Fig 1: In vivo activity of VLX1570 in multiple myeloma xenografts.(a) KMS-11-LUC2 cells (5 × 106) were injected intravenously into female SCID mice. After 7 days, mice were randomized into control and treatment groups (5 mice per group). Mice were treated with vehicle or VLX1570 (3 mg/kg) for 10 consecutive days. The drug was dissolved in PEG/Chremophore/Tween (50/10/40) and diluted 1:10 with saline prior to intravenous injection. Shown is survival over a 142 day period. (b) Quantification of bioluminescence measured at 18, 20, and 30 and 36 days of tumor cell injection. (c) Bioluminescence recorded in individual animals. (d) Growth of subcutaneous RPMI8226 tumors following treatment with VLX1570. Mice were exposed to VLX1570 dissolved in PEG/Chremophore/Tween (50/10/40). Mice were treated with 3 mg/kg VLX1570 for 10 consecutive days (5 mice per group). (e) Immunohistochemical staining showing decreased levels of CXCR4 in RPMI8226 tumors after exposure to 3 mg/kg VLX1570. (f) Increased immunohistochemical staining of K48-linked ubiquitin chains in RPMI8226 tumors after exposure to 3 mg/kg VLX1570. (g) Increased caspase-3 activity after exposure of RPMI8226 tumors to 3 mg/kg VLX1570.
Fig 2: Immunohistochemical analysis of CXCR4 expression in feline mammary carcinomas. Panel A. Representative primary feline carcinoma showing a high number of neoplastic cells with moderate to intense cytoplasmic positivity for CXCR4. (Bar 25 µm). Panel B. Primary tubulopapillary carcinoma: a poorly differentiated area with low number of positive neoplastic cells showing a weak immunoreactivity for CXCR4. (Bar 25 µm). Panel C. Lymph node metastasis of the feline mammary carcinoma showed in Panel B. Metastatic cells show a marked immunoreaction for CXCR4 if compared with the corresponding primary lesion. (Bar 25 µm). Original magnification 40×.
Fig 3: CXCR4 expression in primary cultures of feline mammary carcinoma. Upper panels. Representative immunofluorescence staining using anti-procollagen I (red) of fibroblast and purified feline mammary carcinoma primary cultures, after immunomagnetic fibroblast separation. DAPI-counterstained nuclei in blue. No fibroblast contamination is observed in the tumor cell cultures. Lower panel. A-B-C. Phase-contrast microscopy observation of the cultured cells derived from feline mammary gland tumours with an epithelioid morphology with some elongated spindle-shaped cells growing in monolayer (original magnification 10×) Panels D-E-F: immunofluorescence detection of CXCR4 expression (red) in primary cultures (DAPI-counterstained nuclei in blue). Original magnification 20×.
Fig 4: CXCR4 score in feline mammary carcinomas. Box plots represent the distribution of CXCR4 score in different feline mammary carcinoma histological types. A statistically significant relationship (Pearson's Chi sqr. test) was observed between the increase of CXCR4 scores from normal to benign, malignant and metastatic mammary tissues. Each box shows the median, quartiles, and extreme values within a group.
Fig 5: Immunohistochemical analysis of CXCR4 expression in normal feline mammary gland and benign lesions. Panel A. Representative photomicrograph of a normal lobule of feline mammary gland tissue showing CXCR4 negativity (Bar 50 μm, original magnification 20×). Panel B. Detail of the normal lobule of feline mammary gland tissue showing several CXCR4-negative acini, (Bar 25 μm, original magnification 40×). Panel C. Feline benign mammary lesion (basaloid adenoma, cat n. 25): epithelial cells show negative or weak immunoreaction for CXCR4 (Bar 25 μm, original magnification 40×). Panel D. Feline benign mammary lesion (complex adenoma, cat n. 26): negative immunoreaction for CXCR4. (Bar 25 μm, original magnification 40×).
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