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human monocytic leukemia cell line  (ATCC)


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    ATCC human monocytic leukemia cell line
    Human Monocytic Leukemia Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 19607 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human monocytic leukemia cell line/product/ATCC
    Average 99 stars, based on 19607 article reviews
    human monocytic leukemia cell line - by Bioz Stars, 2026-06
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    Identification and multi-level validation of TPI1 as a pivotal prognostic driver. (A) Lollipop chart showing the selection frequency of feature genes across 101 machine learning models, identifying TPI1 as a high-frequency core gene. (B) Univariate Cox regression analysis of candidate genes; TPI1 exhibited the most substantial Hazard Ratio (HR), characterizing it as a preeminent risk factor. (C) Expression profiling of TPI1 across malignant versus paracancerous tissues within the TCGA-LIHC discovery cohort (upper) and GSE14520 validation cohort (lower). (D) Kaplan-Meier overall survival curves comparing patients with high and low TPI1 expression in the TCGA-LIHC (top) and GSE14520 (bottom) cohorts. (E) Relative mRNA expression levels of TPI1 in the immortalized human hepatocyte line (MIHA) and <t>HCC</t> cell <t>lines</t> <t>(Huh7,</t> SMMC-7721) determined by RT-qPCR. (F) Representative Western blot images (left) and densitometric quantification (right) of TPI1 protein levels in MIHA, Huh7, and SMMC-7721 cells. GAPDH served as the internal loading control. Data are expressed as mean ± SD. ** P < 0.01, *** P < 0.001.
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    ATCC human neuroblastoma cell line sh sy5y
    Effect of BDNF treatment on the neurite outgrowth parameters <t>in</t> <t>SH-SY5Y</t> cells Differentiated SH-SY5Y cells were treated with 10 ng/mL, 50 ng/mL, or 100 ng/mL of BDNF for 48h. (A) Cells were stained for ßIII-tubulin (red) and DAPI (blue). All images were captured 48h post-treatment at 20× magnification on the Agilent BioTek Cytation 5 instrument. Image analysis was performed with the Gen5 software Neurite Outgrowth module where the soma mask overlay is displayed in blue and the neurite mask overlay in yellow. (B) Average neurite length, (C) average neurite branches, (D) average neurite count depending on BDNF concentration, and (E) neurite thickness depending on BDNF concentration. Scale bar: 50 μm. Each data set represents N=2 independent experiments with 4-6 replicates per condition and with 5-9 images per well. The points represent the mean ± SEM for each condition. One-way ANOVA and post hoc Dunnett’s multiple comparison tests. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. BDNF: Brain-derived neurotrophic factor.
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    Human Protein Atlas aldh3a2 expression in human leukemia cell lines and peripheral blood mononuclear cells
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    Aldh3a2 Expression In Human Leukemia Cell Lines And Peripheral Blood Mononuclear Cells, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human pdac cell lines
    Glycolysis inhibitors diminish the virus sensitivity of glycolytic <t>PDAC</t> <t>cells</t> <t>MIA</t> PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
    Human Pdac Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Journal: Genes & Diseases

    Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

    doi: 10.1016/j.gendis.2025.101978

    Figure Lengend Snippet: Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

    Techniques: Transduction, Control, Incubation, Enzyme-linked Immunosorbent Assay, Standard Deviation

    TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.

    Journal: Genes & Diseases

    Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

    doi: 10.1016/j.gendis.2025.101978

    Figure Lengend Snippet: TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.

    Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

    Techniques: Activity Assay, In Vivo, Expressing, Luciferase, In Vivo Imaging

    Identification and multi-level validation of TPI1 as a pivotal prognostic driver. (A) Lollipop chart showing the selection frequency of feature genes across 101 machine learning models, identifying TPI1 as a high-frequency core gene. (B) Univariate Cox regression analysis of candidate genes; TPI1 exhibited the most substantial Hazard Ratio (HR), characterizing it as a preeminent risk factor. (C) Expression profiling of TPI1 across malignant versus paracancerous tissues within the TCGA-LIHC discovery cohort (upper) and GSE14520 validation cohort (lower). (D) Kaplan-Meier overall survival curves comparing patients with high and low TPI1 expression in the TCGA-LIHC (top) and GSE14520 (bottom) cohorts. (E) Relative mRNA expression levels of TPI1 in the immortalized human hepatocyte line (MIHA) and HCC cell lines (Huh7, SMMC-7721) determined by RT-qPCR. (F) Representative Western blot images (left) and densitometric quantification (right) of TPI1 protein levels in MIHA, Huh7, and SMMC-7721 cells. GAPDH served as the internal loading control. Data are expressed as mean ± SD. ** P < 0.01, *** P < 0.001.

