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kcl22 cell lines  (ATCC)


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    ATCC kcl22 cell lines
    A Expression of isolated γδT cells was determined by CFSE-labeling. CFSE-labeled γδT cells were co-cultured with BCR-AB L-knockdown <t>KCL22</t> cells (black bar) or untreated KCL22 cells (open bar). Simvastatin-pretreated, zoledronate-pretreated, or BCR-AB L siRNA-pretreated KCL22 cells were used as the targets for γδT cells at a ratio of 1:1. Zoledronate (Zometa, 5 μM) but not simvastatin (100 nM) rendered KCL22 cell proliferation. B Expression of TNF-α, IFN-γ, and perforin release of isolated γδT cells from six healthy donors was determined by ELISA after co-culture with BCR-ABL siRNA-, TKI-, simvastatin-treated, or untreated K562 cells for 24 h. Treatment with IPP (0.5 μM) was used as a control to activate γδT cells. The ex-vivo killing assays were performed using isolated ( C ) γδT cells and ( D ) naïve γδT cells isolated from healthy donors. The targets could be untreated KU812 cells, or KU812 pretreated with BCR-ABL -specific siRNA or zoledronate. The incubation time for target-γδT cells and for target-naïve subset was 4 h and 24 h, respectively. One-way ANOVA was used for comparison between multiple groups, and paired t test was used to compare selected groups. Statistical significances between these groups are marked with asterisk. Data were presented as mean values ± SD. Data comparison was performed by the paired t test. Statistical significance was defined by * p < 0.05, ** p < 0.01, and *** p < 0.001.
    Kcl22 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 221 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/kcl22+cell+lines/pmc08595379-81-3-9?v=ATCC
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    Images

    1) Product Images from "Activated naïve γδ T cells accelerate deep molecular response to BCR-ABL inhibitors in patients with chronic myeloid leukemia"

    Article Title: Activated naïve γδ T cells accelerate deep molecular response to BCR-ABL inhibitors in patients with chronic myeloid leukemia

    Journal: Blood Cancer Journal

    doi: 10.1038/s41408-021-00572-7

    A Expression of isolated γδT cells was determined by CFSE-labeling. CFSE-labeled γδT cells were co-cultured with BCR-AB L-knockdown KCL22 cells (black bar) or untreated KCL22 cells (open bar). Simvastatin-pretreated, zoledronate-pretreated, or BCR-AB L siRNA-pretreated KCL22 cells were used as the targets for γδT cells at a ratio of 1:1. Zoledronate (Zometa, 5 μM) but not simvastatin (100 nM) rendered KCL22 cell proliferation. B Expression of TNF-α, IFN-γ, and perforin release of isolated γδT cells from six healthy donors was determined by ELISA after co-culture with BCR-ABL siRNA-, TKI-, simvastatin-treated, or untreated K562 cells for 24 h. Treatment with IPP (0.5 μM) was used as a control to activate γδT cells. The ex-vivo killing assays were performed using isolated ( C ) γδT cells and ( D ) naïve γδT cells isolated from healthy donors. The targets could be untreated KU812 cells, or KU812 pretreated with BCR-ABL -specific siRNA or zoledronate. The incubation time for target-γδT cells and for target-naïve subset was 4 h and 24 h, respectively. One-way ANOVA was used for comparison between multiple groups, and paired t test was used to compare selected groups. Statistical significances between these groups are marked with asterisk. Data were presented as mean values ± SD. Data comparison was performed by the paired t test. Statistical significance was defined by * p < 0.05, ** p < 0.01, and *** p < 0.001.
    Figure Legend Snippet: A Expression of isolated γδT cells was determined by CFSE-labeling. CFSE-labeled γδT cells were co-cultured with BCR-AB L-knockdown KCL22 cells (black bar) or untreated KCL22 cells (open bar). Simvastatin-pretreated, zoledronate-pretreated, or BCR-AB L siRNA-pretreated KCL22 cells were used as the targets for γδT cells at a ratio of 1:1. Zoledronate (Zometa, 5 μM) but not simvastatin (100 nM) rendered KCL22 cell proliferation. B Expression of TNF-α, IFN-γ, and perforin release of isolated γδT cells from six healthy donors was determined by ELISA after co-culture with BCR-ABL siRNA-, TKI-, simvastatin-treated, or untreated K562 cells for 24 h. Treatment with IPP (0.5 μM) was used as a control to activate γδT cells. The ex-vivo killing assays were performed using isolated ( C ) γδT cells and ( D ) naïve γδT cells isolated from healthy donors. The targets could be untreated KU812 cells, or KU812 pretreated with BCR-ABL -specific siRNA or zoledronate. The incubation time for target-γδT cells and for target-naïve subset was 4 h and 24 h, respectively. One-way ANOVA was used for comparison between multiple groups, and paired t test was used to compare selected groups. Statistical significances between these groups are marked with asterisk. Data were presented as mean values ± SD. Data comparison was performed by the paired t test. Statistical significance was defined by * p < 0.05, ** p < 0.01, and *** p < 0.001.

    Techniques Used: Expressing, Isolation, Labeling, Cell Culture, Knockdown, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Control, Ex Vivo, Incubation, Comparison



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    ATCC kcl22 cell lines
    A Expression of isolated γδT cells was determined by CFSE-labeling. CFSE-labeled γδT cells were co-cultured with BCR-AB L-knockdown <t>KCL22</t> cells (black bar) or untreated KCL22 cells (open bar). Simvastatin-pretreated, zoledronate-pretreated, or BCR-AB L siRNA-pretreated KCL22 cells were used as the targets for γδT cells at a ratio of 1:1. Zoledronate (Zometa, 5 μM) but not simvastatin (100 nM) rendered KCL22 cell proliferation. B Expression of TNF-α, IFN-γ, and perforin release of isolated γδT cells from six healthy donors was determined by ELISA after co-culture with BCR-ABL siRNA-, TKI-, simvastatin-treated, or untreated K562 cells for 24 h. Treatment with IPP (0.5 μM) was used as a control to activate γδT cells. The ex-vivo killing assays were performed using isolated ( C ) γδT cells and ( D ) naïve γδT cells isolated from healthy donors. The targets could be untreated KU812 cells, or KU812 pretreated with BCR-ABL -specific siRNA or zoledronate. The incubation time for target-γδT cells and for target-naïve subset was 4 h and 24 h, respectively. One-way ANOVA was used for comparison between multiple groups, and paired t test was used to compare selected groups. Statistical significances between these groups are marked with asterisk. Data were presented as mean values ± SD. Data comparison was performed by the paired t test. Statistical significance was defined by * p < 0.05, ** p < 0.01, and *** p < 0.001.
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    A Expression of isolated γδT cells was determined by CFSE-labeling. CFSE-labeled γδT cells were co-cultured with BCR-AB L-knockdown <t>KCL22</t> cells (black bar) or untreated KCL22 cells (open bar). Simvastatin-pretreated, zoledronate-pretreated, or BCR-AB L siRNA-pretreated KCL22 cells were used as the targets for γδT cells at a ratio of 1:1. Zoledronate (Zometa, 5 μM) but not simvastatin (100 nM) rendered KCL22 cell proliferation. B Expression of TNF-α, IFN-γ, and perforin release of isolated γδT cells from six healthy donors was determined by ELISA after co-culture with BCR-ABL siRNA-, TKI-, simvastatin-treated, or untreated K562 cells for 24 h. Treatment with IPP (0.5 μM) was used as a control to activate γδT cells. The ex-vivo killing assays were performed using isolated ( C ) γδT cells and ( D ) naïve γδT cells isolated from healthy donors. The targets could be untreated KU812 cells, or KU812 pretreated with BCR-ABL -specific siRNA or zoledronate. The incubation time for target-γδT cells and for target-naïve subset was 4 h and 24 h, respectively. One-way ANOVA was used for comparison between multiple groups, and paired t test was used to compare selected groups. Statistical significances between these groups are marked with asterisk. Data were presented as mean values ± SD. Data comparison was performed by the paired t test. Statistical significance was defined by * p < 0.05, ** p < 0.01, and *** p < 0.001.
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    Image Search Results


