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1.
Fig. 8.

Fig. 8. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Individual tumor growth data for vehicle- or sunitinib-treated PDAC tumors. Treatment was initiated on day zero. Each panel shows a time-course analysis of an individual PNET tumor in an independent mouse. The top four graphs represent vehicle-treated tumors.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
2.
Fig. 5.

Fig. 5. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Individual tumor growth data for vehicle- or sunitinib-treated PNET tumors. Treatment was initiated on day zero. Each panel shows a time-course analysis of an individual PNET tumor. Of note, PNET mice develop multifocal disease and therefore, one to two tumors were tracked for tumor growth in each mouse.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
3.
Fig. 6.

Fig. 6. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Microbubble perfusion is reduced in 5/6 tumors from Ptf1a-Cre LSL-KrasG12D p53R172H/+ mice treated with sunitinib for 7 d. (A) Microbubble perfusion in vehicle-treated tumors. (B) Microbubble perfusion in sunitinib-treated tumors. Note microbubble perfusion is also reduced in half of the vehicle-treated tumors during the 7-d time course. Blue diamonds, microbubble data acquired before the trial (Pre); red squares, microbubble data acquired at the end of the trial (Post).

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
4.
Fig. 4.

Fig. 4. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Sunitinib reduces blood flow in a GEMM of PNET. (A and C) Vehicle treatment or (B and D) sunitinib treatment for (A and B) 7 or (C and D) 12 d. Blue diamonds, microbubble data acquired before the trial (Pre); red squares, microbubble data acquired at the end of the trial (Post). Comparison of the plateaus of pre- and posttrial microbubble perfusion reveal blood flow is reduced in sunitinib-treated tumors.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
5.
Fig. 9.

Fig. 9. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Microbubble perfusion is reduced by sunitinib treatment to a similar extent in the PNET and PDAC models. Average plateau mb intensity was determined by averaging all values between 20,000 and 30,000 ms which takes into account approximately the second-half of the sequence. Plateau values posttreatment were divided by the pretreatment and multiplied by 100%. Average value across treatment arms was averaged and standard error determined. RT, RIP1-Tag2; Bars, SE; *P < 0.05.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
6.
Fig. 7.

Fig. 7. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Microbubble perfusion is reduced in two of three sunitinib-treated and one of two vehicle-treated PDAC tumors from Ptf1a-Cre LSL-KrasG12D p53R172H/+ mice, treated for 12 d. (A) Microbubble perfusion in vehicle-treated tumors. (B) Microbubble perfusion in sunitinib-treated tumors. Blue diamonds, microbubble data acquired before the trial (Pre); red squares, microbubble data acquired at the end of the trial (Post). Again, one of two untreated controls showed reductions in blood flow over the 12-d period of continuing tumor growth and progression.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
7.
Fig. P1.

Fig. P1. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Ultrasound imaging following infusion of microbubbles into the circulatory system of tumor-bearing mice reveals reduced blood flow following antiangiogenic therapy in a genetically engineered mouse model of pancreatic ductal adenocarcinoma. Cine loops (approximately 1-min movies) were taken while injecting the microbubble contrast agent into the circulation (shown as green) before and after 12 d of treatment with the sunitinib drug. Tumor area is outlined in blue.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
8.
Fig. 11.

Fig. 11. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

The sunitinib-treated PDAC tumor showing a lack of vascular attenuation has atypical morphologic features. The upper and middle rows represent typical PDAC tumors treated with vehicle or sunitinib, whereas the lower row shows the atypical tumor (tumor f from ) that did not suffer loss of vascularity in response to sunitinib therapy. Typical PDAC tumors stained positive for cytokeratins and negative for vimentin. Tumor f demonstrates positivity for both markers as well as more poorly differentiated morphology. CD34, used to demonstrate vasculature, is also aberrantly expressed on tumor f cells.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
9.
Fig. 3.

