PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26065288-3 2015 A-T transversion of the p53 gene is now considered to be a mutational "signature" of aristolochic acid, which is a cause of endemic nephropathy. aristolochic acid I 85-102 tumor protein p53 Homo sapiens 24-27 28477877-0 2017 TP53 mutations in p53-negative dysplastic urothelial cells from Belgian AAN patients: New evidence for aristolochic acid-induced molecular pathogenesis and carcinogenesis. aristolochic acid I 103-120 tumor protein p53 Homo sapiens 0-4 28477877-0 2017 TP53 mutations in p53-negative dysplastic urothelial cells from Belgian AAN patients: New evidence for aristolochic acid-induced molecular pathogenesis and carcinogenesis. aristolochic acid I 103-120 tumor protein p53 Homo sapiens 18-21 26851235-2 2016 Although gene association network analysis demonstrated gene expression profile changes in the liver of human TP53 knock-in mice after acute AAI exposure, to date, whether AAI causes hepatic tumorigenesis is still not confirmed. aristolochic acid I 141-144 tumor protein p53 Homo sapiens 110-114 25184754-1 2014 In the Balkan and Taiwan, the relationship between exposure to aristolochic acid and risk of urothelial neoplasms was inferred from the A>T genetic hallmark in TP53 gene from malignant cells. aristolochic acid I 63-80 tumor protein p53 Homo sapiens 163-167 25184754-2 2014 This study aimed to characterize the TP53 mutational spectrum in urothelial cancers consecutive to Aristolochic Acid Nephropathy in Belgium. aristolochic acid I 99-116 tumor protein p53 Homo sapiens 37-41 23422071-0 2013 Analysis of TP53 mutation spectra reveals the fingerprint of the potent environmental carcinogen, aristolochic acid. aristolochic acid I 98-115 tumor protein p53 Homo sapiens 12-16 23422071-2 2013 Here we review the pieces of evidence that support the role of aristolochic acid (AA) in inducing a mutational fingerprint in the tumor suppressor gene TP53 in urothelial carcinomas of the upper urinary tract (UUT). aristolochic acid I 63-80 tumor protein p53 Homo sapiens 152-156 23434523-7 2013 DNA damage induced by AAI led to an arrest of cells in the S-phase which was associated with the increased expression of p53 and p21 proteins. aristolochic acid I 22-25 tumor protein p53 Homo sapiens 121-124 23445829-0 2013 Variation in presentation and presence of DNA adducts and p53 mutations in patients with endemic nephropathy--an environmental form of the aristolochic acid nephropathy. aristolochic acid I 139-156 tumor protein p53 Homo sapiens 58-61 19428366-0 2009 p53 mutations as fingerprints for aristolochic acid: an environmental carcinogen in endemic (Balkan) nephropathy. aristolochic acid I 34-51 tumor protein p53 Homo sapiens 0-3 22071594-3 2012 Following metabolic activation, aristolochic acid reacts with genomic DNA to form aristolactam-DNA adducts that generate a unique TP53 mutational spectrum in the urothelium. aristolochic acid I 32-49 tumor protein p53 Homo sapiens 130-134 20232387-3 2011 We examined gene expression changes in Hupki (human TP53 knock-in) mice after treatment with aristolochic acid I (AAI) by gavage (5 mg/kg body weight). aristolochic acid I 93-112 tumor protein p53 Homo sapiens 52-56 21413016-0 2011 TP53 Mutational signature for aristolochic acid: an environmental carcinogen. aristolochic acid I 30-47 tumor protein p53 Homo sapiens 0-4 21413016-1 2011 This study was designed to establish the TP53 mutational spectrum of aristolochic acid (AA), examined in the context of endemic (Balkan) nephropathy, an environmental disease associated with transitional cell (urothelial) carcinomas of the upper urinary tract (UUC). aristolochic acid I 69-86 tumor protein p53 Homo sapiens 41-45 16835015-0 2006 Further studies with a cell