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human cd45 hcd45 staining  (Miltenyi Biotec)


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    Structured Review

    Miltenyi Biotec human cd45 hcd45 staining
    (A) NSG mice were engrafted with malignant primary cells derived from the bone marrow of 10 T-ALL patients for tumor expansion. Upon disease establishment, mice were sacrificed, and leukemic cells were harvested from the spleen. To mimic biological replicates, six mice were injected per patient. The percentage of human <t>CD45+</t> cells <t>(hCD45%)</t> was measured by flow cytometry, with only samples exceeding 85% used for downstream analysis. Global hPTM profiling and DNA methylation sequencing were performed for all 10 PDX models. In parallel, PDX cells were treated ex vivo with a panel of eight epidrugs to assess drug sensitivity. Spearman correlation analysis was then conducted to explore the relationship between hPTM levels and drug response. Figure created with Biorender.com . (B) Clustered and annotated heatmap displaying the normalized and summarized single hPTM levels across the 10 PDX models. (C) Volcano plot illustrating the differential analysis of hPTMs between CIMPlow and CIMPhigh PDX models.
    Human Cd45 Hcd45 Staining, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 97/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human cd45 hcd45 staining/product/Miltenyi Biotec
    Average 97 stars, based on 2 article reviews
    human cd45 hcd45 staining - by Bioz Stars, 2026-03
    97/100 stars

    Images

    1) Product Images from "Profiling histone post-translational modifications to identify signatures of epigenetic drug response in T-cell acute lymphoblastic leukemia"

    Article Title: Profiling histone post-translational modifications to identify signatures of epigenetic drug response in T-cell acute lymphoblastic leukemia

    Journal: bioRxiv

    doi: 10.1101/2025.09.01.673463

    (A) NSG mice were engrafted with malignant primary cells derived from the bone marrow of 10 T-ALL patients for tumor expansion. Upon disease establishment, mice were sacrificed, and leukemic cells were harvested from the spleen. To mimic biological replicates, six mice were injected per patient. The percentage of human CD45+ cells (hCD45%) was measured by flow cytometry, with only samples exceeding 85% used for downstream analysis. Global hPTM profiling and DNA methylation sequencing were performed for all 10 PDX models. In parallel, PDX cells were treated ex vivo with a panel of eight epidrugs to assess drug sensitivity. Spearman correlation analysis was then conducted to explore the relationship between hPTM levels and drug response. Figure created with Biorender.com . (B) Clustered and annotated heatmap displaying the normalized and summarized single hPTM levels across the 10 PDX models. (C) Volcano plot illustrating the differential analysis of hPTMs between CIMPlow and CIMPhigh PDX models.
    Figure Legend Snippet: (A) NSG mice were engrafted with malignant primary cells derived from the bone marrow of 10 T-ALL patients for tumor expansion. Upon disease establishment, mice were sacrificed, and leukemic cells were harvested from the spleen. To mimic biological replicates, six mice were injected per patient. The percentage of human CD45+ cells (hCD45%) was measured by flow cytometry, with only samples exceeding 85% used for downstream analysis. Global hPTM profiling and DNA methylation sequencing were performed for all 10 PDX models. In parallel, PDX cells were treated ex vivo with a panel of eight epidrugs to assess drug sensitivity. Spearman correlation analysis was then conducted to explore the relationship between hPTM levels and drug response. Figure created with Biorender.com . (B) Clustered and annotated heatmap displaying the normalized and summarized single hPTM levels across the 10 PDX models. (C) Volcano plot illustrating the differential analysis of hPTMs between CIMPlow and CIMPhigh PDX models.

    Techniques Used: Derivative Assay, Injection, Flow Cytometry, DNA Methylation Assay, Sequencing, Ex Vivo



