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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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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Characterisation of p53 status at the gene, chromosomal and protein levels in oesophageal adenocarcinoma.
PMID 14583777 · PMC2394414 · British journal of cancer · 2003 · 8 claims · 4 setups
p53 gene mutations are infrequent in oesophageal adenocarcinoma (9.6%)
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p53 mutations in urinary bladder cancer.
PMID 11384101 · PMC2363660 · British journal of cancer · 2001 · 6 claims · 5 setups
p53 mutations are strongly associated with high-grade/high-stage bladder tumors and are nearly absent in lowly malignant tumors (Ta, G1-G2a)
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A role for the p53 pathway in the pathology of meningiomas with NF2 loss.
PMID 18974932 · PMC2692701 · Journal of neuro-oncology · 2009 · 7 claims · 4 setups
The Pro72 allele of p53 codon 72 was not selected for in the meningioma cohort, and its distribution did not differ from control populations, indicating no role in meningioma initiation.
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p53 mutations in cervical carcinogenesis--low frequency and lack of correlation with human papillomavirus status.
PMID 8142262 · PMC1968818 · British journal of cancer · 1994 · 7 claims · 6 setups
Somatic mutation in the p53 gene hotspot regions occurs infrequently in cervical carcinomas
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Mutational analysis of the p53 and K-ras genes and allelotype study of the Rb-1 gene for investigating the pathogenesis of combined hapatocellular-cholangiocellular carcinomas.
PMID 8957064 · PMC5921002 · Japanese journal of cancer research : Gann · 1996 · 6 claims · 4 setups
Both components of combined hepatocellular-cholangiocellular carcinoma share the same genetic and phenotypic character and may arise from the same origin in some cases
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Mutation of the p53 gene precedes aneuploid clonal divergence in colorectal carcinoma.
PMID 7841032 · PMC2033599 · British journal of cancer · 1995 · 7 claims · 5 setups
p53 mutation occurs as a single clonal event that precedes and may facilitate aneuploid clonal divergence in colorectal carcinoma
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p53 mutation is a poor prognostic indicator for survival in patients with hepatocellular carcinoma undergoing surgical tumour ablation.
PMID 9514057 · PMC2149958 · British journal of cancer · 1998 · 8 claims · 6 setups
p53 mutations were found in 8 of 12 HCCs with cirrhosis due to viral hepatitis and in both patients with sarcomatoid change
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Abnormalities of the p53 MDM2 and DCC genes in human leiomyosarcomas.
PMID 8198970 · PMC1969417 · British journal of cancer · 1994 · 6 claims · 8 setups
A significant minority of leiomyosarcomas harbor p53 gene point mutations or deletions
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cDNA sequencing improves the detection of P53 missense mutations in colorectal cancer.
PMID 19671129 · PMC2731783 · BMC cancer · 2009 · 8 claims · 6 setups
cDNA sequencing detects P53 missense mutations in colorectal cancer more frequently and reliably than DNA sequencing
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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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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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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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Multiple polymorphisms, but no mutations, in the WAF1/CIP1 gene in human brain tumours.
PMID 7577473 · PMC2033923 · British journal of cancer · 1995 · 8 claims · 5 setups
No somatic mutations of WAF1/CIP1 were found in 158 primary human brain tumours
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Has reproduction · 57
Apoptotic brown adipocytes enhance energy expenditure via extracellular inosine.
PMID 35790189 · PMC9452294 · Nature · 2022 · 8 claims · 8 setups
Apoptotic brown adipocytes release a specific secretome enriched in purine metabolites (including inosine, AMP, hypoxanthine, ATP)
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Advanced colorectal polyps with the molecular and morphological features of serrated polyps and adenomas: concept of a 'fusion' pathway to colorectal cancer.
PMID 16879389 · PMC1619718 · Histopathology · 2006 · 8 claims · 5 setups
KRAS mutation occurs more frequently than BRAF mutation in conventional adenomas, especially those with villous architecture
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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.