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polymerase chain reaction/sequence-specific oligonucleotide probes  (LabCorp)

 
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    LabCorp polymerase chain reaction/sequence-specific oligonucleotide probes
    Polymerase Chain Reaction/Sequence Specific Oligonucleotide Probes, supplied by LabCorp, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sequencing+methods/sequence+specific+oligonucleotide+probe+method/pmc09652741-157-13-17
    Average 90 stars, based on 1 article reviews
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    other:

    Article Title: Association of genetic variations in HLA-B region with hypersensitivity to abacavir in some, but not all, populations.
    Article Snippet: Arlene R Hughes†1, Michael Mosteller1, Aruna T Bansal2, Kirstie Davies2, Stephen A Haneline1, Eric H Lai1, Keith Nangle1, Trevor Scott1, William R Spreen1, Liling L Warren1 & Allen D Roses1, on behalf of the CNA30027 and CNA30032 study teams †Author for correspondence 1GlaxoSmithKline, 5 Moore Drive, RTP, NC 27709, USA E-mail: arh48207@gsk.com 2GlaxoSmithKline, New Frontiers Science Park (North), Third Avenue, Harlow, Essex, CM19 5AW, UK

    Article Title: An epidemiologic study to determine the prevalence of the HLA-B*5701 allele among HIV-positive patients in Europe
    Article Snippet: Results A total of 9720 patients from 272 centres were included in the analysis.. The overall estimate of HLA-B*5701 prevalence in Europe was 4.98%, with country-specific estimates ranging from 1.53 to 7.75%.. HLA-B*5701 prevalence was highest in the self-reported white population (6.49%) and lowest in the black population (0.39%).

    Article Title: Novel sensitive, specific and rapid pharmacogenomic test for the prediction of abacavir hypersensitivity reaction: HLA-B*57:01 detection by real-time PCR.
    Article Snippet: This method was validated during the EPI109367 clinical trial, comparing results from 776 blood samples analyzed with this method with results obtained by LabCorp (NC, USA) on buccal swabs collected from the same subjects by sequence-specific oligonucleotide probe PCR [15].

    Article Title: Prevalence of HLA-B*5701 in HIV-Infected Patients in Spain (Results of the EPI Study)
    Article Snippet: 1Infectious Diseases Unit, H. Donostia, San Sebastian, Spain; 2Medical Department, GlaxoSmithKline, Tres Cantos, Madrid, Spain; 3Immunology Unit, H. Ramón y Cajal, Madrid, Spain; 4Internal Medicine-HIV Unit, H. Xeral de Vigo, Spain; 5Infectious Diseases Unit, H. Bellvitge, Barcelona, Spain; 6HIV Unit, H. Doce de Octubre, Madrid, Spain; 7Infectious Diseases Unit, H. Son Dureta, P. Mallorca, Spain; 8Infectious Diseases Unit, H. La Princesa, Madrid, Spain

    Article Title: HLA-B*5701 Screening for Hypersensitivity to Abacavir
    Article Snippet: HLA-B*5701 screening was performed with the use of DNA-sequence–based typing (at the Centre for Clinical Immunology and Biomedical Statistics, Royal Perth Hospital, Perth, Western Australia) and a sequence-specific oligonucleotide probe method (Laboratory Corporation of America), with additional DNA sequencing for patients for whom the probe results were positive.

    Virus:

    Article Title: Changes in B-lymphocyte stimulator protein levels during treatment with albinterferon alfa-2b in patients with chronic hepatitis C who have failed previous interferon therapy
    Article Snippet: Aim: The pharmacodynamics of albinterferon alfa-2b (albIFN), a novel recombinant protein consisting of interferona-2b genetically fused to human albumin, was evaluated in patients with chronic hepatitis C with a previous nonresponse to interferon-a-based therapy.. B-lymphocyte stimulator (BLyS) is an essential in vivo regulator of B-lymphocyte homeostasis.. This analysis examined the relationship between serum BLyS level and virologic response across a range of alb-IFN doses.

    Hybridization:

    Article Title: Changes in B-lymphocyte stimulator protein levels during treatment with albinterferon alfa-2b in patients with chronic hepatitis C who have failed previous interferon therapy
    Article Snippet: Aim: The pharmacodynamics of albinterferon alfa-2b (albIFN), a novel recombinant protein consisting of interferona-2b genetically fused to human albumin, was evaluated in patients with chronic hepatitis C with a previous nonresponse to interferon-a-based therapy.. B-lymphocyte stimulator (BLyS) is an essential in vivo regulator of B-lymphocyte homeostasis.. This analysis examined the relationship between serum BLyS level and virologic response across a range of alb-IFN doses.