    Journal: Translational Oncology

    Article Title: Integrating spatial and single-cell transcriptomics via machine learning to characterize efferocytosis in hepatocellular carcinoma prognosis and immunotherapy

    doi: 10.1016/j.tranon.2026.102801

    Figure Lengend Snippet: Identification and multi-level validation of TPI1 as a pivotal prognostic driver. (A) Lollipop chart showing the selection frequency of feature genes across 101 machine learning models, identifying TPI1 as a high-frequency core gene. (B) Univariate Cox regression analysis of candidate genes; TPI1 exhibited the most substantial Hazard Ratio (HR), characterizing it as a preeminent risk factor. (C) Expression profiling of TPI1 across malignant versus paracancerous tissues within the TCGA-LIHC discovery cohort (upper) and GSE14520 validation cohort (lower). (D) Kaplan-Meier overall survival curves comparing patients with high and low TPI1 expression in the TCGA-LIHC (top) and GSE14520 (bottom) cohorts. (E) Relative mRNA expression levels of TPI1 in the immortalized human hepatocyte line (MIHA) and HCC cell lines (Huh7, SMMC-7721) determined by RT-qPCR. (F) Representative Western blot images (left) and densitometric quantification (right) of TPI1 protein levels in MIHA, Huh7, and SMMC-7721 cells. GAPDH served as the internal loading control. Data are expressed as mean ± SD. ** P < 0.01, *** P < 0.001.

    Article Snippet: The human HCC cell lines (Huh7 and SMMC-7721) and the immortalized human hepatocyte line MIHA were procured from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: Biomarker Discovery, Selection, Expressing, Quantitative RT-PCR, Western Blot, Control

    Effect of BDNF treatment on the neurite outgrowth parameters in SH-SY5Y cells Differentiated SH-SY5Y cells were treated with 10 ng/mL, 50 ng/mL, or 100 ng/mL of BDNF for 48h. (A) Cells were stained for ßIII-tubulin (red) and DAPI (blue). All images were captured 48h post-treatment at 20× magnification on the Agilent BioTek Cytation 5 instrument. Image analysis was performed with the Gen5 software Neurite Outgrowth module where the soma mask overlay is displayed in blue and the neurite mask overlay in yellow. (B) Average neurite length, (C) average neurite branches, (D) average neurite count depending on BDNF concentration, and (E) neurite thickness depending on BDNF concentration. Scale bar: 50 μm. Each data set represents N=2 independent experiments with 4-6 replicates per condition and with 5-9 images per well. The points represent the mean ± SEM for each condition. One-way ANOVA and post hoc Dunnett’s multiple comparison tests. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. BDNF: Brain-derived neurotrophic factor.

    Journal: STAR Protocols

    Article Title: Protocol for automated quantification of neuronal cells using the Agilent BioTek Cytation system and Gen5 neurite outgrowth module

    doi: 10.1016/j.xpro.2026.104485

    Figure Lengend Snippet: Effect of BDNF treatment on the neurite outgrowth parameters in SH-SY5Y cells Differentiated SH-SY5Y cells were treated with 10 ng/mL, 50 ng/mL, or 100 ng/mL of BDNF for 48h. (A) Cells were stained for ßIII-tubulin (red) and DAPI (blue). All images were captured 48h post-treatment at 20× magnification on the Agilent BioTek Cytation 5 instrument. Image analysis was performed with the Gen5 software Neurite Outgrowth module where the soma mask overlay is displayed in blue and the neurite mask overlay in yellow. (B) Average neurite length, (C) average neurite branches, (D) average neurite count depending on BDNF concentration, and (E) neurite thickness depending on BDNF concentration. Scale bar: 50 μm. Each data set represents N=2 independent experiments with 4-6 replicates per condition and with 5-9 images per well. The points represent the mean ± SEM for each condition. One-way ANOVA and post hoc Dunnett’s multiple comparison tests. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. BDNF: Brain-derived neurotrophic factor.

    Article Snippet: The native human neuroblastoma cell line SH-SY5Y comes from ATCC (CRL-2266).