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    (A) NSG mice were engrafted with malignant primary cells derived from the bone marrow of 10 T-ALL patients for tumor expansion. Upon disease establishment, mice were sacrificed, and leukemic cells were harvested from the spleen. To mimic biological replicates, six mice were injected per patient. The percentage of human <t>CD45+</t> cells <t>(hCD45%)</t> was measured by flow cytometry, with only samples exceeding 85% used for downstream analysis. Global hPTM profiling and DNA methylation sequencing were performed for all 10 PDX models. In parallel, PDX cells were treated ex vivo with a panel of eight epidrugs to assess drug sensitivity. Spearman correlation analysis was then conducted to explore the relationship between hPTM levels and drug response. Figure created with Biorender.com . (B) Clustered and annotated heatmap displaying the normalized and summarized single hPTM levels across the 10 PDX models. (C) Volcano plot illustrating the differential analysis of hPTMs between CIMPlow and CIMPhigh PDX models.
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    (A) NSG mice were engrafted with malignant primary cells derived from the bone marrow of 10 T-ALL patients for tumor expansion. Upon disease establishment, mice were sacrificed, and leukemic cells were harvested from the spleen. To mimic biological replicates, six mice were injected per patient. The percentage of human <t>CD45+</t> cells <t>(hCD45%)</t> was measured by flow cytometry, with only samples exceeding 85% used for downstream analysis. Global hPTM profiling and DNA methylation sequencing were performed for all 10 PDX models. In parallel, PDX cells were treated ex vivo with a panel of eight epidrugs to assess drug sensitivity. Spearman correlation analysis was then conducted to explore the relationship between hPTM levels and drug response. Figure created with Biorender.com . (B) Clustered and annotated heatmap displaying the normalized and summarized single hPTM levels across the 10 PDX models. (C) Volcano plot illustrating the differential analysis of hPTMs between CIMPlow and CIMPhigh PDX models.
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    Miltenyi Biotec human cd45 hcd45 staining staining cd45 fitc antibody
    T-LBL PDX models are sensitive towards in vivo treatment with decitabine. ( A ) T-LBL develops in lymphatic tissues such as the lymph nodes. In T-LBL cells, the DNA methylation pattern is hypermethylated compared to healthy cells. Upon replication, decitabine (DAC) can incorporate into the DNA and irreversibly bind to DNA methyl transferases (DNMTs), thereby countering hypermethylation and restoring transcription. Figure created with BioRender.com . ( B ) NSG mice injected with malignant pleural effusions from patients with T-LBL were treated with vehicle (PBS with 1% DMSO, blue) or decitabine (DAC 0.5 mg/kg body weight, orange). Once engraftment was successful (1% <t>hCD45</t> + cells in the peripheral blood), mice were treated for one or two cycles for five consecutive treatment days followed by two days off. Mice were followed for survival analysis and leukemia burden in the blood. Figure created with BioRender.com . ( C ) Kaplan–Meier analysis of lymphoma-free survival after decitabine treatment (start of treatment is marked with a syringe) is shown (log-rank Mantel-Cox test; p -values: 0.1234 (ns), 0.0332 (*), 0.0021 (**), 0.0002 (***)) for the five T-LBL PDX models analyzed. One treatment cycle (dotted lines) and two treatment cycles (full lines) are compared. ( D ) The treatment effect of 1 cycle of decitabine on hCD45 + cells in the peripheral blood is shown by normalizing tumor growth (average #hCD45 + cells on day 5/average #hCD45 + cells on day 1) in decitabine treated mice to tumor growth in vehicle treated mice.
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    T-LBL PDX models are sensitive towards in vivo treatment with decitabine. ( A ) T-LBL develops in lymphatic tissues such as the lymph nodes. In T-LBL cells, the DNA methylation pattern is hypermethylated compared to healthy cells. Upon replication, decitabine (DAC) can incorporate into the DNA and irreversibly bind to DNA methyl transferases (DNMTs), thereby countering hypermethylation and restoring transcription. Figure created with BioRender.com . ( B ) NSG mice injected with malignant pleural effusions from patients with T-LBL were treated with vehicle (PBS with 1% DMSO, blue) or decitabine (DAC 0.5 mg/kg body weight, orange). Once engraftment was successful (1% <t>hCD45</t> + cells in the peripheral blood), mice were treated for one or two cycles for five consecutive treatment days followed by two days off. Mice were followed for survival analysis and leukemia burden in the blood. Figure created with BioRender.com . ( C ) Kaplan–Meier analysis of lymphoma-free survival after decitabine treatment (start of treatment is marked with a syringe) is shown (log-rank Mantel-Cox test; p -values: 0.1234 (ns), 0.0332 (*), 0.0021 (**), 0.0002 (***)) for the five T-LBL PDX models analyzed. One treatment cycle (dotted lines) and two treatment cycles (full lines) are compared. ( D ) The treatment effect of 1 cycle of decitabine on hCD45 + cells in the peripheral blood is shown by normalizing tumor growth (average #hCD45 + cells on day 5/average #hCD45 + cells on day 1) in decitabine treated mice to tumor growth in vehicle treated mice.
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    Image Search Results


    (A) NSG mice were engrafted with malignant primary cells derived from the bone marrow of 10 T-ALL patients for tumor expansion. Upon disease establishment, mice were sacrificed, and leukemic cells were harvested from the spleen. To mimic biological replicates, six mice were injected per patient. The percentage of human CD45+ cells (hCD45%) was measured by flow cytometry, with only samples exceeding 85% used for downstream analysis. Global hPTM profiling and DNA methylation sequencing were performed for all 10 PDX models. In parallel, PDX cells were treated ex vivo with a panel of eight epidrugs to assess drug sensitivity. Spearman correlation analysis was then conducted to explore the relationship between hPTM levels and drug response. Figure created with Biorender.com . (B) Clustered and annotated heatmap displaying the normalized and summarized single hPTM levels across the 10 PDX models. (C) Volcano plot illustrating the differential analysis of hPTMs between CIMPlow and CIMPhigh PDX models.