    Amplification:

    Article Title: Changes in B-lymphocyte stimulator protein levels during treatment with albinterferon alfa-2b in patients with chronic hepatitis C who have failed previous interferon therapy
    Article Snippet: Aim: The pharmacodynamics of albinterferon alfa-2b (albIFN), a novel recombinant protein consisting of interferona-2b genetically fused to human albumin, was evaluated in patients with chronic hepatitis C with a previous nonresponse to interferon-a-based therapy.. B-lymphocyte stimulator (BLyS) is an essential in vivo regulator of B-lymphocyte homeostasis.. This analysis examined the relationship between serum BLyS level and virologic response across a range of alb-IFN doses.

    Sequencing:

    Article Title: High-resolution HLA genotyping and severe cutaneous adverse reactions in lamotrigine-treated patients
    Article Snippet: Methods High-resolution HLA genotyping was performed for 65 patients of European ancestry treated with lamotrigine (22 cases with lamotrigine-induced SCARs and 43 controls on lamotrigine without SCAR-related symptoms).. Association of HLA genetic variants with SCARs in these patients were evaluated by contrasting allele frequencies between the cases and the controls for each of 112 HLA four-digit alleles.

    Polymerase Chain Reaction:

    Article Title: High-resolution HLA genotyping and severe cutaneous adverse reactions in lamotrigine-treated patients
    Article Snippet: Methods High-resolution HLA genotyping was performed for 65 patients of European ancestry treated with lamotrigine (22 cases with lamotrigine-induced SCARs and 43 controls on lamotrigine without SCAR-related symptoms).. Association of HLA genetic variants with SCARs in these patients were evaluated by contrasting allele frequencies between the cases and the controls for each of 112 HLA four-digit alleles.



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    USP18 Acts as a Key ROS-Responsive Mediator Driving Cisplatin Resistance in Ovarian Cancer. a Mechanisms and incidence of platinum resistance in ovarian cancer (Icons created with BioRender.com ). b Representative images of ROS detection using DCFH-DA probe in cisplatin-resistant and parental SKOV3 cells. Scale bar: 50 μm; GSEA analysis of ROS response genes based on transcriptome sequencing data in cisplatin-resistant and parental SKOV3 cells. c Representative images of ROS detection using DCFH-DA probe in SKOV3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin plus NAC (10 μM) + mito-TEMPO (10 μM). Scale bar: 50 μm; Cell proliferation curves by Real-time cell analysis (RTCA) system (bottom left); LDH release assay in SKOV3 cells treated with cisplatin (20 μM) or cisplatin plus NAC (10 μM) + mito-TEMPO (10 μM) (bottom right). d Representative Immunohistochemistry (IHC) images showing pyroptosis (Cleaved-Caspase-1), apoptosis (Cleaved-Caspase-3), ferroptosis (GPX4), necroptosis (p-MLKL), and autophagy (p62) markers in cisplatin-resistant ovarian cancer PDX model (OV9419) tissues. Scale bar: 100 μm. e Protein expression levels of various cell death markers in OVCAR-3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin plus NAC (10 μM) + mito-TEMPO (10 μM): pyroptosis (Cleaved-Caspase-1), apoptosis (Cleaved-Caspase-3), ferroptosis (GPX4), necroptosis (p-MLKL), and autophagy (LC3 II/LC3 I). f Schematic of DUB screening for cisplatin resistance: DUB plasmid library transfected into A2780 cells, treated with cisplatin (10 μM) after 24h, and cell viability measured by CCK8 after another 48h. Scatter plot shows relative cell viability compared to control. g Protein expression levels of USP18, USP37, and USP39 in parental and cisplatin-resistant SKOV3 cells. h Protein expression levels of USP18, USP37, and USP39 in OVCAR-3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin (20 μM) plus NAC (10 μM) + mito-TEMPO (10 μM). i Protein expression levels of USP18, USP37, and USP39 in tissues from cisplatin-sensitive (n = 4) and -resistant (n = 4) ovarian cancer patients. j Analysis of USP18 expression in ovarian cancer versus normal ovarian tissues using data from The Cancer Genome Atlas (TCGA) ( www.aclbi.com ) k Survival analysis of patients with differential USP18 using data from TCGA. Analysis was performed via the KM-plotter platform ( https://kmplot.com/ ). l Representative IHC staining of USP18 shows its expression patterns in ovarian cancer tissues compared with paired adjacent tissues, and in therapy-sensitive versus resistant cases. Scale bar: 100 μm. Patients were stratified into high and low USP18 expression groups based on the median IHC score, and the distribution was compared using the Chi-squared test. m Analysis of USP18 expression in ovarian cancer patients stratified by response to platinum-based therapy using the ROC plot online platform ( https://rocplot.com/ ). n Protein expression levels of USP18 in ovarian cancer cell lines. o Cisplatin IC 50 values in ovarian cancer cell lines. p Pearson correlation analysis between USP18 protein levels (n) and cisplatin IC 50 (o). Data presented as mean ± SD. Significance calculated by unpaired two-tailed t -test (c). ∗∗P < 0.01; ∗∗∗∗P < 0.0001.

