کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8456797 | 1548774 | 2018 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
DCE-MRI of Sunitinib-Induced Changes in Tumor Microvasculature and Hypoxia: A Study of Pancreatic Ductal Adenocarcinoma Xenografts
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کلمات کلیدی
KtransROIαSMADCE-MRIFOVMVDα smooth muscle actin - α عضله صاف آکتینPancreatic ductal adenocarcinoma - آدنوکارسینوم پانکراس داکتالPDAC یا pancreatic ductal adenocarcinoma - آدنوکارسینومای داکتال پانکراسMicrovessel density - تراکم MicrovesselDynamic contrast-enhanced magnetic resonance imaging - تصویربرداری رزونانس مغناطیسی با کنتراست پویاvolume transfer constant - ثابت انتقال حجمecho time - زمان اکوRepetition time - زمان تکرارregion of interest - منطقه مورد نظرField of view - میدان دیدHematoxylin and Eosin - هماتوکسیلین و ائوزینHypoxic fraction - کسر هیپوکیک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The purpose of this study was dual: to investigate (a) whether sunitinib may induce changes in tumor microvasculature and hypoxia in pancreatic ductal adenocarcinoma (PDAC) and (b) whether any changes can be detected by DCE-MRI. Sunitinib-treated and untreated control tumors of two PDAC xenograft models (BxPC-3 and Panc-1) were subjected to DCE-MRI before the imaged tumors were prepared for quantitative analysis of immunohistochemical preparations. Pimonidazole was used as a hypoxia marker, and fraction of hypoxic tissue (HFPim), density of CD31-positive microvessels (MVDCD31), and density of αSMA-positive microvessels (MVDαSMA) were measured. Parametric images of Ktrans and ve were derived from the DCE-MRI data by using the Tofts pharmacokinetic model. BxPC-3 tumors showed increased HFPim, decreased MVDCD31, unchanged MVDαSMA, and increased vessel maturation index (VMIâ¯=â¯MVDαSMA/MVDCD31) after sunitinib treatment. The increase in VMI was seen because sunitinib induced selective pruning rather than maturation of αSMA-negative microvessels. Even though the microvessels in sunitinib-treated tumors were less abnormal than those in untreated tumors, this microvessel normalization did not improve the function of the microvascular network or normalize the tumor microenvironment. In Panc-1 tumors, HFPim, MVDCD31, MVDαSMA, and VMI were unchanged after sunitinib treatment. Median Ktrans increased with increasing MVDCD31 and decreased with increasing HFPim, and the correlations were similar for treated and untreated BXPC-3 and Panc-1 tumors. These observations suggest that sunitinib may induce significant changes in the microenvironment of PDACs, and furthermore, that Ktrans may be an adequate measure of tumor vascular density and hypoxia in untreated as well as sunitinib-treated PDACs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neoplasia - Volume 20, Issue 7, July 2018, Pages 734-744
Journal: Neoplasia - Volume 20, Issue 7, July 2018, Pages 734-744
نویسندگان
Catherine S. Wegner, Anette Hauge, Trude G. Simonsen, Jon-Vidar Gaustad, Lise Mari K. Andersen, Einar K. Rofstad,