    A Expression of isolated γδT cells was determined by CFSE-labeling. CFSE-labeled γδT cells were co-cultured with BCR-AB L-knockdown KCL22 cells (black bar) or untreated KCL22 cells (open bar). Simvastatin-pretreated, zoledronate-pretreated, or BCR-AB L siRNA-pretreated KCL22 cells were used as the targets for γδT cells at a ratio of 1:1. Zoledronate (Zometa, 5 μM) but not simvastatin (100 nM) rendered KCL22 cell proliferation. B Expression of TNF-α, IFN-γ, and perforin release of isolated γδT cells from six healthy donors was determined by ELISA after co-culture with BCR-ABL siRNA-, TKI-, simvastatin-treated, or untreated K562 cells for 24 h. Treatment with IPP (0.5 μM) was used as a control to activate γδT cells. The ex-vivo killing assays were performed using isolated ( C ) γδT cells and ( D ) naïve γδT cells isolated from healthy donors. The targets could be untreated KU812 cells, or KU812 pretreated with BCR-ABL -specific siRNA or zoledronate. The incubation time for target-γδT cells and for target-naïve subset was 4 h and 24 h, respectively. One-way ANOVA was used for comparison between multiple groups, and paired t test was used to compare selected groups. Statistical significances between these groups are marked with asterisk. Data were presented as mean values ± SD. Data comparison was performed by the paired t test. Statistical significance was defined by * p < 0.05, ** p < 0.01, and *** p < 0.001.

    Journal: Blood Cancer Journal

    Article Title: Activated naïve γδ T cells accelerate deep molecular response to BCR-ABL inhibitors in patients with chronic myeloid leukemia

    doi: 10.1038/s41408-021-00572-7

    Figure Lengend Snippet: A Expression of isolated γδT cells was determined by CFSE-labeling. CFSE-labeled γδT cells were co-cultured with BCR-AB L-knockdown KCL22 cells (black bar) or untreated KCL22 cells (open bar). Simvastatin-pretreated, zoledronate-pretreated, or BCR-AB L siRNA-pretreated KCL22 cells were used as the targets for γδT cells at a ratio of 1:1. Zoledronate (Zometa, 5 μM) but not simvastatin (100 nM) rendered KCL22 cell proliferation. B Expression of TNF-α, IFN-γ, and perforin release of isolated γδT cells from six healthy donors was determined by ELISA after co-culture with BCR-ABL siRNA-, TKI-, simvastatin-treated, or untreated K562 cells for 24 h. Treatment with IPP (0.5 μM) was used as a control to activate γδT cells. The ex-vivo killing assays were performed using isolated ( C ) γδT cells and ( D ) naïve γδT cells isolated from healthy donors. The targets could be untreated KU812 cells, or KU812 pretreated with BCR-ABL -specific siRNA or zoledronate. The incubation time for target-γδT cells and for target-naïve subset was 4 h and 24 h, respectively. One-way ANOVA was used for comparison between multiple groups, and paired t test was used to compare selected groups. Statistical significances between these groups are marked with asterisk. Data were presented as mean values ± SD. Data comparison was performed by the paired t test. Statistical significance was defined by * p < 0.05, ** p < 0.01, and *** p < 0.001.

    Article Snippet: K562, KU812, and KCL22 cell lines were purchased from ATCC.

    Techniques: Expressing, Isolation, Labeling, Cell Culture, Knockdown, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Control, Ex Vivo, Incubation, Comparison

    CML‐derived cell lines. In particular, name of cell line, cell type, sex and age of patient at time of establishment of cell line, disease status, year of establishment of cell line, source of specimen as indicated in the original publication and type of BCR,ABL1 fusion are indicated (BC = blastic crisis, BCP = B‐Cell Precursor, B‐LCL = B‐lymphoblastoid cell line (EBV + ), BM = bone marrow, BMT = bone marrow transplantation, F = female, M = male, NA = not available, R = relapse, PB = peripheral blood, PE = pleural effusion).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: CML‐derived cell lines. In particular, name of cell line, cell type, sex and age of patient at time of establishment of cell line, disease status, year of establishment of cell line, source of specimen as indicated in the original publication and type of BCR,ABL1 fusion are indicated (BC = blastic crisis, BCP = B‐Cell Precursor, B‐LCL = B‐lymphoblastoid cell line (EBV + ), BM = bone marrow, BMT = bone marrow transplantation, F = female, M = male, NA = not available, R = relapse, PB = peripheral blood, PE = pleural effusion).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Transplantation Assay