    Techniques: Staining, Software, Concentration Assay, Comparison, Derivative Assay

    Effect of rotenone treatment on the neurite outgrowth parameters in SH-SY5Y cells Differentiated SH-SY5Y cells were treated with 0.05 μM, 0.1 μM or 0.5 μM of rotenone for 48h. (A) Cells were stained for ß3 tubulin (red color) and DAPI (blue color). All images were captured 48h post-treatment at 20× magnification on the Agilent BioTek Cytation 5 instrument. Image analysis was performed with the Gen5 software Neurite Outgrowth module where the soma mask overlay is displayed in blue and the neurite mask overlay in yellow. (B) Average neurite length, (C) average neurite branches, (D) average neurite count, and (E) neurite thickness depending on rotenone concentration. Scale bar: 50 μm. Each data set represents N=2 independent experiments with 4-6 replicates per condition and with 5-9 pictures per well. The points represent the mean ± SEM for each condition. One-way ANOVA and post hoc Dunnett’s multiple comparison tests. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

    Journal: STAR Protocols

    Article Title: Protocol for automated quantification of neuronal cells using the Agilent BioTek Cytation system and Gen5 neurite outgrowth module

    doi: 10.1016/j.xpro.2026.104485

    Figure Lengend Snippet: Effect of rotenone treatment on the neurite outgrowth parameters in SH-SY5Y cells Differentiated SH-SY5Y cells were treated with 0.05 μM, 0.1 μM or 0.5 μM of rotenone for 48h. (A) Cells were stained for ß3 tubulin (red color) and DAPI (blue color). All images were captured 48h post-treatment at 20× magnification on the Agilent BioTek Cytation 5 instrument. Image analysis was performed with the Gen5 software Neurite Outgrowth module where the soma mask overlay is displayed in blue and the neurite mask overlay in yellow. (B) Average neurite length, (C) average neurite branches, (D) average neurite count, and (E) neurite thickness depending on rotenone concentration. Scale bar: 50 μm. Each data set represents N=2 independent experiments with 4-6 replicates per condition and with 5-9 pictures per well. The points represent the mean ± SEM for each condition. One-way ANOVA and post hoc Dunnett’s multiple comparison tests. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

    Article Snippet: The native human neuroblastoma cell line SH-SY5Y comes from ATCC (CRL-2266).

    Techniques: Staining, Software, Concentration Assay, Comparison

    Impact of the APP and P301L mutation on the neurite outgrowth capacity of SH-SY5Y cells The control condition corresponds to the native cells. The APP condition corresponds to the cells stably overexpressing the Amyloid Precursor Protein (APP). The P301L condition corresponds to the cells stably overexpressing the P301L-Tau mutation. The differentiated cells were treated with 50 ng/mL of BDNF for 48h. (A) Cells were stained for ß3 tubulin (red) and DAPI (blue). All images were captured 48h post-treatment at 20× magnification on the Agilent BioTek Cytation 5 instrument. Image analysis was performed with the Gen5 software Neurite Outgrowth module where the soma mask overlay is displayed in blue and the neurite mask overlay in yellow. (B) Average neurite length, (C) average neurite branches, (D) average neurite count, and (E) neurite thickness in Control, APP, and P301L cells. Scale bar: 50 μm. The boxes represent the median (full line) and the mean (“+” symbol); the whiskers represent the minimum and maximum values. Each data set represents N=2 independent experiments with 4-6 replicates per condition. One-way ANOVA and post hoc Dunnett’s multiple comparison tests. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

    Journal: STAR Protocols

    Article Title: Protocol for automated quantification of neuronal cells using the Agilent BioTek Cytation system and Gen5 neurite outgrowth module

    doi: 10.1016/j.xpro.2026.104485

    Figure Lengend Snippet: Impact of the APP and P301L mutation on the neurite outgrowth capacity of SH-SY5Y cells The control condition corresponds to the native cells. The APP condition corresponds to the cells stably overexpressing the Amyloid Precursor Protein (APP). The P301L condition corresponds to the cells stably overexpressing the P301L-Tau mutation. The differentiated cells were treated with 50 ng/mL of BDNF for 48h. (A) Cells were stained for ß3 tubulin (red) and DAPI (blue). All images were captured 48h post-treatment at 20× magnification on the Agilent BioTek Cytation 5 instrument. Image analysis was performed with the Gen5 software Neurite Outgrowth module where the soma mask overlay is displayed in blue and the neurite mask overlay in yellow. (B) Average neurite length, (C) average neurite branches, (D) average neurite count, and (E) neurite thickness in Control, APP, and P301L cells. Scale bar: 50 μm. The boxes represent the median (full line) and the mean (“+” symbol); the whiskers represent the minimum and maximum values. Each data set represents N=2 independent experiments with 4-6 replicates per condition. One-way ANOVA and post hoc Dunnett’s multiple comparison tests. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

    Article Snippet: The native human neuroblastoma cell line SH-SY5Y comes from ATCC (CRL-2266).

    Techniques: Mutagenesis, Control, Stable Transfection, Staining, Software, Comparison

    Expression of ALDH3A2 in healthy people and patients with AML (A) The expression of ALDH3A2 in various tumors compared with normal tissues. Data are represented as mean ± SEM. (B) Expression of ALDH3A2 in 88 leukemia cell lines. (C) The survival curve of patients with high and low expression of ALDH3A2 (n [low expression] = 121, n [high expression] = 30). (D) The expression of protein ALDH3A2 in HL-60, HL-60/ADM, K562, K562/ADM, and bone marrow in patients. (E) The expression of ALDH3A2 RNA in bone marrow mononuclear cells of AML patients in the CR ( n = 9), C1NR ( n = 8), and R/R ( n = 10) group. Data are represented as mean ± SEM. (F) The expression of ALDH3A2 in bone marrow mononuclear cells of 3 AML patients at their initial and recurrent stage. (G) High/low expression of ALDH3A2 and molecular mutation distribution of 66 AML patients. Data are represented as mean ± SEM. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Journal: iScience

    Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

    doi: 10.1016/j.isci.2026.116202

    Figure Lengend Snippet: Expression of ALDH3A2 in healthy people and patients with AML (A) The expression of ALDH3A2 in various tumors compared with normal tissues. Data are represented as mean ± SEM. (B) Expression of ALDH3A2 in 88 leukemia cell lines. (C) The survival curve of patients with high and low expression of ALDH3A2 (n [low expression] = 121, n [high expression] = 30). (D) The expression of protein ALDH3A2 in HL-60, HL-60/ADM, K562, K562/ADM, and bone marrow in patients. (E) The expression of ALDH3A2 RNA in bone marrow mononuclear cells of AML patients in the CR ( n = 9), C1NR ( n = 8), and R/R ( n = 10) group. Data are represented as mean ± SEM. (F) The expression of ALDH3A2 in bone marrow mononuclear cells of 3 AML patients at their initial and recurrent stage. (G) High/low expression of ALDH3A2 and molecular mutation distribution of 66 AML patients. Data are represented as mean ± SEM. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Article Snippet: ALDH3A2 expression in human leukemia cell lines and peripheral blood mononuclear cells , Human Protein Atlas website ( https://www.proteinatlas.org/ ) , .

    Techniques: Expressing, Mutagenesis, Two Tailed Test, Comparison

    ALDH3A2-V protects AML cells from ferroptosis and cytotoxicity induced by doxorubicin (A) ALDH3A2 mRNA relative expression in HL-60/ADM and K562/ADM cells after transfection of siRNA by electroporation. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The lipid peroxidation degree of HL60ADM and K562ADM cells in the control (ctrl) and ALDH3A2 knockdown (KD) groups after the same dose of doxorubicin treatment for 48 h. (C) The content of ALDH3A2 protein in HL-60, K562, U937, and KG-1α in the ALDH3A2 overexpressing (OE) group and the control (CON) group. (D) The location of ALDH3A2-V overexpression. This representative image was selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. (E) Lipid peroxidation in HL-60, K562, U937, and KG-1α in the ALDH3A2 OE group and the CON group under the same concentration of doxorubicin treatment. (F and G) Cell viability and its fitting curve of HL-60, K562, U937, and KG-1α in the ALDH3A2 OE group and the CON group under the gradient concentration of doxorubicin treatment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Journal: iScience

    Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

    doi: 10.1016/j.isci.2026.116202

    Figure Lengend Snippet: ALDH3A2-V protects AML cells from ferroptosis and cytotoxicity induced by doxorubicin (A) ALDH3A2 mRNA relative expression in HL-60/ADM and K562/ADM cells after transfection of siRNA by electroporation. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The lipid peroxidation degree of HL60ADM and K562ADM cells in the control (ctrl) and ALDH3A2 knockdown (KD) groups after the same dose of doxorubicin treatment for 48 h. (C) The content of ALDH3A2 protein in HL-60, K562, U937, and KG-1α in the ALDH3A2 overexpressing (OE) group and the control (CON) group. (D) The location of ALDH3A2-V overexpression. This representative image was selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. (E) Lipid peroxidation in HL-60, K562, U937, and KG-1α in the ALDH3A2 OE group and the CON group under the same concentration of doxorubicin treatment. (F and G) Cell viability and its fitting curve of HL-60, K562, U937, and KG-1α in the ALDH3A2 OE group and the CON group under the gradient concentration of doxorubicin treatment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Article Snippet: ALDH3A2 expression in human leukemia cell lines and peripheral blood mononuclear cells , Human Protein Atlas website ( https://www.proteinatlas.org/ ) , .

    Techniques: Expressing, Transfection, Electroporation, Control, Knockdown, Over Expression, Concentration Assay, Two Tailed Test, Comparison

    ALDH3A2 affects the sensitivity of AML cells to doxorubicin by altering 4-HNE and fatty acid content (A) The content of 4-HNE in cell lysate and culture supernatant of AML cells in the doxorubicin treatment (ADR) group and control (CON) group. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The content of 4-HNE in HL-60, U937, and KG-1α of the overexpressing ALDH3A2 (OE) group and the CON group under the same concentration of doxorubicin treatment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (C) OPLS-DA was performed on the measured fatty acids. Quantitative data for fatty acid and cell viability were collected from 3 independent experiments. (D) Variable Importance in Projection(VIP) value of different fatty acids; the difference is considered significant when the VIP>1. (E) Content of three different fatty acids in the CON and OE ALDH3A2 group. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (F) Cell viability of AML cells in heptadecanoic acid, oleic acid, and linoleic acid-pretreated groups and the CON group after the treatment of doxorubicin. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (G) Lipid peroxidation in AML cells in heptadecanoic acid-, oleic acid-, and linoleic acid-pretreated groups and the CON group after the treatment of doxorubicin. These images were selected from 3 independent replicates. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, ∗∗ indicates p < 0.01 between the two groups, and ∗∗∗ indicates p < 0.001 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Journal: iScience

    Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

    doi: 10.1016/j.isci.2026.116202

    Figure Lengend Snippet: ALDH3A2 affects the sensitivity of AML cells to doxorubicin by altering 4-HNE and fatty acid content (A) The content of 4-HNE in cell lysate and culture supernatant of AML cells in the doxorubicin treatment (ADR) group and control (CON) group. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The content of 4-HNE in HL-60, U937, and KG-1α of the overexpressing ALDH3A2 (OE) group and the CON group under the same concentration of doxorubicin treatment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (C) OPLS-DA was performed on the measured fatty acids. Quantitative data for fatty acid and cell viability were collected from 3 independent experiments. (D) Variable Importance in Projection(VIP) value of different fatty acids; the difference is considered significant when the VIP>1. (E) Content of three different fatty acids in the CON and OE ALDH3A2 group. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (F) Cell viability of AML cells in heptadecanoic acid, oleic acid, and linoleic acid-pretreated groups and the CON group after the treatment of doxorubicin. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (G) Lipid peroxidation in AML cells in heptadecanoic acid-, oleic acid-, and linoleic acid-pretreated groups and the CON group after the treatment of doxorubicin. These images were selected from 3 independent replicates. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, ∗∗ indicates p < 0.01 between the two groups, and ∗∗∗ indicates p < 0.001 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Article Snippet: ALDH3A2 expression in human leukemia cell lines and peripheral blood mononuclear cells , Human Protein Atlas website ( https://www.proteinatlas.org/ ) , .

    Techniques: Control, Concentration Assay, Two Tailed Test, Comparison

    Effects of fatty acids and ALDH3A2 on plasma membrane fluidity and drug uptake (A) Laurdan staining showed different ratios of order and disorder phases in the control, heptadecanoic acid-, oleic acid-, or linoleic acid-treated groups. These representative images were selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. (B) Flow cytometry was employed to quantify Cy5 fluorescence intensity in control, heptadecanoic acid-, oleic acid-, or linoleic acid-pretreated groups at 2- and 4-h intervals following doxorubicin exposure. The representative image was selected from 3 independent replicate experiments. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (C) Laurdan staining showed different ratios of order and disorder phases in the control and ALDH3A2 high groups. The mCherry fluorescent protein was co-expressed with ALDH3A2, which indicates successful transfection of the overexpression plasmid into the cells. These representative images were selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. (D) U937 cells in the control group and ALDH3A2 high group were treated with Cy5-labeled doxorubicin. The mCherry fluorescent protein was co-expressed with ALDH3A2, which indicates successful transfection of the overexpression plasmid into the cells. These representative images were selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Journal: iScience

    Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

    doi: 10.1016/j.isci.2026.116202

    Figure Lengend Snippet: Effects of fatty acids and ALDH3A2 on plasma membrane fluidity and drug uptake (A) Laurdan staining showed different ratios of order and disorder phases in the control, heptadecanoic acid-, oleic acid-, or linoleic acid-treated groups. These representative images were selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. (B) Flow cytometry was employed to quantify Cy5 fluorescence intensity in control, heptadecanoic acid-, oleic acid-, or linoleic acid-pretreated groups at 2- and 4-h intervals following doxorubicin exposure. The representative image was selected from 3 independent replicate experiments. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (C) Laurdan staining showed different ratios of order and disorder phases in the control and ALDH3A2 high groups. The mCherry fluorescent protein was co-expressed with ALDH3A2, which indicates successful transfection of the overexpression plasmid into the cells. These representative images were selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. (D) U937 cells in the control group and ALDH3A2 high group were treated with Cy5-labeled doxorubicin. The mCherry fluorescent protein was co-expressed with ALDH3A2, which indicates successful transfection of the overexpression plasmid into the cells. These representative images were selected from 3 independent replicate experiments, with 4 fields of view evaluated per replicate. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Article Snippet: ALDH3A2 expression in human leukemia cell lines and peripheral blood mononuclear cells , Human Protein Atlas website ( https://www.proteinatlas.org/ ) , .

    Techniques: Clinical Proteomics, Membrane, Staining, Control, Flow Cytometry, Fluorescence, Transfection, Over Expression, Plasmid Preparation, Labeling, Two Tailed Test, Comparison

    In in vivo experiments, AML with high expression of ALDH3A2 exhibits a poorer response to doxorubicin (A) Schematic diagram of the process for establishing the AML mouse model. (B) In vivo bioimaging shows the success of the model and the leukemia burden in mice before and after treatment. (C) Statistics of fluorescence values ( n = 5) on days 3 and 7 of the experiment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (D) Survival curves of mice in different groups. (E) 4-HNE content in plasma of mice in different groups ( n = 5) on day 7. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (F) 4-HNE content in plasma of AML patients with low ( n = 5) and high ( n = 5) ALDH3A2 expression levels before and after receiving chemotherapy. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired or paired two-tailed Student’s t tests for the comparison of two groups.

    Journal: iScience

    Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

    doi: 10.1016/j.isci.2026.116202

    Figure Lengend Snippet: In in vivo experiments, AML with high expression of ALDH3A2 exhibits a poorer response to doxorubicin (A) Schematic diagram of the process for establishing the AML mouse model. (B) In vivo bioimaging shows the success of the model and the leukemia burden in mice before and after treatment. (C) Statistics of fluorescence values ( n = 5) on days 3 and 7 of the experiment. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (D) Survival curves of mice in different groups. (E) 4-HNE content in plasma of mice in different groups ( n = 5) on day 7. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (F) 4-HNE content in plasma of AML patients with low ( n = 5) and high ( n = 5) ALDH3A2 expression levels before and after receiving chemotherapy. Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired or paired two-tailed Student’s t tests for the comparison of two groups.

    Article Snippet: ALDH3A2 expression in human leukemia cell lines and peripheral blood mononuclear cells , Human Protein Atlas website ( https://www.proteinatlas.org/ ) , .

    Techniques: In Vivo, Expressing, Fluorescence, Clinical Proteomics, Two Tailed Test, Comparison

    X24003 inhibits ALDH3A2 and enhances the cytotoxic effects of doxorubicin on resistant AML cells (A) OPLS-DA was performed on the measured fatty acid containment in the X24003 treatment group and control group. Quantitative data for fatty acid and cell viability were collected from 3 independent experiments. VIP value of different fatty acids; the difference is considered significant when the VIP>1. (B) X24003 exhibits a synergistic effect with doxorubicin in the elimination of doxorubicin-resistant AML cell lines HL-60ADM and K562ADM. (C) X24003 augments doxorubicin-induced lipid peroxidation in doxorubicin-resistant AML cell strains without affecting the parental cell lines. The representative image was selected from three independent replicate experiments. (D) In vivo bioimaging shows the success of the model and the leukemia burden in mice before and after treatment.

