Journal: The Journal of Cell Biology

Article Title: Autophagy gene FIP200 in neural progenitors non–cell autonomously controls differentiation by regulating microglia

doi: 10.1083/jcb.201609093

Figure Lengend Snippet: Suppression of microglia activation and infiltration rescued the defective neurogenesis in 2cKO mice. (A) The percentage of ramified, round, and amoeboid microglia per SVZ section of Ctrl, FIP cKO, 2cKO, and p53 cKO mice treated with vehicle (Veh) or minocycline (Mino; three mice each). (B–D) Number of iNOS + microglia (B), IL-6 + microglia (C), or TNF + microglia (D) per SVZ section in Ctrl, FIP cKO, 2cKO, and p53 cKO mice treated with vehicle (Veh) or minocycline (Mino; mean ± SEM; three mice each). (E–G) Number of DCX + neuroblasts (E) and GFAP + astrocytes (F) per SVZ section or the density of NeuN + neurons per olfactory bulb section (G) in Ctrl, FIP cKO, 2cKO, and p53 cKO mice treated with vehicle or minocycline are shown (mean ± SEM; three mice each). (H) Number of Iba1 + microglia per SVZ section of 2cKO mice treated with vehicle (Veh) or TAK-779 (TAK; mean ± SEM; three mice each). (I–K) Number of DCX + neuroblasts (I) and GFAP + astrocytes (K) per SVZ section or the density of NeuN + neurons per olfactory bulb section (J) in 2cKO mice treated with vehicle (Veh) or TAK-779 (TAK; mean ± SEM; three mice each). (L) Number of Iba1 + microglia per SVZ section in Ctrl, FIP cKO, 2cKO, and p53 cKO mice treated with vehicle (Veh) or PLX3397 (PLX; mean ± SEM; four mice each). (M–O) Number of DCX + neuroblasts (M) and GFAP + astrocytes (O) per SVZ section or the density of NeuN + neurons per olfactory bulb section (N) in Ctrl, FIP cKO, 2cKO, and p53 cKO mice treated with vehicle (Veh) or PLX3397 (PLX) are shown (mean ± SEM; four mice each). **, P < 0.01; ***, P < 0.001.

Article Snippet: PLX3397 (ApexBio) was dissolved in DMSO and then added immediately before using to a solution of 0.5% methyl cellulose (M0512; Sigma-Aldrich) and 1.0% Tween 80 (P1754; Sigma-Aldrich).

Techniques: Activation Assay

Journal: Breast Cancer Research : BCR

Article Title: Eph receptors in breast cancer: roles in tumor promotion and tumor suppression

doi: 10.1186/bcr2207

Figure Lengend Snippet: Therapeutic strategies targeting Eph receptors

Article Snippet: Antibody-conjugates , EphA2 , Prostate cancer, glioma , MedImmune/AstraZeneca , [ ] .

Techniques:

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Tumor cell-derived SPON2 promotes M2-polarized tumor-associated macrophage infiltration and cancer progression by activating PYK2 in CRC

doi: 10.1186/s13046-021-02108-0

Figure Lengend Snippet: Blocking M2 polarization of TAMs and Macrophage depletion inhibited the SPON2-induced tumors growth and invasion. a Gross images of MC38/Vector + PBS, MC38/SPON2 + PBS and MC38/SPON2 + IL10 subcutaneous tumor. b Growth curve in the different treatment groups. Two-way ANOVA test, * p < 0.05, ** p < 0.01. c Anti-IL10 neutralizing antibody treatment time diagram and fold change of tumor volume in each case (final volume / initiate volume). d Hematoxylin and eosin (H&E) staining shows the histology of subcutaneous tumor tissues. IHC shows tumor cells with SPON2 expression. The arrows indicated the tumor invasion. Scale bar, 50 μm. e Flow cytometric quantification showing percentages M2-TAMs of all CD45 + cells in subcutaneous tumors, ** p < 0.01. f Gross images of MC38/Vector and MC38/SPON2 subcutaneous tumors in C57BL/6 mice treated with BLZ945 or isotope control (DMSO). g Tumor growth curve in the different treatment groups. Two-way ANOVA test, **** p < 0.0001. h BLZ945 treatment time diagram and fold change of tumor volume in each case (final volume / initiate volume). i Tumor weights of mice in the different treatment groups at the end point. * p < 0.05. j Hematoxylin and eosin (H&E) staining shows the histology of subcutaneous tumor tissues. IHC shows tumor cells with SPON2 expression. The arrows indicated the tumor invasion. Scale bars, 50 μm. k Flow cytometric quantification showing the effect of SPON2 on the infiltration of M2-TAMs upon BLZ945 treatment. ** p < 0.01

Article Snippet: A CSF1R-specific inhibitor (BLZ945) (T6119, TOPSCIENCE) and DMSO control were administered on days 6, 7, 8, 9, 10, 11 and 12 after tumor inoculation through intragastric administration at a dosage of 200 mg/kg.

Techniques: Blocking Assay, Plasmid Preparation, Staining, Expressing, Control

Journal: Frontiers in Immunology

Article Title: Emerging macrophage-based therapies for cancer: a review of preclinical and clinical advances

doi: 10.3389/fimmu.2025.1679271

Figure Lengend Snippet: Overview of eight therapeutic strategies for targeting tumor-associated macrophages in the tumor microenvironment. Clinical status: CD47–SIRPα (magrolimab, evorpacept and others in trials) , TREM2 (PY314 ± pembrolizumab, Ph1) , LILRB2 (IO-108, Ph1) , PI3Kγ modulators (eganelisib/IPI-549 in Ph1/2 combos) , TLR agonists (e.g., imiquimod approved for sBCC; TLR9 agonist tilsotolimod tested in Ph3 melanoma) , CSF1R inhibitors (emactuzumab and others in trials; pexidartinib approved for tenosynovial giant cell tumor, TGCT) , CAR-macrophages (FIH Ph1 CT-0508) and cross-talk with T/NK cells (mechanistic outcome of CAR-M) , HDAC inhibitors (resminostat in Ph1/2 solid tumor trials ), and DNA methyltransferase inhibitors have human oncology trials; CD24–Siglec-10 (oncology use largely preclinical; CD24Fc tested in non-oncology) ( , ), macrophage-engaging bispecifics , IL-12/STING nanoparticles (STING and IL-12 have clinical trials, but NP-loaded macrophage-targeted formats remain preclinical) , TAM-depleting CAR-T , macrophage-derived EVs , MDCs , most TAM-directed RNA [except saRNA MTL-CEBPA ], and trained immunity induction remain preclinical. Picture created using BioRender.

Article Snippet: CSF1R inhibitor (SM) , Vimseltinib (Romvimza) / Deciphera , TGCT (diffuse/locally advanced, not resectable) , Ph3 MOTION - FDA-approved (14 Feb 2025) , Oral small-molecule, systemic , Monotherapy , Met ORR primary endpoint; QoL 2 benefits , Approved (US).

Techniques: Clinical Proteomics, Derivative Assay