23 research outputs found

    C6 tumour growth is slowed by MLN0518 treatment.

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    <p>The growth rate of tumours in mice treated with 20 mg/kg MLN0518 was significantly slower than tumours in vehicle treated mice over 10 days. Tumour doubling times were calculated on an individual tumour basis (n = 15 per treatment group). Mean ±1s.e.m.</p

    Summary of the quantitative MRI biomarkers acquired from intrinsic susceptibility MRI of C6 xenografts in mice treated with vehicle or 20 mg/kg MLN0518 for 10 days.

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    <p>Mean of median R<sub>2</sub>* and ΔR<sub>2</sub>* values from each tumour ± 1s.e.m. (n≥5 per treatment group). The proportion of voxels in which R<sub>2</sub>* changed significantly, either negatively (ΔR<sub>2</sub>* <0) or positively (ΔR<sub>2</sub>* >0), with carbogen breathing are also shown.</p

    Diffusion-weighted and susceptibility contrast MRI of C6 tumours treated with MLN0518.

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    <p>Parametric maps of apparent diffusion coefficient (ADC, top panel), fractional blood volume (fBV, middle panel) and vessel size index (R<sub>v</sub>, bottom panel) from C6 xenografts in mice treated with vehicle or 20 mg/kg MLN0518 for 10 days show no clear differences between vehicle and treated tumours. Representative maps are shown.</p

    Dynamic contrast-enhanced MRI is sensitive to the response of C6 tumours to MLN0518.

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    <p>Representative parametric maps and quantification of initial area under the gadolinium concentration curve (IAUGC) demonstrate a reduction in tumour blood vessel permeability/flow in mice treated with 20 mg/kg MLN0518 for 3 days compared to controls. Mean parameter values from each tumour ± 1s.e.m. (n≥6 per treatment group), * p<0.05.</p

    Histological assessment of tumour response to MLN0518.

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    <p><b>A.</b> Tumour sections stained for the perfusion marker Hoechst 33342 (blue), endothelial marker CD31 (red) and pimonidazole adduct formation, a marker of hypoxia (green) demonstrate that the hypoxic area was lower in tumours treated with 20 mg/kg MLN0518 for 10 days than vehicle treated controls. The percentage of the total vessels perfused and the overall perfused vessel area was also lower in treated versus control tumours. Representative composite images are shown. <b>B.</b> Alpha smooth muscle actin (α-SMA) immunohistochemistry demonstrates a significant reduction in α-SMA positive blood vessels in MLN0518 treated tumours compared to controls. Magnification ×200.</p

    Gradient calibration protocol flowchart.

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    <p>Flowchart detailing the processes involved in the protocol and the order in which they should be implemented. The two major subdivisions of the technique are the system calibration (a) and the post-processing correction (b). Expected image deformations are illustrated using schematics.</p

    3D grid phantom design.

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    <p>CAD drawing of phantom sections and photograph of the assembled phantom, which was created using 3D printing. To assemble, the grid section (a) was inserted into the outer chamber (b) which was sealed by the chamber cap (c). It can then be filled through the s-bend (d) and sealed using a cap (e). An irregular prism (f) in the centre of the grid structure aids in the orientation of images.</p

    CT and MRI images of phantom.

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    <p>Axial (a) and coronal (b) slices from CT data and corresponding axial (c) and coronal (d) slices from 3D gradient echo MRI data. Landmarks for distance measurements are shown (b) for Z axis (red) and Y axis (blue) (landmarks in X axis are orthogonal to those in the Y axis at same Z coordinates).</p

    Displacement fields generated from post-processing correction.

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    <p>Projection along the X axis from CT phantom data (white) overlaid on MRI images (filler inside phantom shown in green, phantom structure shown in black) show good alignment after post-processing correction (a). Displacement fields generated from the non-rigid registration show displacements increase along the Z axis (b) as distance from the centre increases. This is also observed in the X (c) and Y (d) axes for central slices. Slices taken further from the centre show the displacements in the X (e) and Y (f) directions increase more rapidly with distance from the slice centre.</p

    CD138 expression changes in response to therapy.

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    <p><b>A.</b> Percentage of CD138<sup>+</sup> human myeloma cells measured by flow cytometry in bone aspirates of mice (n = 3), showing a significantly lower percentage of positive cells in both tibias and spine of mice in the two treatment groups than in untreated mice (p<0.05, 2-way ANOVA with Bonferroni post-test). No CD138<sup>+</sup> cells were observed in the organs of any of the mice. <b>B.</b> Histological analysis of sections from the tibias of mice from each group showed distinct differences. (i) Sections from healthy mice displayed classical architecture, with no CD138<sup>+</sup> cells. (ii) In comparison, sections from untreated myeloma mice showed a high infiltration of CD138<sup>+</sup> cells with loss of normal architecture. (iii) Treatment of mice with BZB resulted in the return of normal architecture and loss of CD138<sup>+</sup> cells. (iv) A similar result was observed in mice treated with tosedostat, but with occasional scattered CD138<sup>+</sup> cells.</p
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