adult male nsgs mice (nod-scid; il2rγ null; tg(il3, csf2, kitl)  (Jackson Laboratory)

Journal: Blood Neoplasia

Article Title: Activity of STAMP inhibitors in ABL2 rearranged acute lymphoblastic leukemia is dependent on the Abl2 SH3 domain

doi: 10.1016/j.bneo.2025.100109

Figure Lengend Snippet: Asciminib reduces the leukemic burden and improves survival outcomes in vivo. NSG (NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ) mice injected with patient cells that harbored the ZC3HAV1 :: ABL2 fusion gene were treated with vehicle control (blue curves) or asciminib (red curves). (A) The leukemic burden was evaluated by tracking hCD45 + cells in the peripheral blood. Each line represents an individual mouse. The treatment window is depicted in grey. (B) Kaplan-Meier curves of the control mice (n = 7) and asciminib-treated mice (n = 8) (30 mg/kg per day). ∗∗∗ P = .0003. Statistical significance was measured using the log-rank test. (C) Spleen and (D) liver weights from the control and asciminib-treated mice at the experimental end point. Student t tests were used to determine significance. ∗ P < .05; ∗∗∗ P < .001. (E) Representative hematoxylin and eosin stains of BM, spleen, and liver sections. Images were analyzed using CaseViewer Software (version 2.2 RTM).

Article Snippet: Female, 6-week-old NOD.Cg-Prkdc scid Il2rg tm1Wjl /SzJ (NSG) mice (The Jackson Laboratory, Bar Harbor, ME) were subcutaneously injected with 0.1 mg/mL enrofloxacin (Baytril; Bayer, Leverkusen, Germany) in 0.9% sodium chloride per 10 g of body weight 3 days before sublethal gamma irradiation at 200 cGy.

Techniques: In Vivo, Injection, Control, Software

Journal: Molecular Cancer

Article Title: CircABCA1 promotes ccRCC by reprogramming cholesterol metabolism and facilitating M2 macrophage polarization through IGF2BP3-mediated stabilization of SCARB1 mRNA

doi: 10.1186/s12943-025-02398-4

Figure Lengend Snippet: Upregulated circABCA1 correlates with clinicopathological characteristics, regulates the viability and migration of ccRCC, and maintains the high CHO level in ccRCC. A , B RT-qPCR were utilized to detect circABCA1 expression in adjacent or ccRCC tissue. C - F RT-qPCR were utilized to detect circABCA1 expression in C different WHO/ISUP stages (I + II [ n = 114] vs. III + IV [ n = 40)]), D Tumor stages (T1a–T1b [ n = 130] vs. T2–T4 [ n = 24]), E distant metastases (No [ n = 145] vs. Yes [ n = 9]) and F Ki67 level (Ki67 < 10% [ n = 74] vs. Ki67 ≥ 10% [ n = 44]). G - I CCK-8 and colony formation rescue assay were performed to detect the cell viability activity; Transwell assays were performed in Caki-1 and 786-O cells to detect the cell migration activity after treatment with si-circABCA1. Scale bar = 50 μm. J RNA-seq of cells with circABCA1 knockdown and Gene Ontology (GO) analysis of differential expression genes was conducted. K Representative photographs of ccRCC cells treated with si-circABCA1 for 24 h. L The total-cholesterol (T-CHO) level was detected in Caki-1 or 786-O cells after the overexpression of circABCA1 or interference of circABCA1. M T-CHO level was detected in Caki-1 or 786-O cells treated with MβCD and ov-circABCA1. N The triglyceride (TG) level was detected in Caki-1 or 786-O cells after the overexpression of circABCA1 or interference of circABCA1. NS means P ≥ 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. All Data were presented as mean ± SD. Student’s t-test, n = 3

Article Snippet: For the assessment of in vivo tumorigenesis and metastasis, NSG mice (4 weeks of age, 12–14 g) bearing subcutaneous tumors of 786-O and Caki-1 cells were sourced from the Shanghai Model Organisms Center.

Techniques: Migration, Quantitative RT-PCR, Expressing, CCK-8 Assay, Rescue Assay, Activity Assay, RNA Sequencing, Knockdown, Quantitative Proteomics, Over Expression