Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: The TME of recurrent gliomas accepting radiotherapy (A) Workflow of bulk RNA-seq analysis for glioma tissues. (B) A total of 201 DEGs were identified by RNA-seq, including 171 up-regulated and 30 down-regulated genes. Data were presented as the value of Log 2 FC and q value. (C) The 201 DEGs were classified into different biological pathways based on Reactome annotation. (D) ss-GSEA analysis showing correlations between the expression of 26 immune-related DEGs and immune cell infiltration. (E) Histogram showing the fold change of the 26 immune-related DEGs. Data were presented as the value of log 2 FC. (F) The mRNA level of selected immune-related DEGs in glioma tissues. Data were presented as mean ± SD. (unpaired t test, ∗ p < 0.05, ∗∗ p < 0.01). (G) Relative fold-change of MARCO, CD163, and CD47. Data were presented as the value of log 2 FC (unpaired t test). Data were obtained from 5 primary glioma tissues, 4 recurrent glioma tissues after radiotherapy (A and B). Data were from 4 primary glioma tissues and 4 recurrent glioma tissues after radiotherapy (F).

Article Snippet: GL261 , DSMZ , ACC-802.

Techniques: RNA Sequencing, Analysis, Expressing, Immune Cell

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: Increased M2-TAMs suggest poor prognosis in recurrent glioma patients (A) Representative images of IHC staining of IBA1, CD68, CD163, and iNOS in paired primary and recurrent glioma samples accepting radiotherapy. Scale bars: 200 μm and 100 μm (enlarged view). (B–E) Quantification of IHC results in (A). The percent of IBA1 (B), CD68 (C), CD163 (D) positive cells and the integral optical density of iNOS (E) in glioma samples accepting radiotherapy. Data were presented as paired individual-value (two-tailed paired t test, ∗ p < 0.05, ∗∗ p < 0.01). (F) Representative images of IHC staining of IBA1, CD68, CD163, and iNOS in paired primary and recurrent glioma samples without radiotherapy. Scale bars: 200 μm and 100 μm (enlarged view). (G–J) Quantification of IHC results in (F). The percent of IBA1 (G), CD68 (H), CD163 (I) positive cells and the integral optical density of iNOS (J) in glioma samples without radiotherapy. Data were presented as paired individual value (two-tailed paired t test). (K–N) The correlation between tumor volume doubling time and the level of IBA1 (K), CD68 (L), CD163 (M), iNOS (N). Data were presented as Pearson correlation coefficient. (O–R) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of IBA1 (O), CD68 (P), CD163 (Q), and iNOS (R). Data were presented as median ± 95% confidence intervals (∗ p < 0.05, ∗∗ p < 0.01). Data were obtained from 14 paired primary glioma and recurrent glioma with radiotherapy (B, K, and O), 15 paired primary glioma and recurrent glioma with radiotherapy (C–E, L–N, and P–R), and 8 paired primary glioma and recurrent glioma without radiotherapy (G–J).

Article Snippet: GL261 , DSMZ , ACC-802.

Techniques: Immunohistochemistry, Two Tailed Test, Expressing

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 may be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).

Article Snippet: GL261 , DSMZ , ACC-802.

Techniques: Analysis, Immunohistochemistry, Irradiation, Two Tailed Test, Expressing

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 does not mediate glioma cell proliferation following radiotherapy in vitro (A) Viability of GBM cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 1.9, p = 0.21, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative images of colony formation assay after CCL-18 (100 ng/mL) treatment. (C) Quantitative results from (B). Data were presented as mean ± SD (unpaired t test, ∗∗∗ p < 0.001). (D) Schematic workflow for the co-culture experiment. (E) Representative images of colony formation assay. (F) Quantitative results from (E). Data were presented as mean ± SD (unpaired t test, ∗ p < 0.05). (G) The mRNA level of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. Data were presented as mean ± SEM (unpaired t test, ∗∗∗ p < 0.001). (H) Representative immunoblot of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. (I) Quantitative results from (H). Data were presented as mean ± SEM (unpaired t test, ∗ p < 0.05, ∗∗ p < 0.01). (J) Immunoblot of CCR8 after overexpression. (K) Representative images of colony formation assay on irradiated GBM cells after CCL-18 (100 ng/mL) treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (two-way ANOVA, F = 4.9, p = 0.06, ∗ p < 0.05, ∗∗ p < 0.01). Data were obtained from 3 independent experiments (A–L).

Article Snippet: GL261 , DSMZ , ACC-802.

Techniques: In Vitro, Colony Assay, Co-culture Assay, Irradiation, Western Blot, Over Expression

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of ACP5, Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).

Article Snippet: GL261 , DSMZ , ACC-802.

Techniques: In Vivo, Western Blot, Derivative Assay

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet:

Article Snippet: GL261 , DSMZ , ACC-802.

