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eg7 ova  (ATCC)


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    ATCC eg7 ova
    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures <t>(E).</t> <t>EG7.OVA</t> tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
    Eg7 Ova, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 624 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Targeting phosphodiesterase 10A disrupts MAPK signaling pathways in the tumor microenvironment to unleash antitumor immunity"

    Article Title: Targeting phosphodiesterase 10A disrupts MAPK signaling pathways in the tumor microenvironment to unleash antitumor immunity

    Journal: bioRxiv

    doi: 10.64898/2026.02.26.708383

    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures (E). EG7.OVA tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
    Figure Legend Snippet: (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures (E). EG7.OVA tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Techniques Used: Expressing, Cell Culture, Activation Assay

    (A) ADT-030 exhibits curative antitumor effect in EG7.OVA tumor model. Following the workflow depicted in the schema, WT C57BL/6 mice were implanted s.c. with EG7.OVA tumor cells. Mice with established tumors (50-100mm2) were treated with ADT-030 for 12 consecutive days. 3 mice that achieved complete tumor regression were rechallenged with EG7.OVA tumor cells. Naïve mice inoculated with EG7.OVA tumors at the same time servied as controls. (B) ADT-030 antitumor efficacy is compromised in Batf3KO mice. Following the workflow depicted in the schema, EG7.OVA cells were s.c. implanted to WT or Batf3KO mice. Mice with established tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05.
    Figure Legend Snippet: (A) ADT-030 exhibits curative antitumor effect in EG7.OVA tumor model. Following the workflow depicted in the schema, WT C57BL/6 mice were implanted s.c. with EG7.OVA tumor cells. Mice with established tumors (50-100mm2) were treated with ADT-030 for 12 consecutive days. 3 mice that achieved complete tumor regression were rechallenged with EG7.OVA tumor cells. Naïve mice inoculated with EG7.OVA tumors at the same time servied as controls. (B) ADT-030 antitumor efficacy is compromised in Batf3KO mice. Following the workflow depicted in the schema, EG7.OVA cells were s.c. implanted to WT or Batf3KO mice. Mice with established tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05.

    Techniques Used:



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    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures <t>(E).</t> <t>EG7.OVA</t> tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures <t>(E).</t> <t>EG7.OVA</t> tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures <t>(E).</t> <t>EG7.OVA</t> tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures <t>(E).</t> <t>EG7.OVA</t> tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures <t>(E).</t> <t>EG7.OVA</t> tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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    Image Search Results


    (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures (E). EG7.OVA tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: bioRxiv

    Article Title: Targeting phosphodiesterase 10A disrupts MAPK signaling pathways in the tumor microenvironment to unleash antitumor immunity

    doi: 10.64898/2026.02.26.708383

    Figure Lengend Snippet: (A-C) Detection of ICD markers. Tumor cells were treated with DMSO or ADT-030 for 24 hours. Cell surface expression of CRT was detected by FACS, and MFI values are summarized in (A) as mean ± SEM. Extracellular ATP and HMGB1 levels from the indicated cells were measured and results shown as mean +/- SEM are summarized in (B) and (C), respectively. (D) ADT-030-treated tumor cells promote DC maturation. The schema depicts the experimental setup in which BMDCs were co-cultured with ADT-030 or DMSO pre-treated 4T1.GFP cells for 48 hrs. Uptake of the GFP signal by DCs and DC activation markers (MHC-II, CD80 and CD86) were assessed by FACS. MFIs are summarized as mean ± SEM in bar graphs. (E, F) cDC1-dependent priming of tumor-specific CD8⁺ T cells. The schema depicts the experimental procedures (E). EG7.OVA tumor cells were s.c. implanted to the flanks of WT or Batf3KO mice. Mice with palpable tumors were treated with vehicle or ADT-030. Peripheral blood was collected 10 days after treatment to detect OVA-specific CD8+ T cells by OVA-Kb tetramer. Representative dot plots are shown in (F). Numbers of the gated region demark percent of tetramer-positive cells in CD8+ T cell population. Results shown as mean +/- SEM are summarized in the bar graph. (G) ADT-030 efficacy in mice diminishes in the absence of cDC1. As depicted in the schema, EL4 or KPC cells were s.c. implanted to WT or Batf3KO mice. Mice with palpable tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: Murine tumor cell lines 4T1, A20, B16F10, CT26, EL4, EG7.OVA and MC38 were purchased from ATCC.

    Techniques: Expressing, Cell Culture, Activation Assay

    (A) ADT-030 exhibits curative antitumor effect in EG7.OVA tumor model. Following the workflow depicted in the schema, WT C57BL/6 mice were implanted s.c. with EG7.OVA tumor cells. Mice with established tumors (50-100mm2) were treated with ADT-030 for 12 consecutive days. 3 mice that achieved complete tumor regression were rechallenged with EG7.OVA tumor cells. Naïve mice inoculated with EG7.OVA tumors at the same time servied as controls. (B) ADT-030 antitumor efficacy is compromised in Batf3KO mice. Following the workflow depicted in the schema, EG7.OVA cells were s.c. implanted to WT or Batf3KO mice. Mice with established tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05.

    Journal: bioRxiv

    Article Title: Targeting phosphodiesterase 10A disrupts MAPK signaling pathways in the tumor microenvironment to unleash antitumor immunity

    doi: 10.64898/2026.02.26.708383

    Figure Lengend Snippet: (A) ADT-030 exhibits curative antitumor effect in EG7.OVA tumor model. Following the workflow depicted in the schema, WT C57BL/6 mice were implanted s.c. with EG7.OVA tumor cells. Mice with established tumors (50-100mm2) were treated with ADT-030 for 12 consecutive days. 3 mice that achieved complete tumor regression were rechallenged with EG7.OVA tumor cells. Naïve mice inoculated with EG7.OVA tumors at the same time servied as controls. (B) ADT-030 antitumor efficacy is compromised in Batf3KO mice. Following the workflow depicted in the schema, EG7.OVA cells were s.c. implanted to WT or Batf3KO mice. Mice with established tumors were treated daily with vehicle or ADT-030 daily till the endpoint. Tumor growth curves are shown as mean ± SEM, with the number of mice per group indicated. *, P < 0.05.

    Article Snippet: Murine tumor cell lines 4T1, A20, B16F10, CT26, EL4, EG7.OVA and MC38 were purchased from ATCC.

    Techniques: