Review



human chronic myelogenous leukemia cancer cell line k562  (ATCC)


Bioz Verified Symbol ATCC is a verified supplier
Bioz Manufacturer Symbol ATCC manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 99
      Buy from Supplier

    Structured Review

    ATCC human chronic myelogenous leukemia cancer cell line k562
    Tumor targeting of Allo HSC-iNKT cells through intrinsic NK function (A and B) FACS analyses of surface NK receptor expression and intracellular cytotoxic molecule production by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. (A) Representative FACS plots. (B) Quantification of (A) (n = 9). (C–E) In vitro direct killing of human tumor cells by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. Both fresh and frozen-thawed cells were studied. Five human tumor cell lines were studied: A375 (melanoma), <t>K562</t> <t>(myelogenous</t> leukemia), H292 (lung cancer), PC3 (prostate cancer), and MM.1S (multiple myeloma). All tumor cell lines were engineered to express firefly luciferase and green fluorescence protein (FG) dual reporters. (C) Experimental design. (D and E) Tumor killing data of A375-FG human melanoma cells (D) and K562-FG human myelogenous leukemia cells (E) at 24 h (n = 4). (F–H) Tumor killing mechanisms of Allo HSC-iNKT cells. NKG2D- and DNAM-1-mediated pathways were studied. (F) Experimental design. (G) Tumor killing data of A375-FG human melanoma cells at 24 h (tumor/iNKT ratio 1:2; n = 4). (H) Tumor killing data of K562-FG human myelogenous leukemia cells at 24 h (tumor/iNKT ratio 1:1; n = 4). (I–K) Studying the in vivo antitumor efficacy of Allo HSC-iNKT cells in an A375-FG human melanoma xenograft NSG mouse model. (I) Experimental design. BLI, live animal bioluminescence imaging. (J) BLI images showing tumor loads in experimental mice over time. (K) Tumor size measurements over time (n = 4–5). Representative of three experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001 by Student’s t test (B) or one-way ANOVA (D, E, G, H, and K). See also <xref ref-type=Figure S1 . " width="250" height="auto" />
    Human Chronic Myelogenous Leukemia Cancer Cell Line K562, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 11235 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human chronic myelogenous leukemia cancer cell line k562/product/ATCC
    Average 99 stars, based on 11235 article reviews
    human chronic myelogenous leukemia cancer cell line k562 - by Bioz Stars, 2026-02
    99/100 stars

    Images

    1) Product Images from "Development of allogeneic HSC-engineered iNKT cells for off-the-shelf cancer immunotherapy"

    Article Title: Development of allogeneic HSC-engineered iNKT cells for off-the-shelf cancer immunotherapy

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2021.100449

    Tumor targeting of Allo HSC-iNKT cells through intrinsic NK function (A and B) FACS analyses of surface NK receptor expression and intracellular cytotoxic molecule production by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. (A) Representative FACS plots. (B) Quantification of (A) (n = 9). (C–E) In vitro direct killing of human tumor cells by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. Both fresh and frozen-thawed cells were studied. Five human tumor cell lines were studied: A375 (melanoma), K562 (myelogenous leukemia), H292 (lung cancer), PC3 (prostate cancer), and MM.1S (multiple myeloma). All tumor cell lines were engineered to express firefly luciferase and green fluorescence protein (FG) dual reporters. (C) Experimental design. (D and E) Tumor killing data of A375-FG human melanoma cells (D) and K562-FG human myelogenous leukemia cells (E) at 24 h (n = 4). (F–H) Tumor killing mechanisms of Allo HSC-iNKT cells. NKG2D- and DNAM-1-mediated pathways were studied. (F) Experimental design. (G) Tumor killing data of A375-FG human melanoma cells at 24 h (tumor/iNKT ratio 1:2; n = 4). (H) Tumor killing data of K562-FG human myelogenous leukemia cells at 24 h (tumor/iNKT ratio 1:1; n = 4). (I–K) Studying the in vivo antitumor efficacy of Allo HSC-iNKT cells in an A375-FG human melanoma xenograft NSG mouse model. (I) Experimental design. BLI, live animal bioluminescence imaging. (J) BLI images showing tumor loads in experimental mice over time. (K) Tumor size measurements over time (n = 4–5). Representative of three experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001 by Student’s t test (B) or one-way ANOVA (D, E, G, H, and K). See also <xref ref-type=Figure S1 . " title="... tumor cell lines were studied: A375 (melanoma), K562 (myelogenous leukemia), H292 (lung cancer), PC3 (prostate cancer), and ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Tumor targeting of Allo HSC-iNKT cells through intrinsic NK function (A and B) FACS analyses of surface NK receptor expression and intracellular cytotoxic molecule production by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. (A) Representative FACS plots. (B) Quantification of (A) (n = 9). (C–E) In vitro direct killing of human tumor cells by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. Both fresh and frozen-thawed cells were studied. Five human tumor cell lines were studied: A375 (melanoma), K562 (myelogenous leukemia), H292 (lung cancer), PC3 (prostate cancer), and MM.1S (multiple myeloma). All tumor cell lines were engineered to express firefly luciferase and green fluorescence protein (FG) dual reporters. (C) Experimental design. (D and E) Tumor killing data of A375-FG human melanoma cells (D) and K562-FG human myelogenous leukemia cells (E) at 24 h (n = 4). (F–H) Tumor killing mechanisms of Allo HSC-iNKT cells. NKG2D- and DNAM-1-mediated pathways were studied. (F) Experimental design. (G) Tumor killing data of A375-FG human melanoma cells at 24 h (tumor/iNKT ratio 1:2; n = 4). (H) Tumor killing data of K562-FG human myelogenous leukemia cells at 24 h (tumor/iNKT ratio 1:1; n = 4). (I–K) Studying the in vivo antitumor efficacy of Allo HSC-iNKT cells in an A375-FG human melanoma xenograft NSG mouse model. (I) Experimental design. BLI, live animal bioluminescence imaging. (J) BLI images showing tumor loads in experimental mice over time. (K) Tumor size measurements over time (n = 4–5). Representative of three experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001 by Student’s t test (B) or one-way ANOVA (D, E, G, H, and K). See also Figure S1 .