Fig. 3. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Independent replicate experiments shown in A and B evaluating tumor blood flow by microbubble-enhanced ultrasound. Microbubble perfusion data are very similar in different planes of PNET and PDAC tumors, shown in both replicate experiments (A and B). In both A and B, red and blue are consecutive injections in different planes of a PNET tumor, whereas green and purple are consecutive injections in different planes of a PDAC tumor. The increase in signal around 10,000 ms is when microbubbles enter the field. After a short “wash-in” period, a plateau is achieved. Note the lower plateau in the PDAC tumors, indicative of comparatively less blood flow despite the fact that these tumors are larger, which further exemplifies the low vascularity of treatment-naïve PDAC tumors.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
10.
Fig. 2.

Fig. 2. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Effects of sunitinib and gemcitabine in mouse models of PNET and PDAC. (A) In PNET, sunitinib caused a reduction in tumor burden following 5 wk of sunitinib treatment. (B) Sunitinib showed no efficacy following 4 wk of treatment in Ptf1a-Cre LSL-KrasG12D p53lox/+ mice. The combination of sunitinib plus gemcitabine produced no added benefit to that of gemcitabine alone. (C) Gemcitabine at 150 mg/kg twice a week elicited a statistically significant decrease in tumor burden. (D) Gemcitabine at 150 mg/kg twice a week affords a survival benefit over the course of the trial. (E) Sunitnib or gemcitabine plus sunitinib had no affect on survival during the trial. Bars, SE; *P < 0.05; C, vehicle-treated control; Su, sunitinib; Gem, gemcitabine.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
11.
Fig. 10.

Fig. 10. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

Vessel density is reduced in PDAC arising in Ptf1a-Cre LSL-KrasG12D p53R172H/+ mice treated with sunitinib. (A) Staining of tumors with endothelial markers CD31 and CD34 in control and sunitinib-treated mice to assess microvessel density. Tumors were also stained with PDGFR-beta to evaluate effect of sunitinib treatment on tumor stroma. Magnification bar (shown in the upper left panel) represents 37.5 µm for the PDGFR-beta panel. CD31 and CD34 panels are depicted at twofold lower magnification; a bar of the same length represents 75 µm. All analyses (PDGFR-beta, CD31, and CD34) were performed on seven sunitinib-treated mice and seven controls (five vehicle, two no treatment). The photomicrographs of invasive tumors immunostained for various antigens is representative of staining multiple tissue sections through each tumor. The staining pattern among mice within each group showed similar patterns except for tumor “f” (see ). (B) CD31 and CD34 positive blood vessels were counted in tumors and averaged over four representative regions and plotted with SEM. Analysis of tumor microvessel density in mice receiving NT, no treatment; V, vehicle; or S, sunitinib.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.
12.
Fig. 1.

Fig. 1. From: Imaging guided trials of the angiogenesis inhibitor sunitinib in mouse models predict efficacy in pancreatic neuroendocrine but not ductal carcinoma.

PDAC arising in Ptf1a-Cre LSL-KrasG12D p53R172H/+ mice have abundant stroma and sparse vasculature. (A) Normal mouse pancreas (i, ii) and PDAC (iii, iv) stained with H&E (i, iii) and anti-FITC tomato lectin (ii, iv). Perfused FITC tomato lectin identifies functional vasculature during physiologic conditions of assay. (B) Comparison of total vasculature (anti-CD34; i, iii) to functionally perfused vasculature (anti-FITC lectin; ii, iv) within PDAC (i, ii) and duodenum (iii, iv) of a single mouse. Red arrows highlight infrequent CD34+ and anti-FITC lectin positive vessels in adjacent sections of PDAC; in the normal tissue, the two are largely concordant. (C and D) Mouse (C) and human (D) PDAC stained with (i) CD34+ for blood vessels, (ii) cytokeratin to highlight tumor cells, (iii) α-SMA to identify activated myofibroblasts, and (iv) PDGFR-beta. (Magnification: AC, 50 µm; D. 100 µm.) The lectin perfusion experiment was performed on four untreated mice. All other analyses (CD34, α-SMA, PDGFR-beta, and cytokeratin) were performed on seven untreated or vehicle-treated mice (five vehicle, two no treatment). The selected photomicrographs of invasive tumors immunostained for various antigens are representative of multiple sections of such tumors. Staining pattern among mice within each group showed similar patterns.

Peter Olson, et al. Proc Natl Acad Sci U S A. 2011 December 6;108(49):E1275-E1284.

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