    Journal: iScience

    Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

    doi: 10.1016/j.isci.2026.116202

    Figure Lengend Snippet: X24003 inhibits ALDH3A2 and enhances the cytotoxic effects of doxorubicin on resistant AML cells (A) OPLS-DA was performed on the measured fatty acid containment in the X24003 treatment group and control group. Quantitative data for fatty acid and cell viability were collected from 3 independent experiments. VIP value of different fatty acids; the difference is considered significant when the VIP>1. (B) X24003 exhibits a synergistic effect with doxorubicin in the elimination of doxorubicin-resistant AML cell lines HL-60ADM and K562ADM. (C) X24003 augments doxorubicin-induced lipid peroxidation in doxorubicin-resistant AML cell strains without affecting the parental cell lines. The representative image was selected from three independent replicate experiments. (D) In vivo bioimaging shows the success of the model and the leukemia burden in mice before and after treatment.

    Article Snippet: ALDH3A2 expression in human leukemia cell lines and peripheral blood mononuclear cells , Human Protein Atlas website ( https://www.proteinatlas.org/ ) , .

    Techniques: Control, In Vivo

    HDAC2 binds to the promoter of the ALDH3A2 gene and regulates its expression (A) CUT&RUN indicates that HDAC2 binds to the promoter of the ALDH3A2 gene; the binding affinity is observed to decrease after treatment with chidamide. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The expression of ALDH3A2 protein in AML cells following treatment with doxorubicin or chidamide. (C) Treatment of chidamide enhances lipid peroxidation induced by doxorubicin in AML cells. The representative image was selected from three independent replicate experiments. (D) Chidamide exhibits a synergistic effect with doxorubicin in the elimination of AML cells. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Journal: iScience

    Article Title: ALDH3A2-mediated fatty acid synthesis induces ferroptosis and AML drug resistance

    doi: 10.1016/j.isci.2026.116202

    Figure Lengend Snippet: HDAC2 binds to the promoter of the ALDH3A2 gene and regulates its expression (A) CUT&RUN indicates that HDAC2 binds to the promoter of the ALDH3A2 gene; the binding affinity is observed to decrease after treatment with chidamide. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . (B) The expression of ALDH3A2 protein in AML cells following treatment with doxorubicin or chidamide. (C) Treatment of chidamide enhances lipid peroxidation induced by doxorubicin in AML cells. The representative image was selected from three independent replicate experiments. (D) Chidamide exhibits a synergistic effect with doxorubicin in the elimination of AML cells. Data are represented as mean ± SEM. The specific data are shown in the supplemental table . Ns indicates no statistical difference between the two groups, ∗ indicates p < 0.05 between the two groups, and ∗∗ indicates p < 0.01 between the two groups. Statistical significance was determined using unpaired two-tailed Student’s t tests for the comparison of two groups.

    Article Snippet: ALDH3A2 expression in human leukemia cell lines and peripheral blood mononuclear cells , Human Protein Atlas website ( https://www.proteinatlas.org/ ) , .

    Techniques: Expressing, Binding Assay, Two Tailed Test, Comparison

    Glycolysis inhibitors diminish the virus sensitivity of glycolytic PDAC cells MIA PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: Glycolysis inhibitors diminish the virus sensitivity of glycolytic PDAC cells MIA PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Virus, Infection, Control, Western Blot, Staining, Fluorescence, Microscopy, XTT Assay, Expressing

    p53 activation modulates glutamine metabolism in PDAC cells (A) Glutamine consumption in PDAC cells, presented as fold-increase compared with PBS, which was set as 1.0. (B) Outline of glutamine metabolism, shown from glutamine uptake to α-KG production. (C) Lysates of PDAC cells were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (D) PDAC cells were infected with OBP-301 or OBP-702 at an MOI of 100 for 48 h. The amount of intracellular α-KG in PDAC cells is shown as fold-increase compared with the mock-infected group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (E) PDAC cells were infected with OBP-301 or OBP-702 at the indicated MOIs for 72 h. Cell lysates were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (F) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 24 h. The amount of intracellular αKG in PDAC cells is presented as fold-increase compared with mock-infected control groups. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences among four groups was determined using one-way ANOVA followed by Turkey’s multiple comparison procedure. (G) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 48 h. Cell lysates were subjected to western blot analysis for p53, GDH1/2, OGDH, and IDH1. β-Actin was assayed as a loading control. The expression level of each protein was calculated relative to that of MIAPaCa-2 cells or mock-treated cells, which was set at 1.0. ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: p53 activation modulates glutamine metabolism in PDAC cells (A) Glutamine consumption in PDAC cells, presented as fold-increase compared with PBS, which was set as 1.0. (B) Outline of glutamine metabolism, shown from glutamine uptake to α-KG production. (C) Lysates of PDAC cells were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (D) PDAC cells were infected with OBP-301 or OBP-702 at an MOI of 100 for 48 h. The amount of intracellular α-KG in PDAC cells is shown as fold-increase compared with the mock-infected group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (E) PDAC cells were infected with OBP-301 or OBP-702 at the indicated MOIs for 72 h. Cell lysates were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (F) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 24 h. The amount of intracellular αKG in PDAC cells is presented as fold-increase compared with mock-infected control groups. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences among four groups was determined using one-way ANOVA followed by Turkey’s multiple comparison procedure. (G) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 48 h. Cell lysates were subjected to western blot analysis for p53, GDH1/2, OGDH, and IDH1. β-Actin was assayed as a loading control. The expression level of each protein was calculated relative to that of MIAPaCa-2 cells or mock-treated cells, which was set at 1.0. ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Activation Assay, Western Blot, Infection, Control, Comparison, Expressing