Techniques: Cell-Signaling, Virus, Tissue, Microarray, Recombinant, cDNA Synthesis, Enzyme-linked Immunosorbent Assay, Software, Biomarker Discovery, In Vivo Imaging

Journal: Blood Advances

Article Title: Distinct epitope engagement confers differential activity of linvoseltamab vs teclistamab across BCMA mutations ∗

doi: 10.1182/bloodadvances.2026020381

Figure Lengend Snippet: Effect of BCMA mutations on T-cell–mediated cytotoxicity against HEK293h/CD20 cells treated with linvoseltamab and teclistamab. HEK293 or OPM-2 myeloma cells were incubated for 3 days with isolated human T cells, with E:T of 12.5 (HEK293) and 5 (OPM-2). Target cell survival was determined by flow cytometry. Percentage survival was normalized to untreated cells. The OPM-2 cell line was used as a comparator because this is an MM cell line that endogenously expresses BCMA. E:T, effector-to-target ratio.

Article Snippet: T-cell‒mediated cytotoxicity was evaluated by flow cytometry in target HEK293/hCD20 cells (with WT BCMA or mutated BCMA) and OPM-2 cells (human MM BCMA-expressing cell line; DSMZ ACC 50).

Techniques: Incubation, Isolation, Flow Cytometry

Journal: Blood Advances

Article Title: Distinct epitope engagement confers differential activity of linvoseltamab vs teclistamab across BCMA mutations ∗

doi: 10.1182/bloodadvances.2026020381

Figure Lengend Snippet: Effect of BCMA-binding interface mutations on primary T-cell activation by linvoseltamab and teclistamab. HEK293 or OPM-2 myeloma cells were incubated for 3 days with isolated human T cells, with E:T of 12.5 (HEK293) and 5 (OPM-2). T-cell activation was determined by flow cytometry based on the percentage of CD8 + T cells expressing CD25. The OPM-2 cell line was used as a comparator because this is an MM cell line that endogenously expresses BCMA.

Article Snippet: T-cell‒mediated cytotoxicity was evaluated by flow cytometry in target HEK293/hCD20 cells (with WT BCMA or mutated BCMA) and OPM-2 cells (human MM BCMA-expressing cell line; DSMZ ACC 50).

Techniques: Binding Assay, Activation Assay, Incubation, Isolation, Flow Cytometry, Expressing

Journal: Chemmedchem

Article Title: Scaffold Hopping Provides Liver X Receptor Agonist With Preference for the β Subtype

doi: 10.1002/cmdc.70509

Figure Lengend Snippet: In vitro characterization of the optimized LXR agonist 7 . (a) Full‐length LXR reporter gene assay in HEK293T cells. N ≥ 3. (b) Quantification of LXR target genes in HepG2 cells. Both 2 and ( S )‐ 7 robustly induced expression of target genes involved in cholesterol metabolism (ABCA1, ABCG1) and DNL (FAS, SREBP1c). Data are the mean ± SEM of N = 4; ** p < 0.01, *** p < 0.001 (ANOVA with post hoc Bonferroni test against 0.1% DMSO or as indicated by the bars). Full agonist T0901317 ( 32 ) was tested for comparison. (c,d) Lipogenesis assay. Incubation of HepG2 cells with pan LXR full agonist T0901317 ( 32 ) for 72 h led to a substantial accumulation of lipids that were stained with Oil Red O. In comparison to 32 , both the parent compound 2 and ( S )‐ 7 displayed less lipogenic potential. Data are the mean ± SEM of N = 3; * p < 0.05, ** p < 0.01, *** p < 0.001 (one‐sided t ‐test against 0.1% DMSO). The images shown in (d) are representative details from the full images that can be found in Figure S3. (e) In a cytotoxicity assay, 2 and ( rac )‐ 7 did not influence the metabolic activity of HepG2 cells but induced cytotoxicity to HEK293T cells in the micromolar concentration region. While these concentrations are well above the EC 50 value of ( S )‐ 7 in the Gal4 reporter gene assay (red dashed line), compound 2 showed partially toxic effects at its EC 50 value (green dashed line). (f) Metabolic stability of 2 and ( rac )‐ 7 in rat liver microsomes. After 60 min, ( rac )‐ 7 was almost recovered completely, whereas approximately half of 2 had been metabolized. 7‐Ethoxycoumarine (7‐EC) served as internal standard. Data are the mean ± SEM of N = 3.

Article Snippet: HEK293T and HepG2 cells (German Collection of Microorganisms and Cell Cultures, DSMZ) were grown in Dulbecco's modified Eagle's medium (DMEM) high glucose supplemented with 10% fetal bovine serum (FBS), sodium pyruvate (1 mM), penicillin (100 U/mL), and streptomycin (100 μg/mL) at 37 °C and 5% CO 2 .

Techniques: In Vitro, Reporter Gene Assay, Expressing, Comparison, Incubation, Staining, Cytotoxicity Assay, Activity Assay, Concentration Assay, Stability