    Panel of images illustrating the seven different treatment conditions of K562, LAMA84, and KCL22 cell lines obtained using the Invitrogen EVOS XL Core Imaging System with a 20× zoom. Areas of the well that best showed the cellular conditions were selected (including color, shape, size, and the formation of dead cell clusters). Panel A1, A2, A3: Control at 20× zoom in the three cell lines; Panel B1, B2, B3: DMSO at 20X zoom in the three cell lines; Panel C1, C2, C3: imatinib at 20× zoom in the three cell lines; Panel D1, D2, D3: nilotinib at 20× zoom in the three cell lines; Panel E1, E2, E3: dasatinib at 20× zoom in the three cell lines; Panel F1, F2, F3: bosutinib at 20× zoom in the three cell lines; Panel G1, G2, G3: ponatinib at 20× zoom in the three cell lines. Red arrows indicate significantly larger sized cells; blue arrow indicate cell clusters; orange arrows indicate larger sized cells; green arrows indicate irregularly shaped cells; blue boxes highlight apoptotic bodies. (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Panel of images illustrating the seven different treatment conditions of K562, LAMA84, and KCL22 cell lines obtained using the Invitrogen EVOS XL Core Imaging System with a 20× zoom. Areas of the well that best showed the cellular conditions were selected (including color, shape, size, and the formation of dead cell clusters). Panel A1, A2, A3: Control at 20× zoom in the three cell lines; Panel B1, B2, B3: DMSO at 20X zoom in the three cell lines; Panel C1, C2, C3: imatinib at 20× zoom in the three cell lines; Panel D1, D2, D3: nilotinib at 20× zoom in the three cell lines; Panel E1, E2, E3: dasatinib at 20× zoom in the three cell lines; Panel F1, F2, F3: bosutinib at 20× zoom in the three cell lines; Panel G1, G2, G3: ponatinib at 20× zoom in the three cell lines. Red arrows indicate significantly larger sized cells; blue arrow indicate cell clusters; orange arrows indicate larger sized cells; green arrows indicate irregularly shaped cells; blue boxes highlight apoptotic bodies. (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Imaging, Control

    The average area, diameter, and circularity resulting from each treatment in the three cell lines utilized. Values that have shown statistically significant differences during comparison are highlighted in green. (BOSU, bosutinib; CTR, control; DASA, dasatinib; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; PONA, ponatinib; TKIs, tyrosine kinase inhibitors). (Two Way ANOVA).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: The average area, diameter, and circularity resulting from each treatment in the three cell lines utilized. Values that have shown statistically significant differences during comparison are highlighted in green. (BOSU, bosutinib; CTR, control; DASA, dasatinib; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; PONA, ponatinib; TKIs, tyrosine kinase inhibitors). (Two Way ANOVA).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Comparison, Control

    Cells viability (%) measured by MTT assay in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Cells viability (%) measured by MTT assay in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: MTT Assay, Comparison, Control

    Number of cells measured by CCK8 assay in the three cell lines considered, K562, LAMA84 and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Number of cells measured by CCK8 assay in the three cell lines considered, K562, LAMA84 and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: CCK-8 Assay, Comparison, Control

    Extracellular glutamate concentration (μM) in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA: imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Extracellular glutamate concentration (μM) in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA: imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Concentration Assay, Comparison, Control

    Expression of BCR::ABL1 transcript (normalised for GAPDH) in the three cell lines considered, K562, LAMA84 and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Expression of BCR::ABL1 transcript (normalised for GAPDH) in the three cell lines considered, K562, LAMA84 and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Expressing, Comparison, Control

    Expression of CD33 transcript (normalized for GAPDH) in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Expression of CD33 transcript (normalized for GAPDH) in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Expressing, Comparison, Control

    Expression of CD11b transcript (normalized for GAPDH) in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Expression of CD11b transcript (normalized for GAPDH) in the three cell lines considered, K562, LAMA84, and KCL22, representative of the comparison across individual treatment conditions (CTR, control; DMSO, dimethylsulfoxide; IMA, imatinib; NILO, nilotinib; DASA, dasatinib; BOSU, bosutinib; PONA, ponatinib) (Two‐way ANOVA with Tukey's post hoc test).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Expressing, Comparison, Control