    Journal: Redox Biology

    Article Title: Redox-triggered USP18 confers cisplatin resistance in ovarian cancer by selectively activating a non-canonical FSP1-dependent ferroptosis escape pathway

    doi: 10.1016/j.redox.2026.104179

    Figure Lengend Snippet: USP18 Acts as a Key ROS-Responsive Mediator Driving Cisplatin Resistance in Ovarian Cancer. a Mechanisms and incidence of platinum resistance in ovarian cancer (Icons created with BioRender.com ). b Representative images of ROS detection using DCFH-DA probe in cisplatin-resistant and parental SKOV3 cells. Scale bar: 50 μm; GSEA analysis of ROS response genes based on transcriptome sequencing data in cisplatin-resistant and parental SKOV3 cells. c Representative images of ROS detection using DCFH-DA probe in SKOV3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin plus NAC (10 μM) + mito-TEMPO (10 μM). Scale bar: 50 μm; Cell proliferation curves by Real-time cell analysis (RTCA) system (bottom left); LDH release assay in SKOV3 cells treated with cisplatin (20 μM) or cisplatin plus NAC (10 μM) + mito-TEMPO (10 μM) (bottom right). d Representative Immunohistochemistry (IHC) images showing pyroptosis (Cleaved-Caspase-1), apoptosis (Cleaved-Caspase-3), ferroptosis (GPX4), necroptosis (p-MLKL), and autophagy (p62) markers in cisplatin-resistant ovarian cancer PDX model (OV9419) tissues. Scale bar: 100 μm. e Protein expression levels of various cell death markers in OVCAR-3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin plus NAC (10 μM) + mito-TEMPO (10 μM): pyroptosis (Cleaved-Caspase-1), apoptosis (Cleaved-Caspase-3), ferroptosis (GPX4), necroptosis (p-MLKL), and autophagy (LC3 II/LC3 I). f Schematic of DUB screening for cisplatin resistance: DUB plasmid library transfected into A2780 cells, treated with cisplatin (10 μM) after 24h, and cell viability measured by CCK8 after another 48h. Scatter plot shows relative cell viability compared to control. g Protein expression levels of USP18, USP37, and USP39 in parental and cisplatin-resistant SKOV3 cells. h Protein expression levels of USP18, USP37, and USP39 in OVCAR-3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin (20 μM) plus NAC (10 μM) + mito-TEMPO (10 μM). i Protein expression levels of USP18, USP37, and USP39 in tissues from cisplatin-sensitive (n = 4) and -resistant (n = 4) ovarian cancer patients. j Analysis of USP18 expression in ovarian cancer versus normal ovarian tissues using data from The Cancer Genome Atlas (TCGA) ( www.aclbi.com ) k Survival analysis of patients with differential USP18 using data from TCGA. Analysis was performed via the KM-plotter platform ( https://kmplot.com/ ). l Representative IHC staining of USP18 shows its expression patterns in ovarian cancer tissues compared with paired adjacent tissues, and in therapy-sensitive versus resistant cases. Scale bar: 100 μm. Patients were stratified into high and low USP18 expression groups based on the median IHC score, and the distribution was compared using the Chi-squared test. m Analysis of USP18 expression in ovarian cancer patients stratified by response to platinum-based therapy using the ROC plot online platform ( https://rocplot.com/ ). n Protein expression levels of USP18 in ovarian cancer cell lines. o Cisplatin IC 50 values in ovarian cancer cell lines. p Pearson correlation analysis between USP18 protein levels (n) and cisplatin IC 50 (o). Data presented as mean ± SD. Significance calculated by unpaired two-tailed t -test (c). ∗∗P < 0.01; ∗∗∗∗P < 0.0001.

    Article Snippet: All sequencing procedures were performed by Annoroad Gene Tech. (Beijing) Co., Ltd.

