The molecular mechanism that is suggested to explain the etiology of AA exposure-associated cancers relies on the metabolic activation of AAs to reactive metabolites which target DNA and produce adducts (Kim and Guengerich 2005; Neumann 2010; Turesky and Le Marchand 2011).
Sample text:```Unlabeled DNA substrates containing consensus 12-RSS, 23-RSS, Hox11 or non-specific DNA sequences (DAR81/82) were prepared from oligonucleotides described previously [11,24].```
Sample intent: background
Sample text:```In line with our results, several previous studies demonstrated the anti-proliferative effect of PPARs agonists in several cell types [11-15].```
Sample intent: result



Sample text:```Therefore, one manifestation of the BRCA1–TONSL genetic interaction may well operate at sites of UV-induced damage, where both proteins are normally engaged in complex DNA damage responses (Duro et al. 2010; O’Connell et al. 2010; O’Donnell et al. 2010; Piwko et al. 2010; Pathania et al. 2011).```
Sample intent: method



Sample text:```Quantitative geneticists have documented numerous cases of such interactions (Stuber et al. 1992; Ragot et al. 1995; Cockerham and Zeng 1996; Melchinger et al. 1998).```
Sample intent: method



Sample text:```Intriguingly, using MPRs-deficient MEF cells, mouse and human CLN5 have been shown to reach lysosomes in an MPRindependent manner [12].```
Sample intent: background



Sample text:```In addition, consistent with the result of our preclinical study, recent clinical study showed that alectinib was also highly active against ALK-positive NSCLC patients after treatment with crizotinib [21].```
Sample intent: result
Sample text:```Quantitative geneticists have documented numerous cases of such interactions (Stuber et al. 1992; Ragot et al. 1995; Cockerham and Zeng 1996; Melchinger et al. 1998).```
Sample intent: method



Sample text:```In line with our results, several previous studies demonstrated the anti-proliferative effect of PPARs agonists in several cell types [11-15].```
Sample intent: result



Sample text:```Classification of Genetic Variants All genetic variants in our cohort and those reported in the manuscripts uncovered by the literature search were reassessed and classified according to the current guidelines of the American College of Medical Genetics.13 For this evaluation, we used MAF data derived from the Exome Aggregation Consortium and the Exome Variant Server.```
Sample intent: background



Sample text:```In our previous study, we found that RAG-mediated nicking and cleavage of oligonucleotide substrates containing cRSSs identified from lymphoid malignancies were either unchanged or slightly reduced in the presence of HMGB1 for most cRSSs tested (including LMO2, TAL1, Hox11, SIL, SCL), except Ttg-1 [24].```
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Sample text:```The vast majority of mutations in FUS/TLS-related familial ALS cases were identified in C-terminal NLS, which result in the retention and the inclusion of FUS/TLS in the cytoplasm [2,3,5,8,14], and FUS/TLS as well as TDP-43 is recruited to SGs under stress conditions such as arsenite, heat shock and hypoxia [28,29,30].```
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Sample text:```Therefore, one manifestation of the BRCA1–TONSL genetic interaction may well operate at sites of UV-induced damage, where both proteins are normally engaged in complex DNA damage responses (Duro et al. 2010; O’Connell et al. 2010; O’Donnell et al. 2010; Piwko et al. 2010; Pathania et al. 2011).```
Sample intent: method



Sample text:```Previous studies revealed that acylcarnitines were elevated early after APAP treatment and that their elevation was indicative of mitochondrial damage and dysfunction.(15,19) In the present study these observations were confirmed, as palmitoylcarnitine was elevated by toxic doses of APAP and maintained at normal levels (compared with untreated controls) by Wy-14,643 pretreatment.```
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Sample text:```due to mitochondrial dysfunction caused by age-related mitochondrial DNA mutations, deletions 151 (10, 21) and damage (25, 59).```
Sample intent: method



Sample text:```This study supports the theory of a tumor origin from multipotential progenitor cells.(14) Reports of the Ki67 labeling index have demonstrated great variety.```
Sample intent: result



Sample text:```Our genealogy, based on many alleles but only the first exon of bindin, is not entirely consistent with that of McCartney and Lessios (2004), based on fewer alleles but incorporating the entire molecule.```
Sample intent: result