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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Improving melanoma classification by integrating genetic and morphologic features.
PMID 18532874 · PMC2408611 · PLoS medicine · 2008 · 7 claims · 5 setups
BRAF-mutant melanomas show distinct morphological features (upward migration and nesting of intraepidermal melanocytes, epidermal thickening, sharper lateral demarcation, larger/rounder/more pigmented tumor cells) compared to non-mutant melanomas
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Different molecular patterns in glioblastoma multiforme subtypes upon recurrence.
PMID 19644652 · PMC2811648 · Journal of neuro-oncology · 2010 · 7 claims · 5 setups
Type 1 GBM (p53 mutation, no EGFR amplification) and type 2 GBM (EGFR amplification, no p53 mutation) conserve their original molecular pattern at relapse.
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RExPrimer: an integrated primer designing tool increases PCR effectiveness by avoiding 3' SNP-in-primer and mis-priming from structural variation.
PMID 19958502 · PMC2788391 · BMC genomics · 2009 · 7 claims · 4 setups
RExPrimer integrates local SNP, indel, pseudogene, and CNV/structural variation databases with the Primer3 core algorithm to avoid mis-priming and SNP-in-Primer effects.
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Mosaicism in von Hippel-Lindau disease: an event important to recognize.
PMID 18205710 · PMC4401302 · Journal of cellular and molecular medicine · 2007 · 7 claims · 5 setups
The proband's father is a somatic mosaic for a VHL missense mutation (R161Q), explaining his mild, late-onset phenotype compared to his daughter's severe early-onset disease.
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Epidermal growth factor receptor abnormalities in the pathogenesis and progression of lung adenocarcinomas.
PMID 19138956 · PMC3369271 · Cancer prevention research (Philadelphia, Pa.) · 2008 · 8 claims · 4 setups
EGFR mutations and protein overexpression are early phenomena in the pathogenesis of lung adenocarcinoma, occurring in histologically normal bronchial/bronchiolar epithelium (NBE)