immortalization assay to investigate the mutation signature of aristolochic acid in human p53 sequences. aristolochic acid I 91-108 tumor protein p53 Homo sapiens 118-121 19030178-0 2009 TP53 mutation signature supports involvement of aristolochic acid in the aetiology of endemic nephropathy-associated tumours. aristolochic acid I 48-65 tumor protein p53 Homo sapiens 0-4 19030178-3 2009 Using a novel mutation assay in which we can induce and select mutations in human TP53 sequences in vitro by exposure of cultured cells to a mutagen, we found that A to T mutations were elicited by aristolochic acid at sites in TP53 rarely mutated in human cancers in general, but which were observed in the BEN patients. aristolochic acid I 198-215 tumor protein p53 Homo sapiens 82-86 19030178-3 2009 Using a novel mutation assay in which we can induce and select mutations in human TP53 sequences in vitro by exposure of cultured cells to a mutagen, we found that A to T mutations were elicited by aristolochic acid at sites in TP53 rarely mutated in human cancers in general, but which were observed in the BEN patients. aristolochic acid I 198-215 tumor protein p53 Homo sapiens 228-232 18639569-0 2008 Gene expression profiles modulated by the human carcinogen aristolochic acid I in human cancer cells and their dependence on TP53. aristolochic acid I 59-78 tumor protein p53 Homo sapiens 125-129 18639569-3 2008 We compared transcriptional and translational responses of two isogenic HCT116 cell lines, one expressing TP53 (p53-WT) and the other with this gene knocked out (p53-null), to treatment with aristolochic acid I (AAI) (50-100 microM) for 6-48 h. Modulation of 118 genes was observed in p53-WT cells and 123 genes in p53-null cells. aristolochic acid I 191-208 tumor protein p53 Homo sapiens 162-165 18639569-3 2008 We compared transcriptional and translational responses of two isogenic HCT116 cell lines, one expressing TP53 (p53-WT) and the other with this gene knocked out (p53-null), to treatment with aristolochic acid I (AAI) (50-100 microM) for 6-48 h. Modulation of 118 genes was observed in p53-WT cells and 123 genes in p53-null cells. aristolochic acid I 191-208 tumor protein p53 Homo sapiens 162-165 18639569-3 2008 We compared transcriptional and translational responses of two isogenic HCT116 cell lines, one expressing TP53 (p53-WT) and the other with this gene knocked out (p53-null), to treatment with aristolochic acid I (AAI) (50-100 microM) for 6-48 h. Modulation of 118 genes was observed in p53-WT cells and 123 genes in p53-null cells. aristolochic acid I 191-208 tumor protein p53 Homo sapiens 162-165 17942951-6 2007 A "signature" p53 mutation in the upper urothelial cancer associated with this disease provides evidence of long-term exposure to aristolochic acid. aristolochic acid I 130-147 tumor protein p53 Homo sapiens 14-17 16835015-3 2006 Here we examine p53 mutations induced by aristolochic acid I (AAI)), the carcinogen probably responsible for Chinese herbal nephropathy. aristolochic acid I 41-60 tumor protein p53 Homo sapiens 16-19 16835015-6 2006 One of the mutations was identical in position (codon 139) and base change (A to T on the non-transcribed strand) to the single p53 mutation that has thus far been characterized in a urothelial tumor of a nephropathy patient with documented AAI exposure. aristolochic acid I 241-244 tumor protein p53 Homo sapiens 128-131 15042566-0 2004 DNA adducts and p53 mutations in a patient with aristolochic acid-associated nephropathy. aristolochic acid I 48-65 tumor protein p53 Homo sapiens 16-19 11159751-0 2001 Sequence-specific detection of aristolochic acid-DNA adducts in the human p53 gene by terminal transferase-dependent PCR. aristolochic acid I 31-48 tumor protein p53 Homo sapiens 74-77