    Comparison of metabolic phenotypes and virus sensitivity in subcutaneous tumor models with glycolytic and non-glycolytic PDAC cells (A) Representative photographs of immunohistochemical staining for LDHA, GLUT1, and IDH1 in each group. Scale bars, 100 μm. (B) Expression levels of LDHA, GLUT1, and IDH1, calculated by dividing the DAB intensity by the number of cells in randomly selected fields. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (C) MIA PaCa-2 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (green arrows) every other day for 3 cycles. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (D) PK-59 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (orange arrows). The upper right photographs show tumor-bearing mice in the control and OBP-702-treated groups. The lower right photographs show tumors in the mock and OBP-702 groups. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: Comparison of metabolic phenotypes and virus sensitivity in subcutaneous tumor models with glycolytic and non-glycolytic PDAC cells (A) Representative photographs of immunohistochemical staining for LDHA, GLUT1, and IDH1 in each group. Scale bars, 100 μm. (B) Expression levels of LDHA, GLUT1, and IDH1, calculated by dividing the DAB intensity by the number of cells in randomly selected fields. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (C) MIA PaCa-2 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (green arrows) every other day for 3 cycles. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (D) PK-59 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (orange arrows). The upper right photographs show tumor-bearing mice in the control and OBP-702-treated groups. The lower right photographs show tumors in the mock and OBP-702 groups. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Comparison, Virus, Immunohistochemical staining, Staining, Expressing, Control

    Investigation of the relationship between PET/CT metabolic parameters and glycolytic activity of PDAC tumors (A and B) PET/CT images of MIA PaCa-2 tumor (A) and PK-59 tumor (B). The upper left (a) shows the horizontal section, whereas the lower left (b) shows the sagittal section, and the right (c) shows the coronal section. Dotted circles indicate the tumor area. (C) Comparison of SUVmax values for MIA PaCa-2 and PK-59 tumors. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D and E) Comparison of MTV (D) and TLG (E) values for MIA PaCa-2 and PK-59 tumors at the indicated thresholds. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (F and G) Scatter diagrams demonstrating correlations between expression of LDHA (F) or GLUT1 (G) and preoperative SUVmax (left), MTV (40%) (center), and TLG (40%) (right) values in patients with PDAC ( n = 30). The statistical significance of the correlations in the scatterplots was determined using Pearson’s correlation analysis. N.S., not significant; ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: Investigation of the relationship between PET/CT metabolic parameters and glycolytic activity of PDAC tumors (A and B) PET/CT images of MIA PaCa-2 tumor (A) and PK-59 tumor (B). The upper left (a) shows the horizontal section, whereas the lower left (b) shows the sagittal section, and the right (c) shows the coronal section. Dotted circles indicate the tumor area. (C) Comparison of SUVmax values for MIA PaCa-2 and PK-59 tumors. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D and E) Comparison of MTV (D) and TLG (E) values for MIA PaCa-2 and PK-59 tumors at the indicated thresholds. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (F and G) Scatter diagrams demonstrating correlations between expression of LDHA (F) or GLUT1 (G) and preoperative SUVmax (left), MTV (40%) (center), and TLG (40%) (right) values in patients with PDAC ( n = 30). The statistical significance of the correlations in the scatterplots was determined using Pearson’s correlation analysis. N.S., not significant; ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Positron Emission Tomography-Computed Tomography, Activity Assay, Comparison, Expressing