALK kinase domain mutations occur in 8% of primary neuroblastomas, with F1174L being the most frequent
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Genomics: applications in mechanism elucidation.
PMID 19166886 · PMC2698023 · Advanced drug delivery reviews · 2009 · 8 claims · 8 setups
Genomic tools require no a priori knowledge of a compound's mode of action and can reveal biological pathways (metabolism, distribution, off-target effects) in addition to the precise mechanism of action.
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Nitrosative stress-induced s-glutathionylation of protein disulfide isomerase leads to activation of the unfolded protein response.
PMID 19773442 · PMC2756322 · Cancer research · 2009 · 7 claims · 8 setups
PABA/NO treatment causes S-glutathionylation (not S-nitrosylation) of PDI in cells and in vitro
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In B-CLL, the codon 72 polymorphic variants of p53 are not related to drug resistance and disease prognosis.
PMID 16109171 · PMC1208864 · BMC cancer · 2005 · 7 claims · 5 setups
The p53 codon 72 polymorphism is not associated with drug resistance or overall survival in B-CLL
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Incidence of mutation and deletion in topoisomerase II alpha mRNA of etoposide and mAMSA-resistant cell lines.
PMID 11676865 · PMC5926608 · Japanese journal of cancer research : Gann · 2001 · 7 claims · 6 setups
Acquired mutations of the topoisomerase IIα gene are an important and frequent mechanism of resistance to topoisomerase II inhibitors, independent of the degree of resistance.