    Techniques: Sequencing, Control, Cell Analysis, Lactate Dehydrogenase Assay, Immunohistochemistry, Expressing, Plasmid Preparation, Transfection, Two Tailed Test

    Elevated ROS levels upregulate c-JUN expression, which transcriptionally activates downstream USP18 in cisplatin-resistant ovarian cancer cells. a GSEA analysis of hallmark ROS pathway genes from transcriptome sequencing in OVCAR-3 cells overexpressing USP18 plasmid and vector. b Heatmap of transcriptome sequencing expression values for ROS pathway-related genes in A2780 cells overexpressing USP18 plasmid and vector. c Differentially expressed genes in OVCAR-3 cells treated with sodium arsenite (NaAsO2, 0.5 mM) versus vehicle control. d Differentially expressed genes in SKOV3 cells treated with cisplatin (20 μM) vs vehicle control. e Venn diagram of ROS pathway-related upregulated transcription factors identified from transcriptome sequencing data in c and d. f Analysis of JUN expression in ovarian cancer patients stratified by response to platinum-based therapy using the ROC plot online platform. g Survival analysis of patients with differential JUN expression using data from TCGA. Analysis was performed via the KM-plotter platform. h Protein expression levels of c-JUN and USP18 in OVCAR-3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin (20 μM) plus NAC (10 μM) + mito-TEMPO (10 μM). i Protein expression levels of c-JUN and USP18 in OVCAR-3 cells treated with vehicle control, NaAsO2 (0.5 mM), or NaAsO2(0.5 mM) plus NAC (10 μM) + mito-TEMPO (10 μM). j Cell viability measured by CCK8 assay in OVCAR-3 and A2780 cells overexpressing USP18 and treated with cisplatin (10 μM) plus NAC (10 μM) + mito-TEMPO (10 μM) k RT-qPCR analysis of USP18 mRNA expression levels in OVCAR-3 cells treated with vehicle control, cisplatin (10 μM), or cisplatin combined with c-JUN knockdown. l Schematic of predicted c-JUN binding sites in the USP18 promoter region ( https://jaspar.elixir.no/ ). m ChIP assay in CAOV3 cells validating c-JUN binding to USP18. n-p Dual-luciferase reporter assay confirming c-JUN binding and transcriptional regulation of USP18. n Schematic diagram of the dual-luciferase reporter assay. o Overexpression of c-JUN activates the USP18 promoter. OVCAR-3/CAOV3 cells were co-transfected with the USP18 promoter reporter construct and a c-JUN expression plasmid (or empty vector control). p OVCAR-3 cells transfected with the USP18 promoter reporter were treated with vehicle control, cisplatin (10 μM), or cisplatin (10 μM) combined with c-JUN knockdown (sic-JUN). Data presented as mean ± SD. Significance calculated by unpaired two-tailed t -test (j, k, m, o, p). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001.

    Journal: Redox Biology

    Article Title: Redox-triggered USP18 confers cisplatin resistance in ovarian cancer by selectively activating a non-canonical FSP1-dependent ferroptosis escape pathway

    doi: 10.1016/j.redox.2026.104179

    Figure Lengend Snippet: Elevated ROS levels upregulate c-JUN expression, which transcriptionally activates downstream USP18 in cisplatin-resistant ovarian cancer cells. a GSEA analysis of hallmark ROS pathway genes from transcriptome sequencing in OVCAR-3 cells overexpressing USP18 plasmid and vector. b Heatmap of transcriptome sequencing expression values for ROS pathway-related genes in A2780 cells overexpressing USP18 plasmid and vector. c Differentially expressed genes in OVCAR-3 cells treated with sodium arsenite (NaAsO2, 0.5 mM) versus vehicle control. d Differentially expressed genes in SKOV3 cells treated with cisplatin (20 μM) vs vehicle control. e Venn diagram of ROS pathway-related upregulated transcription factors identified from transcriptome sequencing data in c and d. f Analysis of JUN expression in ovarian cancer patients stratified by response to platinum-based therapy using the ROC plot online platform. g Survival analysis of patients with differential JUN expression using data from TCGA. Analysis was performed via the KM-plotter platform. h Protein expression levels of c-JUN and USP18 in OVCAR-3 cells treated with vehicle control, cisplatin (20 μM), or cisplatin (20 μM) plus NAC (10 μM) + mito-TEMPO (10 μM). i Protein expression levels of c-JUN and USP18 in OVCAR-3 cells treated with vehicle control, NaAsO2 (0.5 mM), or NaAsO2(0.5 mM) plus NAC (10 μM) + mito-TEMPO (10 μM). j Cell viability measured by CCK8 assay in OVCAR-3 and A2780 cells overexpressing USP18 and treated with cisplatin (10 μM) plus NAC (10 μM) + mito-TEMPO (10 μM) k RT-qPCR analysis of USP18 mRNA expression levels in OVCAR-3 cells treated with vehicle control, cisplatin (10 μM), or cisplatin combined with c-JUN knockdown. l Schematic of predicted c-JUN binding sites in the USP18 promoter region ( https://jaspar.elixir.no/ ). m ChIP assay in CAOV3 cells validating c-JUN binding to USP18. n-p Dual-luciferase reporter assay confirming c-JUN binding and transcriptional regulation of USP18. n Schematic diagram of the dual-luciferase reporter assay. o Overexpression of c-JUN activates the USP18 promoter. OVCAR-3/CAOV3 cells were co-transfected with the USP18 promoter reporter construct and a c-JUN expression plasmid (or empty vector control). p OVCAR-3 cells transfected with the USP18 promoter reporter were treated with vehicle control, cisplatin (10 μM), or cisplatin (10 μM) combined with c-JUN knockdown (sic-JUN). Data presented as mean ± SD. Significance calculated by unpaired two-tailed t -test (j, k, m, o, p). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001.

