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Journal articles on the topic 'Tumor vascularization'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Zhang, Li-Zhi, Chang-Qing Zhang, Zhen-Yu Yan, Qing-Cheng Yang, Yao Jiang, and Bing-Fang Zeng. "Tumor-initiating cells and tumor vascularization." Pediatric Blood & Cancer 56, no. 3 (November 8, 2010): 335–40. http://dx.doi.org/10.1002/pbc.22886.

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2

Brossa, Alessia, Lola Buono, Sofia Fallo, Alessandra Fiorio Pla, Luca Munaron, and Benedetta Bussolati. "Alternative Strategies to Inhibit Tumor Vascularization." International Journal of Molecular Sciences 20, no. 24 (December 7, 2019): 6180. http://dx.doi.org/10.3390/ijms20246180.

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Endothelial cells present in tumors show different origin, phenotype, and genotype with respect to the normal counterpart. Various mechanisms of intra-tumor vasculogenesis sustain the complexity of tumor vasculature, which can be further modified by signals deriving from the tumor microenvironment. As a result, resistance to anti-VEGF therapy and activation of compensatory pathways remain a challenge in the treatment of cancer patients, revealing the need to explore alternative strategies to the classical anti-angiogenic drugs. In this review, we will describe some alternative strategies to inhibit tumor vascularization, including targeting of antigens and signaling pathways overexpressed by tumor endothelial cells, the development of endothelial vaccinations, and the use of extracellular vesicles. In addition, anti-angiogenic drugs with normalizing effects on tumor vessels will be discussed. Finally, we will present the concept of endothelial demesenchymalization as an alternative approach to restore normal endothelial cell phenotype.

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RAJORIA, SHILPI, ROBERT SURIANO, YUSHAN L. WILSON, ANDREA L. GEORGE, JAN GELIEBTER, STIMSON P. SCHANTZ, and RAJ K. TIWARI. "Estradiol-mediated tumor neo-vascularization." Oncology Letters 2, no. 3 (March 21, 2011): 453–57. http://dx.doi.org/10.3892/ol.2011.283.

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4

Auguste, Patrick, Sylvie Lemiere, Fréderic Larrieu-Lahargue, and Andreas Bikfalvi. "Molecular mechanisms of tumor vascularization." Critical Reviews in Oncology/Hematology 54, no. 1 (April 2005): 53–61. http://dx.doi.org/10.1016/j.critrevonc.2004.11.006.

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5

Ribatti, Domenico, and Francesco Pezzella. "Overview on the Different Patterns of Tumor Vascularization." Cells 10, no. 3 (March 13, 2021): 639. http://dx.doi.org/10.3390/cells10030639.

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Angiogenesis is a crucial event in the physiological processes of embryogenesis and wound healing. During malignant transformation, dysregulation of angiogenesis leads to the formation of a vascular network of tumor-associated capillaries promoting survival and proliferation of the tumor cells. Starting with the hypothesis formulated by Judah Folkman that tumor growth is angiogenesis-dependent, this area of research has a solid scientific foundation and inhibition of angiogenesis is a major area of therapeutic development for the treatment of cancer. Over this period numerous authors published data of vascularization of tumors, which attributed the cause of neo-vascularization to various factors including inflammation, release of angiogenic cytokines, vasodilatation, and increased tumor metabolism. More recently, it has been demonstrated that tumor vasculature is not necessarily derived by endothelial cell proliferation and sprouting of new capillaries, but alternative vascularization mechanisms have been described, namely vascular co-option and vasculogenic mimicry. In this article, we have analyzed the mechanisms involved in tumor vascularization in association with classical angiogenesis, including post-natal vasculogenesis, intussusceptive microvascular growth, vascular co-option, and vasculogenic mimicry. We have also discussed the role of these alternative mechanism in resistance to anti-angiogenic therapy and potential therapeutic approaches to overcome resistance.

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6

Lejeune, Ferdy J. "Improving drug penetration in tumors by targeting tumor vascularization." Targeted Oncology 1, no. 2 (April 2006): 90–96. http://dx.doi.org/10.1007/s11523-006-0019-0.

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7

Grunstein, Jeremy, Joseph J. Masbad, Reed Hickey, Frank Giordano, and Randall S. Johnson. "Isoforms of Vascular Endothelial Growth Factor Act in a Coordinate Fashion To Recruit and Expand Tumor Vasculature." Molecular and Cellular Biology 20, no. 19 (October 1, 2000): 7282–91. http://dx.doi.org/10.1128/mcb.20.19.7282-7291.2000.

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ABSTRACT Vascular endothelial growth factor (VEGF) is an essential regulator of vascularization. It is expressed as several splice variants; the major forms contain 120 amino acids, 164 amino acids, and 188 amino acids. We utilized transformed cells nullizygous for VEGF to specifically express each of these isoforms in isolation, in order to determine the role of each in tumorigenic neo-vascularization. We found that only the intermediate isoform, VEGF164, could fully rescue tumor growth; VEGF120 partially rescued tumor growth, and VEGF188 failed completely to rescue tumor expansion. Surprisingly, the vascular density of VEGF188 isoform-expressing tumors is significantly greater than that of wild-type VEGF cells and the other isoform-specific tumors. The failure of the hypervascular VEGF188-expressing tumors to grow may be due to inadequate perfusion of the massive number of microvessels in these tumors; three-dimensional imaging of the tumorigenic vasculature indicated little or no recruitment of the peripheral vasculature. This demonstrates that the VEGF isoforms perform unique functions which together enable tumorigenic vascularization.

