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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Expression genomics in breast cancer research: microarrays at the crossroads of biology and medicine.
PMID 17397520 · PMC1868923 · Breast cancer research : BCR · 2007 · 8 claims · 8 setups
Genome-wide expression microarray studies reveal transcriptional networks/signatures that explain breast cancer biological and clinical heterogeneity
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Heterogeneity of p53 mutational status in esophageal squamous cell carcinoma.
PMID 9617346 · PMC5921814 · Japanese journal of cancer research : Gann · 1998 · 6 claims · 4 setups
Three of 10 esophageal squamous cell carcinomas showed heterogeneous p53 mutational status, but only within the pre-invasive (carcinoma in situ) area.
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Alteration of the p53 tumor suppressor gene occurs independently of K-ras activation and more frequently in serous adenocarcinomas than in other common epithelial tumors of the human ovary.
PMID 7852189 · PMC5919385 · Japanese journal of cancer research : Gann · 1994 · 7 claims · 4 setups
p53 gene mutations occur more frequently in serous adenocarcinomas than in other common epithelial ovarian tumors combined
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Association between cyclo-oxygenase-2 overexpression and missense p53 mutations in gastric cancer.
PMID 11161397 · PMC2363738 · British journal of cancer · 2001 · 8 claims · 4 setups
p53 missense mutation is associated with COX-2 overexpression in gastric cancer
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High incidence of p53 gene mutation in human ovarian cancer and its association with nuclear accumulation of p53 protein and tumor DNA aneuploidy.
PMID 1429209 · PMC5918982 · Japanese journal of cancer research : Gann · 1992 · 7 claims · 4 setups
p53 gene mutations occur at high incidence in human ovarian carcinoma, especially common epithelial type
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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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An oncogenomics-based in vivo RNAi screen identifies tumor suppressors in liver cancer.
PMID 19012953 · PMC2990916 · Cell · 2008 · 7 claims · 8 setups
shRNA pools targeting genes recurrently deleted in human HCC accelerate hepatocarcinogenesis in vivo, whereas randomly selected shRNA pools do not.
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Detection of p53 gene mutations in aspiration biopsy specimens from suspected breast cancers by polymerase chain reaction-single strand conformation polymorphism analysis.
PMID 7730136 · PMC5920757 · Japanese journal of cancer research : Gann · 1995 · 4 claims · 4 setups
Detection of p53 gene mutation by PCR-SSCP in aspirated breast biopsy specimens is a helpful method for more accurate diagnosis of suspected breast cancer
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Large-scale mutagenesis in p19(ARF)- and p53-deficient mice identifies cancer genes and their collaborative networks.
PMID 18485879 · PMC2405818 · Cell · 2008 · 8 claims · 8 setups
A large-scale retroviral insertional mutagenesis screen identified 10,806 insertion sites implicating over 300 loci in tumorigenesis
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Correlation of mutation and immunohistochemistry of p53 in hepatocellular carcinomas in Korean people.
PMID 12483005 · PMC3054961 · Journal of Korean medical science · 2002 · 6 claims · 3 setups
5% immunoreactive tumor cells is a reliable IHC threshold to detect p53 mutations in HCC
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Genomic and mutational profiling to assess clonal relationships between multiple non-small cell lung cancers.
PMID 19671847 · PMC2892178 · Clinical cancer research : an official journal of the American Association for Cancer Research · 2009 · 8 claims · 5 setups
Genomic profiling by aCGH can distinguish clonal tumors from independent primaries with high confidence by identifying matching versus non-matching regions of allelic gain/loss.
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High-resolution aCGH and expression profiling identifies a novel genomic subtype of ER negative breast cancer.
PMID 17925008 · PMC2246289 · Genome biology · 2007 · 7 claims · 8 setups
A novel subtype of high-grade ER-negative breast cancer exists, characterized by a low genomic instability index (GII)
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Mutation of ERBB2 provides a novel alternative mechanism for the ubiquitous activation of RAS-MAPK in ovarian serous low malignant potential tumors.
PMID 19010816 · PMC6953412 · Molecular cancer research : MCR · 2008 · 8 claims · 8 setups
Activating RAS-MAPK pathway mutations are present in >70% of serous LMP tumors versus ~12.5% of serous ovarian carcinomas
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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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ATBF1 and NQO1 as candidate targets for allelic loss at chromosome arm 16q in breast cancer: absence of somatic ATBF1 mutations and no role for the C609T NQO1 polymorphism.
PMID 18416817 · PMC2377272 · BMC cancer · 2008 · 8 claims · 7 setups
Five genes (NQO1, ATBF1, DBNDD1, HSBP1, CGI-38) at 16q show significantly lower mRNA expression in breast tumors with LOH at 16q compared to tumors without LOH
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WAF1/CIP1 structural abnormalities do not contribute to cell cycle deregulation in ovarian cancer.
PMID 8645586 · PMC2074480 · British journal of cancer · 1996 · 7 claims · 5 setups
No WAF1/CIP1 coding mutations were found in any of 36 ovarian carcinomas sequenced, including tumors with LOH on 6p and those lacking p53 mutations
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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