    Article Snippet: All sequencing procedures were performed by Annoroad Gene Tech. (Beijing) Co., Ltd.

    Techniques: Expressing, Sequencing, Plasmid Preparation, Control, CCK-8 Assay, Quantitative RT-PCR, Knockdown, Binding Assay, Luciferase, Reporter Assay, Over Expression, Transfection, Construct, Two Tailed Test

    CD32b distinguishes transcriptionally and functionally distinct GM-DC subsets derived from MDPs and GMPs. (A) Principal component analysis (PCA) of bulk RNA-seq data from GM-DCs sorted on day 7 and day 21. DCs were generated from cultures of whole bone marrow (BM), sorted MDPs, or sorted GMPs with GM-CSF. (B) Heatmap showing the expression of genes upregulated and downregulated in MDP GM-DCs at day 7, identified through Venn diagram analysis and mapped onto BM GM-DCs at both time points. (C) Volcano plot of differentially expressed genes (DEGs) between MDP GM-DCs (day 7) and GMP GM-DCs (day 21). The thresholds for significance (dotted lines) are set at a log 2 (fold change) ≥ 3 or raw p -value ≤ 10 -16 . (D) Flow cytometric validation of selected surface marker candidates identified in the volcano plot (C) . Normalized Mean fluorescence intensity (MFI) of four representative markers is shown for each DC subset. Normalized MFI was calculated by subtracting the isotype control mean fluorescence from the sample mean fluorescence, and then dividing the result by the isotype control mean. Representative histograms are shown below the bar graphs, with the isotype control overlaid in gray. Data are representative of two independent experiments.

    Journal: Frontiers in Immunology

    Article Title: CD32b defines distinct dendritic cell lineages generated from the culture of bone marrow with GM-CSF

    doi: 10.3389/fimmu.2026.1703978

    Figure Lengend Snippet: CD32b distinguishes transcriptionally and functionally distinct GM-DC subsets derived from MDPs and GMPs. (A) Principal component analysis (PCA) of bulk RNA-seq data from GM-DCs sorted on day 7 and day 21. DCs were generated from cultures of whole bone marrow (BM), sorted MDPs, or sorted GMPs with GM-CSF. (B) Heatmap showing the expression of genes upregulated and downregulated in MDP GM-DCs at day 7, identified through Venn diagram analysis and mapped onto BM GM-DCs at both time points. (C) Volcano plot of differentially expressed genes (DEGs) between MDP GM-DCs (day 7) and GMP GM-DCs (day 21). The thresholds for significance (dotted lines) are set at a log 2 (fold change) ≥ 3 or raw p -value ≤ 10 -16 . (D) Flow cytometric validation of selected surface marker candidates identified in the volcano plot (C) . Normalized Mean fluorescence intensity (MFI) of four representative markers is shown for each DC subset. Normalized MFI was calculated by subtracting the isotype control mean fluorescence from the sample mean fluorescence, and then dividing the result by the isotype control mean. Representative histograms are shown below the bar graphs, with the isotype control overlaid in gray. Data are representative of two independent experiments.

    Article Snippet: RNA sequencing (RNA-seq) procedure and analysis were performed by Macrogen (Seoul, Korea).

    Techniques: Derivative Assay, RNA Sequencing, Generated, Expressing, Biomarker Discovery, Marker, Fluorescence, Control