    Techniques Used: Expressing, Control, In Vitro, Luciferase, Fluorescence, In Vivo, Imaging


    Figure Legend Snippet:

    Techniques Used: Enzyme-linked Immunosorbent Assay, Blocking Assay, Purification, Control, Virus, Recombinant, Cell Culture, Saline, Cell Isolation, RNA Sequencing, Gene Expression, Sequencing, Derivative Assay, Plasmid Preparation, Software, Imaging



    Similar Products

    human chronic myelogenous leukemia cancer cell line k562  (ATCC)
    99
    ATCC human chronic myelogenous leukemia cancer cell line k562
    Tumor targeting of Allo HSC-iNKT cells through intrinsic NK function (A and B) FACS analyses of surface NK receptor expression and intracellular cytotoxic molecule production by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. (A) Representative FACS plots. (B) Quantification of (A) (n = 9). (C–E) In vitro direct killing of human tumor cells by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. Both fresh and frozen-thawed cells were studied. Five human tumor cell lines were studied: A375 (melanoma), <t>K562</t> <t>(myelogenous</t> leukemia), H292 (lung cancer), PC3 (prostate cancer), and MM.1S (multiple myeloma). All tumor cell lines were engineered to express firefly luciferase and green fluorescence protein (FG) dual reporters. (C) Experimental design. (D and E) Tumor killing data of A375-FG human melanoma cells (D) and K562-FG human myelogenous leukemia cells (E) at 24 h (n = 4). (F–H) Tumor killing mechanisms of Allo HSC-iNKT cells. NKG2D- and DNAM-1-mediated pathways were studied. (F) Experimental design. (G) Tumor killing data of A375-FG human melanoma cells at 24 h (tumor/iNKT ratio 1:2; n = 4). (H) Tumor killing data of K562-FG human myelogenous leukemia cells at 24 h (tumor/iNKT ratio 1:1; n = 4). (I–K) Studying the in vivo antitumor efficacy of Allo HSC-iNKT cells in an A375-FG human melanoma xenograft NSG mouse model. (I) Experimental design. BLI, live animal bioluminescence imaging. (J) BLI images showing tumor loads in experimental mice over time. (K) Tumor size measurements over time (n = 4–5). Representative of three experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001 by Student’s t test (B) or one-way ANOVA (D, E, G, H, and K). See also <xref ref-type=Figure S1 . " width="250" height="auto" />
    Human Chronic Myelogenous Leukemia Cancer Cell Line K562, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human chronic myelogenous leukemia cancer cell line k562/product/ATCC
    Average 99 stars, based on 1 article reviews
    human chronic myelogenous leukemia cancer cell line k562 - by Bioz Stars, 2026-02
    99/100 stars
    		  Buy from Supplier