    Panel of images illustrating asciminib treatment of K562, LAMA84, and KCL22 cell lines obtained using the Invitrogen EVOS XL Core Imaging System with a 20× zoom. Areas of the well that best showed the cellular conditions were selected (including color, shape, size, and the formation of dead cell clusters). Panel A1, A2, A3: Control at 20× zoom in the three cell lines; Panel B1, B2, B3: asciminib at 20× zoom in the three cell lines. Red arrows indicate significantly larger sized cells; blue arrow indicate cell clusters; orange arrows indicate larger sized cells; green arrows indicate irregularly shaped cells. (CTR, control; ASCI, asciminib).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Panel of images illustrating asciminib treatment of K562, LAMA84, and KCL22 cell lines obtained using the Invitrogen EVOS XL Core Imaging System with a 20× zoom. Areas of the well that best showed the cellular conditions were selected (including color, shape, size, and the formation of dead cell clusters). Panel A1, A2, A3: Control at 20× zoom in the three cell lines; Panel B1, B2, B3: asciminib at 20× zoom in the three cell lines. Red arrows indicate significantly larger sized cells; blue arrow indicate cell clusters; orange arrows indicate larger sized cells; green arrows indicate irregularly shaped cells. (CTR, control; ASCI, asciminib).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Imaging, Control

    The average area, diameter, and circularity resulting from asciminib treatment in the three cell lines utilized. Values that have shown statistically significant differences during comparison are highlighted in green. (ASCI, asciminib; CTR, control). (Two Way ANOVA).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: The average area, diameter, and circularity resulting from asciminib treatment in the three cell lines utilized. Values that have shown statistically significant differences during comparison are highlighted in green. (ASCI, asciminib; CTR, control). (Two Way ANOVA).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: Comparison, Control

    Cell viability (%) measured by MTT assay (A), number of cells measured by CCK8 assay (B), extracellular glutamate concentration (μM) (C) and expression of BCR::ABL1 (D), CD33 (E) and CD11b (F) transcripts all normalized for GAPDH in the three cell lines considered, K562, LAMA84 and KCL22, following asciminib treatment. (CTR, control; ASCI, asciminib) (Two‐way ANOVA with Tukey's post hoc test).

    Journal: Cell Biology International

    Article Title: Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent

    doi: 10.1002/cbin.70007

    Figure Lengend Snippet: Cell viability (%) measured by MTT assay (A), number of cells measured by CCK8 assay (B), extracellular glutamate concentration (μM) (C) and expression of BCR::ABL1 (D), CD33 (E) and CD11b (F) transcripts all normalized for GAPDH in the three cell lines considered, K562, LAMA84 and KCL22, following asciminib treatment. (CTR, control; ASCI, asciminib) (Two‐way ANOVA with Tukey's post hoc test).

    Article Snippet: This observation can be attributed to the fact that the KCL22 cell line has a faster doubling time (24 h) compared to K562 and LAMA84 (35 h and 50 h, respectively) ( https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-168 ; https://www.Dsmz.de/Collection/Catalogue/Details/Culture/ACC-519 ; https://www.Sigmaaldrich.Com/IT/It/Product/Sigma/Cb_89121407 ).

    Techniques: MTT Assay, CCK-8 Assay, Concentration Assay, Expressing, Control

    Cell lines and culture conditions

    Journal: American Journal of Cancer Research

    Article Title: Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I -compound mutations

    doi:

    Figure Lengend Snippet: Cell lines and culture conditions

    Article Snippet: Patients’ characteristics: CML samples used for in vitro studies and response to ‘asciminib+ponatinib’ table ft1 table-wrap mode="anchored" t5 caption a7 Cell line (Name) Provider/Origin Comments K562 Provided by Dr. M. Deininger (University of Utah, Salt Lake City, UT, USA) - KU812 Provided by Dr. K. Kishi (Niigata University, Niigata, Japan) Basophil-committed KCL22 Purchased from the German Collection of Microorganism and Cell Culture (DSMZ, Braunschweig, Germany) Complex karyotype; 2 Philadelphia Chromosomes KCL22 T315I Produced in our lab: Dr. K. Byrgazov and Dr. T. Lion (Children’s Cancer Research Institute (CCRI), Vienna, Austria) Complex karyotype; 2 Philadelphia Chromosomes Imatinib-resistant; Kept in 5 μM imatinib.

