Gareth Jenkins
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View article: Tungsten carbide–cobalt can function as a particle positive control for genotoxicity <i>in vitro</i> in specific cell lines
Tungsten carbide–cobalt can function as a particle positive control for genotoxicity <i>in vitro</i> in specific cell lines Open
Nanoparticle genotoxicity can be induced through several mechanisms, but there are currently no nanoparticle positive controls available for the evaluation of in vitro genotoxicity. Tungsten carbide–cobalt (WC/Co) has been proposed as one …
View article: Harnessing the power of an advanced <i>in vitro</i> 3D liver model and error-corrected duplex sequencing for the detection of mutational signatures
Harnessing the power of an advanced <i>in vitro</i> 3D liver model and error-corrected duplex sequencing for the detection of mutational signatures Open
Genotoxicity testing plays a crucial role in evaluating the hazards posed by various chemicals. Traditional methods, such as the Ames test, mammalian cell mutation assays and the transgenic rodent assay have certain limitations, including …
View article: Microenvironment and Biomarkers in Esophageal Cancers: An Approach for Early Detection and Identification
Microenvironment and Biomarkers in Esophageal Cancers: An Approach for Early Detection and Identification Open
Background Esophageal cancer is a prevalent and highly lethal malignancy worldwide, comprising two main subtypes: esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC). While both subtypes are frequently encountered…
View article: Supplementary Table S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
A VCF file containing putatively pathogenic variants found in 1142 intestinal cancer associated genes in 21 of the duodenal adenomas studied here (see supplementary table 1 for sample details). Full genomic datasets for these samples are a…
View article: Supplementary Table S4 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S4 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
A VCF file containing putatively pathogenic variants found in 1142 intestinal cancer associated genes in 27 of the duodenal adenomas studied here (see supplementary table 1 for sample details). Full genomic datasets for these samples are a…
View article: Supplementary Figure S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Gene Ontology of DEGs between duodenal adenomas with and without PIGA somatic mutation. Enriched terms are plotted for Biological process(BP), A. Cellular Component (CC), B. and Molecular Function(MF), C. Terms are coloured by Log2-Padj va…
View article: Supplementary Table S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Summary statistics for all FAP and MAP patient-derived intestinal samples analysed in this study. Data sets are from two centres, Cardiff University (CU) and MD Anderson Cancer Center (MDACC). Statistically significant P-values < 0.05 are …
View article: Supplementary Figure S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Whole transcriptome sequencing quality control and read distribution for data sets from Cardiff and MD Anderson. A. Sequencing quality assessment, batch aggregates are shown. B. Read distribution across the genome per batch demonstrating t…
View article: Supplementary Figure S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
The gating tree was set as follows, shown for an organoid line without a PIGA somatic variant. A: FSC/SSC to isolate cells (represents the distribution of cells in the light scatter based on size and intracellular composition, respectively…
View article: Figure 3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Figure 3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Volcano plot of DEGs of FAP and MAP patients with and without PIGA mutation. Genes have been filtered to remove those with a mean expression ≤10 read counts. Red dots indicate DEGs with Padj ≤ 0.01 at ≥±1.5 LFC. Purple do…
View article: Figure 2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Figure 2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Flow cytometry analysis of FLAER positive cells in 11 FAP duodenal organoids with and without somatic PIGA variants. Fluorescence from FLAER is detected using the FITC-A channel (emission:475–650 nm). A, Abundance of FLAER po…
View article: Data from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Data from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
The pathogenesis of duodenal tumors in the inherited tumor syndromes familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP) is poorly understood. This study aimed to identify genes that are significantly mutated in these…
View article: Figure 3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Figure 3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Volcano plot of DEGs of FAP and MAP patients with and without PIGA mutation. Genes have been filtered to remove those with a mean expression ≤10 read counts. Red dots indicate DEGs with Padj ≤ 0.01 at ≥±1.5 LFC. Purple do…
View article: Figure 2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Figure 2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Flow cytometry analysis of FLAER positive cells in 11 FAP duodenal organoids with and without somatic PIGA variants. Fluorescence from FLAER is detected using the FITC-A channel (emission:475–650 nm). A, Abundance of FLAER po…