    Image Search Results


    Tumor targeting of Allo HSC-iNKT cells through intrinsic NK function (A and B) FACS analyses of surface NK receptor expression and intracellular cytotoxic molecule production by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. (A) Representative FACS plots. (B) Quantification of (A) (n = 9). (C–E) In vitro direct killing of human tumor cells by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. Both fresh and frozen-thawed cells were studied. Five human tumor cell lines were studied: A375 (melanoma), K562 (myelogenous leukemia), H292 (lung cancer), PC3 (prostate cancer), and MM.1S (multiple myeloma). All tumor cell lines were engineered to express firefly luciferase and green fluorescence protein (FG) dual reporters. (C) Experimental design. (D and E) Tumor killing data of A375-FG human melanoma cells (D) and K562-FG human myelogenous leukemia cells (E) at 24 h (n = 4). (F–H) Tumor killing mechanisms of Allo HSC-iNKT cells. NKG2D- and DNAM-1-mediated pathways were studied. (F) Experimental design. (G) Tumor killing data of A375-FG human melanoma cells at 24 h (tumor/iNKT ratio 1:2; n = 4). (H) Tumor killing data of K562-FG human myelogenous leukemia cells at 24 h (tumor/iNKT ratio 1:1; n = 4). (I–K) Studying the in vivo antitumor efficacy of Allo HSC-iNKT cells in an A375-FG human melanoma xenograft NSG mouse model. (I) Experimental design. BLI, live animal bioluminescence imaging. (J) BLI images showing tumor loads in experimental mice over time. (K) Tumor size measurements over time (n = 4–5). Representative of three experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001 by Student’s t test (B) or one-way ANOVA (D, E, G, H, and K). See also <xref ref-type=Figure S1 . " width="100%" height="100%">

    Journal: Cell Reports Medicine

    Article Title: Development of allogeneic HSC-engineered iNKT cells for off-the-shelf cancer immunotherapy

    doi: 10.1016/j.xcrm.2021.100449

    Figure Lengend Snippet: Tumor targeting of Allo HSC-iNKT cells through intrinsic NK function (A and B) FACS analyses of surface NK receptor expression and intracellular cytotoxic molecule production by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. (A) Representative FACS plots. (B) Quantification of (A) (n = 9). (C–E) In vitro direct killing of human tumor cells by Allo HSC-iNKT cells. PBMC-NK cells were included as a control. Both fresh and frozen-thawed cells were studied. Five human tumor cell lines were studied: A375 (melanoma), K562 (myelogenous leukemia), H292 (lung cancer), PC3 (prostate cancer), and MM.1S (multiple myeloma). All tumor cell lines were engineered to express firefly luciferase and green fluorescence protein (FG) dual reporters. (C) Experimental design. (D and E) Tumor killing data of A375-FG human melanoma cells (D) and K562-FG human myelogenous leukemia cells (E) at 24 h (n = 4). (F–H) Tumor killing mechanisms of Allo HSC-iNKT cells. NKG2D- and DNAM-1-mediated pathways were studied. (F) Experimental design. (G) Tumor killing data of A375-FG human melanoma cells at 24 h (tumor/iNKT ratio 1:2; n = 4). (H) Tumor killing data of K562-FG human myelogenous leukemia cells at 24 h (tumor/iNKT ratio 1:1; n = 4). (I–K) Studying the in vivo antitumor efficacy of Allo HSC-iNKT cells in an A375-FG human melanoma xenograft NSG mouse model. (I) Experimental design. BLI, live animal bioluminescence imaging. (J) BLI images showing tumor loads in experimental mice over time. (K) Tumor size measurements over time (n = 4–5). Representative of three experiments. Data are presented as the mean ± SEM. ns, not significant; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001 by Student’s t test (B) or one-way ANOVA (D, E, G, H, and K). See also Figure S1 .

    Article Snippet: Human chronic myelogenous leukemia cancer cell line K562 , ATCC , CCL-243.

    Techniques: Expressing, Control, In Vitro, Luciferase, Fluorescence, In Vivo, Imaging

    Journal: Cell Reports Medicine

    Article Title: Development of allogeneic HSC-engineered iNKT cells for off-the-shelf cancer immunotherapy

    doi: 10.1016/j.xcrm.2021.100449

    Figure Lengend Snippet:

    Article Snippet: Human chronic myelogenous leukemia cancer cell line K562 , ATCC , CCL-243.

    Techniques: Enzyme-linked Immunosorbent Assay, Blocking Assay, Purification, Control, Virus, Recombinant, Cell Culture, Saline, Cell Isolation, RNA Sequencing, Gene Expression, Sequencing, Derivative Assay, Plasmid Preparation, Software, Imaging