Journal: bioRxiv

Article Title: Radioligand therapy in combination with CAR T cells overcomes the heterogeneous immunosuppressive prostate tumor microenvironment

doi: 10.64898/2026.07.02.736191

Figure Lengend Snippet: ( a ) Summary of PSMA and PSCA expression in prostate cancer PDX from the MURAL collection. Cx, sublines in castrated mice. ( b-c ) Representative IHC staining of PSCA ( b ) and PSMA ( c ) in selected PDX models, organized from top to bottom based on PSCA expression levels (high, low, and negative). Scale bar, 100 µm. ( d-e ) Transcriptomic expression levels of FOLH1 (PSMA) and PSCA from public datasets (HuPSA).

Article Snippet: For antigen expression, antibodies used include: APC anti-human PSMA (clone REA408/LNI-17, Miltenyi Biotec/Biolegend) and anti-human PSCA (clone 1G8, UCLA), followed by PE goat anti-mouse secondary antibody (BD Biosciences).

Techniques: Expressing, Immunohistochemistry

Journal: bioRxiv

Article Title: Radioligand therapy in combination with CAR T cells overcomes the heterogeneous immunosuppressive prostate tumor microenvironment

doi: 10.64898/2026.07.02.736191

Figure Lengend Snippet: ( a ) Schematic of tumor injection and treatment schedule in hPSCA-KI C57BL/6J mice bearing antigen-heterogeneous subcutaneous prostate tumors. s.c. subcutaneous; i.v., intravenous. RM9-PSMA-ffLuc and RM9-PSCA-ffLuc were mixed prior to tumor injection, and 1.5 × 10 6 total cells were engrafted into the left flank. On day 5 post-tumor injection, mice received Lu-177 RLT (74 MBq, i.v.), followed by Cy (100 mg/kg, i.p.) on day 8, and CAR T cells (PSCA-CAR, non-targeting TAG72-CAR control, or PSMA-CAR positive control, 1 × 10 6 , i.v.). The positive control group received 2 × 10⁶ total CAR T cells (1 × 10⁶ of each CAR). Blood samples were collected on day 9 (prior to CAR T cell infusion) and day 18 (tumor regression phase) for CBC analysis (n = 3 per group). ( b ) Individual tumor growth curves. Tumor volume was measured by caliper twice weekly until the survival endpoint (n = 9 for RLT + Cy + PSCA-CAR/TAG72-CAR; n = 6 for RLT + PSCA-CAR and Cy + PSMA-CAR + PSCA-CAR; n = 4 for PSCA-CAR, RLT + PSCA-CAR, and Cy + TAG72-CAR; and n = 3 for RLT + TAG72-CAR). ( c ) Kaplan-Meier survival curves for each treatment group. P-value is calculated using multiple comparisons with Holm-Šídák’s correction. ( d ) Body weight changes over time, normalized to baseline (day 5, prior to RLT). Data are presented as mean ± SEM. ( e-h ) Hematologic analysis by CBC, including white blood cells (WBCs, e ), lymphocytes ( f ), red blood cells (RBCs, g ), and platelets (PLTs, h ) from each group (n = 3 per group). Controls include tumor-bearing untreated (UT) mice at day 9, and tumor-naïve mice at day 18. Data are presented as mean ± SEM. Statistical significance was assessed using two-way ANOVA, followed by Tukey’s multiple comparison test.

Article Snippet: For antigen expression, antibodies used include: APC anti-human PSMA (clone REA408/LNI-17, Miltenyi Biotec/Biolegend) and anti-human PSCA (clone 1G8, UCLA), followed by PE goat anti-mouse secondary antibody (BD Biosciences).

Techniques: Injection, Control, Positive Control, Comparison

Journal: medRxiv

Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

doi: 10.64898/2026.03.18.26348533

Figure Lengend Snippet: Composite images of α-bungarotoxin (red) targeting postsynaptic neuromuscular junctions (i.e., motor endplates), anti-neurofilament H (purple) targeting the axonal cytoskeletons, and anti-GCPII (green) demonstrating muscle innervation after nerve transection with or without repair; arrowheads emphasize axons. (A) Healthy muscle after sham surgery demonstrating a normal innervated neuromuscular junction with surrounding GCPII expression. Contrast this with the appearance of neuromuscular junctions at (B) 4 weeks, (C) 8 weeks, and (D) 16 weeks after sciatic nerve transection with repair; note progressive flattening and fragmentation of endplates consistent with chronic denervation, the absence of axons, and lack of GCPII expression. Nerve transection with immediate repair demonstrates infiltration of axons and neuromuscular junction reinnervation between (E) 4 weeks and (F) 8 weeks. Also note recovery of GCPII expression near the reinnervated neuromuscular junction, which persists at (G) 16 weeks after nerve repair. Panels are 20× magnification, scale bar: 20 μm.

Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

Techniques: Expressing

Journal: medRxiv

Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

doi: 10.64898/2026.03.18.26348533

Figure Lengend Snippet: Images of anti-GCPII (green), anti-cytochrome C (red) targeting mitochondria, and DAPI (blue) targeting nuclei at 12 weeks after nerve transection with or without repair. White boxes around key area of each image. Panel D (sham surgery) is a composite of Panels A-C; Panel H (sciatic nerve transection without repair) is a composite of Panels E-G; Panel L (nerve transection with repair) is a composite of Panels I-K. Note localization of GCPII staining near clusters of subsarcolemmal mitochondria overlying myocyte nuclei, irrespective of denervation. A similar staining pattern was present at all tested timepoints between two and 16 weeks after nerve transection with or without repair. Panels are 63× magnification, scale bar: 10 μm.

Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

Techniques: Staining

Journal: medRxiv

Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

doi: 10.64898/2026.03.18.26348533

Figure Lengend Snippet: (A) Representative Western blot and corresponding densitometric analysis (n=2–3 per group) show increased GCPII band intensity in denervated samples at 2-, 8-, 12-, and 24-weeks post-denervation, compared to low baseline expression in naïve muscle (i.e., control). Band intensities were normalized to denervation-duration-matched controls and plotted as relative expression. Statistical analysis was not performed due to the limited sample size. (B) GCPII enzymatic assay demonstrating significantly increased GCPII activity at 8-, 12-, and 24-week timepoints. Activity is expressed in femtomoles of N-acetyl-aspartyl-glutamate (NAAG) hydrolysis per mg GCPII per hour (fmol/mg/h).

Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

Techniques: Western Blot, Expressing, Control, Enzymatic Assay, Activity Assay

Journal: medRxiv

Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

doi: 10.64898/2026.03.18.26348533

Figure Lengend Snippet: (A) Mean gastrocnemius muscle uptake administration 2, 4, and 16 weeks after injury. White: sham surgery (uninjured nerve); Gray: repaired nerve; Black: unrepaired nerve; n = 5-6 per group per timepoint. Note persistent muscle uptake in the unrepaired group over time (B) Tissue [ 18 F]DCFPyL uptake after blocking GCPII binding with ZJ-43 coadministration; White: sham surgery (uninjured nerve), pooled across all timepoints; Gray: unrepaired nerve, pooled across all timepoints; Black: ZJ-43 co-administration, 4 weeks after sciatic nerve transection without repair. One outlier in biceps muscle unrepaired group (1.2 % ID/g) was excluded in the plot for improved visibility of remaining data; the outlier was included in statistical comparisons. Groupwise comparisons performed using Kruskal-Wallis test. %ID/g: percent injected dose per gram.

Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

Techniques: Blocking Assay, Binding Assay, Injection