    Techniques: Cell Culture, Produced

    Asciminib and ponatinib synergize in producing growth inhibition in BCR-ABL1+ cell lines. The human CML cell lines KU812, K562, KCL22 and KCL22T315I (A) and Ba/F3 cells expressing various BCR-ABL1-mutations (Ba/F3p210T315I, Ba/F3p210T315I/E255V, Ba/F3p210T315I/F359V, Ba/F3p210T315I/F311L, Ba/F3p210T315I/G250E) or untransfected Ba/F3 cells supplemented with 10 ng/ml IL-3 (B) were kept in control medium or in the presence of asciminib (■-■), ponatinib (●-●), or a combination of both drugs at a fixed ratio (▲-▲) for 48 hours before 3H-thymidine-uptake was evaluated. Results are calculated as percent of control and represent the mean ± S.D. of triplicates. (C) The nature of drug interaction (additive versus synergistic) shown in (A) and (B) was determined for each experiment by calculating combination index (CI) values using Calcusyn software. A CI value of 1 indicates an additive effect, whereas CI values below 1 indicate synergistic drug effects. Examples are shown for K562 and KU812 as well as Ba/F3p210T315I and Ba/F3p210T315I/G250E cells as indicated.

    Journal: American Journal of Cancer Research

    Article Title: Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I -compound mutations

    doi:

    Figure Lengend Snippet: Asciminib and ponatinib synergize in producing growth inhibition in BCR-ABL1+ cell lines. The human CML cell lines KU812, K562, KCL22 and KCL22T315I (A) and Ba/F3 cells expressing various BCR-ABL1-mutations (Ba/F3p210T315I, Ba/F3p210T315I/E255V, Ba/F3p210T315I/F359V, Ba/F3p210T315I/F311L, Ba/F3p210T315I/G250E) or untransfected Ba/F3 cells supplemented with 10 ng/ml IL-3 (B) were kept in control medium or in the presence of asciminib (■-■), ponatinib (●-●), or a combination of both drugs at a fixed ratio (▲-▲) for 48 hours before 3H-thymidine-uptake was evaluated. Results are calculated as percent of control and represent the mean ± S.D. of triplicates. (C) The nature of drug interaction (additive versus synergistic) shown in (A) and (B) was determined for each experiment by calculating combination index (CI) values using Calcusyn software. A CI value of 1 indicates an additive effect, whereas CI values below 1 indicate synergistic drug effects. Examples are shown for K562 and KU812 as well as Ba/F3p210T315I and Ba/F3p210T315I/G250E cells as indicated.

    Article Snippet: Patients’ characteristics: CML samples used for in vitro studies and response to ‘asciminib+ponatinib’ table ft1 table-wrap mode="anchored" t5 caption a7 Cell line (Name) Provider/Origin Comments K562 Provided by Dr. M. Deininger (University of Utah, Salt Lake City, UT, USA) - KU812 Provided by Dr. K. Kishi (Niigata University, Niigata, Japan) Basophil-committed KCL22 Purchased from the German Collection of Microorganism and Cell Culture (DSMZ, Braunschweig, Germany) Complex karyotype; 2 Philadelphia Chromosomes KCL22 T315I Produced in our lab: Dr. K. Byrgazov and Dr. T. Lion (Children’s Cancer Research Institute (CCRI), Vienna, Austria) Complex karyotype; 2 Philadelphia Chromosomes Imatinib-resistant; Kept in 5 μM imatinib.

    Techniques: Inhibition, Expressing, Control, Software

    Asciminib and ponatinib synergize in producing apoptosis in BCR-ABL1+ cell lines. KU812, K562 and KCL22T315I (A) and Ba/F3 cells expressing various BCR-ABL1-mutations (Ba/F3p210T315I, Ba/F3p210T315I/E255V, Ba/F3p210T315I/F359V, Ba/F3p210T315I/F311L, Ba/F3p210T315I/G250E) (B) were kept in control medium or in the presence of asciminib, ponatinib or a combination of both drugs as indicated for 48 hours before apoptosis was determined by Annexin V-FITC/DAPI staining and flow cytometry. One typical experiment (left panels) or the mean ± S.D. of three independent experiments. (right panels) are shown. Asterisk (right panels): P<0.05 compared to control.

    Journal: American Journal of Cancer Research

    Article Title: Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I -compound mutations

    doi:

    Figure Lengend Snippet: Asciminib and ponatinib synergize in producing apoptosis in BCR-ABL1+ cell lines. KU812, K562 and KCL22T315I (A) and Ba/F3 cells expressing various BCR-ABL1-mutations (Ba/F3p210T315I, Ba/F3p210T315I/E255V, Ba/F3p210T315I/F359V, Ba/F3p210T315I/F311L, Ba/F3p210T315I/G250E) (B) were kept in control medium or in the presence of asciminib, ponatinib or a combination of both drugs as indicated for 48 hours before apoptosis was determined by Annexin V-FITC/DAPI staining and flow cytometry. One typical experiment (left panels) or the mean ± S.D. of three independent experiments. (right panels) are shown. Asterisk (right panels): P<0.05 compared to control.

