Journal: Molecular Therapy Oncology

Article Title: AAV immuno-gene therapy platform delivering vectorized cytokines defines a new modality for high-grade glioma treatment

doi: 10.1016/j.omton.2026.201183

Figure Lengend Snippet: The standard GL261 syngeneic GBM model fails to recapitulate interferon responses due to species-specific differences (A) Schematic of the syngeneic allograft study in immunocompetent C57BL/6J mice orthotopically engrafted with GL261-FL cells and treated intratumorally via CED with saline, AAV9-GFP (2E11 vg/brain), or AAV9-mIFNβ (2E11 vg/brain). (B) Longitudinal BLI of FLuc+ tumor growth in mice treated as in (A). Saline = black, AAV9-GFP = green, AAV9-mIFNβ = orange. Thin lines = individual mice, thick lines = geometric mean. Vertical dashed line = day of treatment (day 5). n = 45 (15 per arm). (C) Kaplan-Meier survival curves for treated mice from (B). p = 0.05 by log-rank (Mantel-Cox) test for AAV9-mIFNβ vs. AAV9-GFP. (D) UMAP of single-cell RNA-seq profiles from brains of mice treated with saline, AAV9-GFP, or AAV9-mIFNβ, colored by cell type (left) and treatment type (right). (E) Differential gene expression analysis (DESeq2) of tumor cells from AAV9-mIFNβ-treated vs. AAV9-GFP-treated mice. Red = p -Adj<0.01, gray = p -Adj>0.01. (F) Differentially expressed genes in mouse PBMCs treated with mIFNβ vs. media control (left), human PBMCs treated with hIFNβ vs. media control (middle), and mouse PBMCs treated with hIFNβ vs. media control (right). Significantly differentially expressed genes ( p -Adj<0.01) = red, with select genes labeled. (G) Venn diagrams showing minimal overlap of significantly upregulated (left) and downregulated (right) genes between mouse and human PBMCs treated with species-matched IFNβ. (H) Concordance plot comparing fold change responses to species-matched IFNβ in mouse vs. human PBMCs reveals no correlation (R 2 = 0.012), indicating that interferon responses are strongly species specific.

Article Snippet: Human PBMCs were treated with either recombinant human IFNβ (PBL Cat#11415-1) or media control and placed in an incubator (37°C, 5% CO 2 , with saturating humidity) for 24 ± 1 h. Mouse PBMCs were treated with recombinant mouse IFNβ (PBL Cat#12405-1 Lot:7573R), recombinant human IFNβ, or media control and placed in an incubator (37°C, 5% CO 2 , with saturating humidity) for 24 ± 1 h. At the time of collection, plates were spun in a swinging bucket rotor centrifuge (350 × g , 5 min).

Techniques: Saline, Single Cell, RNA Sequencing, Gene Expression, Control, Labeling

Journal: Frontiers in Immunology

Article Title: Reorganization and functional divergence of the CD4+ memory T cell compartment in hidradenitis suppurativa

doi: 10.3389/fimmu.2026.1831664

Figure Lengend Snippet: Expansion of central memory T cells (T CM ) in HS skin. Flow cytometric analysis of total CD4+ and CD8+ T cell subsets in (A) the skin and (B) peripheral blood. Frequency of naïve and memory subsets within the CD4+ and CD8+ compartments are shown for (C) skin and (D) peripheral blood. Each dot represents an individual donor (Healthy, diamonds; HS, circles); bars indicate the mean frequency of the population relative to the indicated gate ± standard deviation (SD). Healthy PBMCs, n = 8; Healthy skin, n = 5; HS skin and PBMCs matched samples ( n = 5). Detailed gating strategies for T cell memory subsets (Naïve, T CM , T EM and T RM ) are provided in Supplementary Figure 1 . * P < 0.05, ** P < 0.01 and *** P < 0.001 (Two-way ANOVA with Šídák’s multiple comparisons test).

Article Snippet: Peripheral blood mononuclear cells (PBMCs) from blood were isolated with StraightFrom ® Whole Blood PBMC Isolation Kit, human (130-126-359, Miltenyi Biotec), and resuspended in the same culture medium as skin cells.

Techniques: Standard Deviation

Journal: Frontiers in Immunology

Article Title: Reorganization and functional divergence of the CD4+ memory T cell compartment in hidradenitis suppurativa

doi: 10.3389/fimmu.2026.1831664

Figure Lengend Snippet: Heightened pro-inflammatory potential of skin vs peripheral blood CD4+ memory T cells. Frequencies of cytokine-expressing memory T cell subsets from matched skin and PBMC samples ( n = 4). Bars represent the mean percentage (± SD) of cytokine-expressing memory T cells vs parent, under unstimulated baseline conditions (“Unstim”, blue bars/circles) and following stimulation with anti-CD3/anti-CD28 coated beads (“aCD3/aCD28”, red bars/triangles). Data are shown for TNF-α-producing CD4+ T EM (A) and T CM (D) cells, IFN-γ-producing CD4+ T EM (B) and T CM (E) , IL-17A-producing CD4+ T EM (C) and T CM (F) . Statistical differences between skin and PBMCs and stimulation condition were evaluated by 2-way repeated measures ANOVA and Fisher’s LSD test (* P < 0.05 and ** P < 0.01).

Article Snippet: Peripheral blood mononuclear cells (PBMCs) from blood were isolated with StraightFrom ® Whole Blood PBMC Isolation Kit, human (130-126-359, Miltenyi Biotec), and resuspended in the same culture medium as skin cells.

Techniques: Expressing

Journal: Journal of Medicinal Chemistry

Article Title: Biocompatible Glycoconjugation Enables Sensitive In Vivo Cell Tracking by PET/CT

doi: 10.1021/acs.jmedchem.6c00538

Figure Lengend Snippet: Region of Interest (ROI) analysis of PET/CT imaging. A) [ 89 Zr]­Zr–U937 cells. B) [ 89 Zr]­Zr-PBMCs. C) [ 89 Zr]­Zr-NHP-Neutrophils. D) [ 89 Zr]­Zr-NHP-T cells.

Article Snippet: Human primary nonmobilized PBMCs were obtained from healthy donor peripheral blood using an institutional review board (IRB)-approved protocol (2017–0170) and isolated using the MACSprep PBMC Isolation Kit (Miltenyi Biotec, San Jose, CA) without density gradient centrifugation.

Techniques: Positron Emission Tomography-Computed Tomography, Imaging

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

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

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

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

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

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

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