View article: Supplementary Figure S4 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S4 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
RNASeq WTS pipeline validation by quantitative RT-PCR (qRT-PCR) and IHC A. Comparison of normalised RNA-Seq read counts (orange) to relative qRT-PCR expression levels (purple) for four top DEGs. Δ CT values are shown, with low values indic…
View article: Supplementary Table S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Germline and somatic mutations in FAP patient derived duodenal organoids
View article: Supplementary Figure S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Gene Ontology of DEGs between duodenal adenomas with and without PIGA somatic mutation. Enriched terms are plotted for Biological process(BP), A. Cellular Component (CC), B. and Molecular Function(MF), C. Terms are coloured by Log2-Padj va…
View article: Supplementary Figure S4 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S4 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
RNASeq WTS pipeline validation by quantitative RT-PCR (qRT-PCR) and IHC A. Comparison of normalised RNA-Seq read counts (orange) to relative qRT-PCR expression levels (purple) for four top DEGs. Δ CT values are shown, with low values indic…
View article: Supplementary Figure S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Whole transcriptome sequencing quality control and read distribution for data sets from Cardiff and MD Anderson. A. Sequencing quality assessment, batch aggregates are shown. B. Read distribution across the genome per batch demonstrating t…
View article: Supplementary Table S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Summary statistics for all FAP and MAP patient-derived intestinal samples analysed in this study. Data sets are from two centres, Cardiff University (CU) and MD Anderson Cancer Center (MDACC). Statistically significant P-values < 0.05 are …
View article: Supplementary Table S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Overview of all intestinal samples used in this study. *Sequenced previously (Thomas et al, 2017) and reanalysed here. Somatic mutations in APC, KRAS and PIGA as identified by WES and WTS analysis of CU and MDACC duodenal adenomas. Samples…
View article: Figure 1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Figure 1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
A,PIGA mutations identified in 19 duodenal adenomas and two duodenal adenoma patient-derived organoid lines. Relative location in comparison with known protein domains is shown. B, The VAF of four types of somatic muta…
View article: Supplementary Table S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S5 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
A VCF file containing putatively pathogenic variants found in 1142 intestinal cancer associated genes in 21 of the duodenal adenomas studied here (see supplementary table 1 for sample details). Full genomic datasets for these samples are a…
View article: Supplementary Figure S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S3 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
The gating tree was set as follows, shown for an organoid line without a PIGA somatic variant. A: FSC/SSC to isolate cells (represents the distribution of cells in the light scatter based on size and intracellular composition, respectively…
View article: Figure 1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Figure 1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
A,PIGA mutations identified in 19 duodenal adenomas and two duodenal adenoma patient-derived organoid lines. Relative location in comparison with known protein domains is shown. B, The VAF of four types of somatic muta…
View article: Supplementary Table S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Germline and somatic mutations in FAP patient derived duodenal organoids
View article: Supplementary Table S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Table S1 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Overview of all intestinal samples used in this study. *Sequenced previously (Thomas et al, 2017) and reanalysed here. Somatic mutations in APC, KRAS and PIGA as identified by WES and WTS analysis of CU and MDACC duodenal adenomas. Samples…
View article: Supplementary Figure S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Somatic mutation rates in FAP and MAP-associated duodenal adenomas. A. Total, non-silent and silent mutation rate for all FAP and MAP adenomas. For FAP-associated duodenal adenomas, the average total mutation rate was 3.3 mutations per Mb …
View article: Data from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Data from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
The pathogenesis of duodenal tumors in the inherited tumor syndromes familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP) is poorly understood. This study aimed to identify genes that are significantly mutated in these…
View article: Supplementary Figure S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis
Supplementary Figure S2 from PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis Open
Somatic mutation rates in FAP and MAP-associated duodenal adenomas. A. Total, non-silent and silent mutation rate for all FAP and MAP adenomas. For FAP-associated duodenal adenomas, the average total mutation rate was 3.3 mutations per Mb …