    Journal: bioRxiv

    Article Title: Profiling histone post-translational modifications to identify signatures of epigenetic drug response in T-cell acute lymphoblastic leukemia

    doi: 10.1101/2025.09.01.673463

    Figure Lengend Snippet: (A) NSG mice were engrafted with malignant primary cells derived from the bone marrow of 10 T-ALL patients for tumor expansion. Upon disease establishment, mice were sacrificed, and leukemic cells were harvested from the spleen. To mimic biological replicates, six mice were injected per patient. The percentage of human CD45+ cells (hCD45%) was measured by flow cytometry, with only samples exceeding 85% used for downstream analysis. Global hPTM profiling and DNA methylation sequencing were performed for all 10 PDX models. In parallel, PDX cells were treated ex vivo with a panel of eight epidrugs to assess drug sensitivity. Spearman correlation analysis was then conducted to explore the relationship between hPTM levels and drug response. Figure created with Biorender.com . (B) Clustered and annotated heatmap displaying the normalized and summarized single hPTM levels across the 10 PDX models. (C) Volcano plot illustrating the differential analysis of hPTMs between CIMPlow and CIMPhigh PDX models.

    Article Snippet: Lymphoblast engraftment and leukemic burden was monitored by flow cytometric analysis on peripheral blood, using human CD45+ (hCD45) staining (CD45-FITC antibody; Miltenyi Biotec, Bergish Gladbag, Germany).

    Techniques: Derivative Assay, Injection, Flow Cytometry, DNA Methylation Assay, Sequencing, Ex Vivo

    T-LBL PDX models are sensitive towards in vivo treatment with decitabine. ( A ) T-LBL develops in lymphatic tissues such as the lymph nodes. In T-LBL cells, the DNA methylation pattern is hypermethylated compared to healthy cells. Upon replication, decitabine (DAC) can incorporate into the DNA and irreversibly bind to DNA methyl transferases (DNMTs), thereby countering hypermethylation and restoring transcription. Figure created with BioRender.com . ( B ) NSG mice injected with malignant pleural effusions from patients with T-LBL were treated with vehicle (PBS with 1% DMSO, blue) or decitabine (DAC 0.5 mg/kg body weight, orange). Once engraftment was successful (1% hCD45 + cells in the peripheral blood), mice were treated for one or two cycles for five consecutive treatment days followed by two days off. Mice were followed for survival analysis and leukemia burden in the blood. Figure created with BioRender.com . ( C ) Kaplan–Meier analysis of lymphoma-free survival after decitabine treatment (start of treatment is marked with a syringe) is shown (log-rank Mantel-Cox test; p -values: 0.1234 (ns), 0.0332 (*), 0.0021 (**), 0.0002 (***)) for the five T-LBL PDX models analyzed. One treatment cycle (dotted lines) and two treatment cycles (full lines) are compared. ( D ) The treatment effect of 1 cycle of decitabine on hCD45 + cells in the peripheral blood is shown by normalizing tumor growth (average #hCD45 + cells on day 5/average #hCD45 + cells on day 1) in decitabine treated mice to tumor growth in vehicle treated mice.

    Journal: Cancers

    Article Title: Pre-Clinical Evaluation of the Hypomethylating Agent Decitabine for the Treatment of T-Cell Lymphoblastic Lymphoma

    doi: 10.3390/cancers15030647

    Figure Lengend Snippet: T-LBL PDX models are sensitive towards in vivo treatment with decitabine. ( A ) T-LBL develops in lymphatic tissues such as the lymph nodes. In T-LBL cells, the DNA methylation pattern is hypermethylated compared to healthy cells. Upon replication, decitabine (DAC) can incorporate into the DNA and irreversibly bind to DNA methyl transferases (DNMTs), thereby countering hypermethylation and restoring transcription. Figure created with BioRender.com . ( B ) NSG mice injected with malignant pleural effusions from patients with T-LBL were treated with vehicle (PBS with 1% DMSO, blue) or decitabine (DAC 0.5 mg/kg body weight, orange). Once engraftment was successful (1% hCD45 + cells in the peripheral blood), mice were treated for one or two cycles for five consecutive treatment days followed by two days off. Mice were followed for survival analysis and leukemia burden in the blood. Figure created with BioRender.com . ( C ) Kaplan–Meier analysis of lymphoma-free survival after decitabine treatment (start of treatment is marked with a syringe) is shown (log-rank Mantel-Cox test; p -values: 0.1234 (ns), 0.0332 (*), 0.0021 (**), 0.0002 (***)) for the five T-LBL PDX models analyzed. One treatment cycle (dotted lines) and two treatment cycles (full lines) are compared. ( D ) The treatment effect of 1 cycle of decitabine on hCD45 + cells in the peripheral blood is shown by normalizing tumor growth (average #hCD45 + cells on day 5/average #hCD45 + cells on day 1) in decitabine treated mice to tumor growth in vehicle treated mice.

    Article Snippet: Lymphoma engraftment was regularly monitored by flow cytometry, using human CD45 + (hCD45) staining (CD45-FITC antibody (Miltenyi Biotec, Bergish Gladbag, Germany)).

    Techniques: In Vivo, DNA Methylation Assay, Injection