    Article Snippet: Patients’ characteristics: CML samples used for in vitro studies and response to ‘asciminib+ponatinib’ table ft1 table-wrap mode="anchored" t5 caption a7 Cell line (Name) Provider/Origin Comments K562 Provided by Dr. M. Deininger (University of Utah, Salt Lake City, UT, USA) - KU812 Provided by Dr. K. Kishi (Niigata University, Niigata, Japan) Basophil-committed KCL22 Purchased from the German Collection of Microorganism and Cell Culture (DSMZ, Braunschweig, Germany) Complex karyotype; 2 Philadelphia Chromosomes KCL22 T315I Produced in our lab: Dr. K. Byrgazov and Dr. T. Lion (Children’s Cancer Research Institute (CCRI), Vienna, Austria) Complex karyotype; 2 Philadelphia Chromosomes Imatinib-resistant; Kept in 5 μM imatinib.

    Techniques: Expressing, Control, Staining, Flow Cytometry

    Asciminib and ponatinib synergize in inhibiting CRKL phosphorylation in human CML cell lines. KU812, K562, KCL22 and KCL22T315I were kept in control medium (Control) or in the presence of asciminib (Asci), ponatinib (Pona) or a combination (Combi) of both drugs as indicated for 4 hours before expression of p-CRKL and β-tubulin (loading control) were analyzed by Western blotting.

    Journal: American Journal of Cancer Research

    Article Title: Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I -compound mutations

    doi:

    Figure Lengend Snippet: Asciminib and ponatinib synergize in inhibiting CRKL phosphorylation in human CML cell lines. KU812, K562, KCL22 and KCL22T315I were kept in control medium (Control) or in the presence of asciminib (Asci), ponatinib (Pona) or a combination (Combi) of both drugs as indicated for 4 hours before expression of p-CRKL and β-tubulin (loading control) were analyzed by Western blotting.

    Article Snippet: Patients’ characteristics: CML samples used for in vitro studies and response to ‘asciminib+ponatinib’ table ft1 table-wrap mode="anchored" t5 caption a7 Cell line (Name) Provider/Origin Comments K562 Provided by Dr. M. Deininger (University of Utah, Salt Lake City, UT, USA) - KU812 Provided by Dr. K. Kishi (Niigata University, Niigata, Japan) Basophil-committed KCL22 Purchased from the German Collection of Microorganism and Cell Culture (DSMZ, Braunschweig, Germany) Complex karyotype; 2 Philadelphia Chromosomes KCL22 T315I Produced in our lab: Dr. K. Byrgazov and Dr. T. Lion (Children’s Cancer Research Institute (CCRI), Vienna, Austria) Complex karyotype; 2 Philadelphia Chromosomes Imatinib-resistant; Kept in 5 μM imatinib.

    Techniques: Phospho-proteomics, Control, Expressing, Western Blot

    Calculated LogP and anti-proliferation activities of alkynyl analogs

    Journal: ChemMedChem

    Article Title: Alkynylnicotinamide-based compounds as ABL1 inhibitors with potent activities against drug-resistant CML harboring ABL1(T315I) mutant kinase.

    doi: 10.1002/cmdc.201700829

    Figure Lengend Snippet: Calculated LogP and anti-proliferation activities of alkynyl analogs

    Article Snippet: Evaluation of compounds activity against ABL1 and ABL1(T315I) inside CML cell lines KCL22 and KCL22-IR (by KinaSense, West Lafayette, IN, USA).

    Techniques:

    Inhibition of cellular ABL1 activity by imatinib, ponatinib and HSN compounds

    Journal: ChemMedChem

    Article Title: Alkynylnicotinamide-based compounds as ABL1 inhibitors with potent activities against drug-resistant CML harboring ABL1(T315I) mutant kinase.

    doi: 10.1002/cmdc.201700829

    Figure Lengend Snippet: Inhibition of cellular ABL1 activity by imatinib, ponatinib and HSN compounds

    Article Snippet: Evaluation of compounds activity against ABL1 and ABL1(T315I) inside CML cell lines KCL22 and KCL22-IR (by KinaSense, West Lafayette, IN, USA).

    Techniques: Inhibition, Activity Assay