A semiautomatic lesion segmentation and histogram analysis approach can provide a significant reduction in interobserver variability for DCE MR imaging measurements of K(trans) when compared with manual ROI methods, whereas intraobserver reproducibility is improved to some extent.

Current methods of assessing tumor response at skeletal sites with metastatic disease use a combination of imaging tests, serum and urine biochemical markers, and symptoms assessment. These methods do not always enable the positive assessment of therapeutic benefit to be made but instead provide an evaluation of progression, which then guides therapy decisions in the clinic. Functional imaging techniques such as whole-body diffusion magnetic resonance imaging (MRI) when combined with anatomic imaging and other emerging "wet" biomarkers can improve the classification of therapy response in patients with metastatic bone disease. A range of imaging findings can be seen in the clinic depending on the type of therapy and duration of treatment. Successful response to systemic therapy is usually depicted by reductions in signal intensity accompanied by apparent diffusion coefficient (ADC) increases. Rarer patterns of successful treatment include no changes in signal intensity accompanying increases in ADC values (T2 shine-through pattern) or reductions in signal intensity without ADC value changes. Progressive disease results in increases in extent/intensity of disease on high b-value images with variable ADC changes. Diffusion MRI therapy response criteria need to be developed and tested in prospective studies in order to address current, unmet clinical and pharmaceutical needs for reliable measures of tumor response in metastatic bone disease.

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These preliminary results suggest that the determination of kep of high K(trans) area permits the noninvasive estimation of tumor angiogenesis in rectal cancer and that DCE-MRI parameters can be used as imaging biomarkers to predict the biologic aggressiveness of the tumor and patient prognosis.

Purpose:To assess vascular remodeling in tumors during two different antiangiogenic therapies with dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and vessel size imaging and to evaluate the vessel size index (VSI) as a novel biomarker of therapy response. Materials and Methods:In two independent experiments, nude mice bearing human skin squamous cell carcinoma xenografts were treated with a vascular endothelial growth factor (VEGF) inhibitor (bevacizumab) or a multitargeted tyrosine kinase inhibitor (SU11248). Changes in tumor vascularity were assessed by DCE-MRI and vessel size imaging. DCE-MRI data were analyzed applying a two-compartment model (Brix), calculating the parameters Amplitude and k ep . Results:For both experiments Amplitude decreased significantly in treated tumors while k ep did not change significantly. VSI showed controversial results. VSI was significantly increased in SU11248-treated A431 tumors, whereas no changes were found in bevacizumab-treated HaCaT-ras-A-5RT3 tumors. Immunohistology confirmed these results and suggest differences in the maturation of tumor vascularization as a possible explanation.Conclusion: DCE-MRI and vessel size imaging provide reliable and supplementing biomarkers of antiangiogenic therapy response. The results of both methods are in excellent agreement with histology. Nevertheless, our results also indicate that vascular remodeling is complex and that a uniform response cannot be expected for different tumors and therapies.

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The aim of this study was to test the feasibility of vessel size imaging with precise evaluation of apparent diffusion coefficient and cerebral blood volume and to apply this novel technique in acute stroke patients within a pilot group to observe the microvascular responses in acute ischemic tissue. Microvessel density-related quantity Q and mean vessel size index (VSI) were assessed in 9 healthy volunteers and 13 acute stroke patients with vessel occlusion within 6 hours after symptom onset. Our results in healthy volunteers matched with general anatomical observations. Given the limitation of a small patient cohort, the median VSI in the ischemic area was higher than that in the mirrored region in the contralateral hemisphere (P < 0.05). Decreased Q was observed in the ischemic region in 2 patients, whereas no obvious changes of Q were found in the remaining 11 patients. In a patient without recanalization, the VSI hyperintensity in the subcortical area matched well with the final infarct. These data reveal that different observations of microvascular response in the acute ischemic tissue seem to emerge and vessel size imaging may provide useful information for the definition of ischemic penumbra and have an impact on future therapeutic approaches.

The correlation between VSI and vessel size from histopathology is in good accordance with the animal studies. The overestimation of small capillary sizes is also known from the animal trials. Vessel size and CBV showed similar results, both for the correlation with the histopathological vessel size and the progression-free interval.