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8

Dock, W., F. Grabenwöger, V. Metz, K. Eibenberger, and M. T. Farrés. "Tumor vascularization: assessment with duplex sonography." Radiology 181, no. 1 (October 1991): 241–44. http://dx.doi.org/10.1148/radiology.181.1.1887039.

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9

Conejo-Garcia, Jose R., Ronald J. Buckanovich, Fabian Benencia, Maria C. Courreges, Stephen C. Rubin, Richard G. Carroll, and George Coukos. "Vascular leukocytes contribute to tumor vascularization." Blood 105, no. 2 (January 15, 2005): 679–81. http://dx.doi.org/10.1182/blood-2004-05-1906.

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Abstract There is no proof that hematopoietic cells contribute significantly to vasculogenesis in postnatal life. Here we report a novel leukocyte subset within ovarian carcinoma that coexpresses endothelial and dendritic cell markers. Fluorescence-activated cell sorter (FACS) analysis identified a high frequency of VE-cadherin+ CD45+ leukocytes (39% of host cells) in 10 of 10 solid tumors evaluated. This population represented less than 1% of nontumor cells in ascites and peripheral blood. At the protein level, more than 86% of these cells expressed the endothelial markers P1H12, CD34, and CD31 and leukocyte markers CD11c and major histocompatibility complex (MHC) class II. At the mRNA level, we detected TEM1, TEM7, and Thy-1, specific markers of angiogenic endothelium. Finally, this population has the capacity to generate functional blood vessels in vivo. Because of its mixed phenotype, we named this population vascular leukocytes (VLCs). Our data provide an important link between hematopoietic endothelial precursors and vascular development in postnatal life and a possible novel therapeutic target.

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10

Belotti, Dorina, Denise Pinessi, and Giulia Taraboletti. "Alternative Vascularization Mechanisms in Tumor Resistance to Therapy." Cancers 13, no. 8 (April 15, 2021): 1912. http://dx.doi.org/10.3390/cancers13081912.

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Blood vessels in tumors are formed through a variety of different mechanisms, each generating vessels with peculiar structural, molecular, and functional properties. This heterogeneity has a major impact on tumor response or resistance to antineoplastic therapies and is now emerging as a promising target for strategies to prevent drug resistance and improve the distribution and efficacy of antineoplastic treatments. This review presents evidence of how different mechanisms of tumor vessel formation (vasculogenesis, glomeruloid proliferation, intussusceptive angiogenesis, vasculogenic mimicry, and vessel co-option) affect tumor responses to antiangiogenic and antineoplastic therapies, but also how therapies can promote alternative mechanisms of vessel formation, contributing to tumor recurrence, malignant progression, and acquired drug resistance. We discuss the possibility of tailoring treatment strategies to overcome vasculature-mediated drug resistance or to improve drug distribution and efficacy.

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11

Winder, Mateusz, Wojciech Spychałowicz, Aleksander Owczarek, and Jerzy Chudek. "Comparison of Adrenal Tumor Size in Ultrasound Examinations with and without the Use of a Contrast Agent." Medicina 55, no. 5 (May 20, 2019): 165. http://dx.doi.org/10.3390/medicina55050165.

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Background and objectives: Patients diagnosed with incidentally found adrenal tumors (incidentaloma) that do not meet the criteria for surgical treatment require follow-ups with repeated imaging. The aim of this study is to compare the accuracy of the measurements of the adrenal tumor size in ultrasound (US) with and without contrast in comparison to computed tomography (CT) or magnetic resonance (MRI). Further, this study attempts to answer the question of whether contrast-enhanced ultrasound (CEUS) can improve imaging accuracy and replace CT/MRI in the monitoring of patients with adrenal tumors. Materials and Methods: The retrospective analysis included 79 adult patients with adrenal incidentalomas not exceeding a dimension of 6 cm who underwent a CT or MRI scan, US, and CEUS with the use of SonoVue in two-dimensional (2D) and three-dimensional (3D) projections and Doppler techniques. Tumor vascularization in CEUS was classified as follows: peripheral, peripheral-central, central, or poor. Results: Of 79 adrenal tumors, 48.1% showed peripheral, 29.1% showed poor, 21.5% showed peripheral-central, and only 1.3% showed central vascularization. The median volume of tumors detected with CEUS (69.9 cm3) was significantly higher than with US (44.5 cm3) and CT or MRI (57.1 cm3). The relative error of the adrenal volume with CEUS compared with CT or MRI was significantly higher than with standard US, regardless of the type of tumor vascularization. Conclusions: CEUS does not improve the accuracy of adrenal tumor size assessment regardless of the type of vascularization.

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Guo, Chunqing, Annicole Buranych, Devanand Sarkar, Paul B. Fisher, and Xiang-Yang Wang. "The role of tumor-associated macrophages in tumor vascularization." Vascular Cell 5, no. 1 (2013): 20. http://dx.doi.org/10.1186/2045-824x-5-20.

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13

Kaak, Cinja, Vinodh Kakkassery, Björn O. Scheef, Marco Zschoche, Felix Rommel, Guido Hildebrandt, Steffen Emmert, et al. "Evaluation of Choroidal Melanoma Vascularization by Color Doppler Flow Imaging: An Option for Follow-Up Tumor Control Assessment after CyberKnife®?" Medicina 57, no. 6 (May 31, 2021): 553. http://dx.doi.org/10.3390/medicina57060553.

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Background and Objectives: Thus far, tumor control for choroidal melanoma after teletherapeutic radiation is clinically difficult. In contrast to brachytherapy, the tumor height does not necessarily have to shrink as a result of teletherapy. Therefore, the objective of this study was to evaluate tumor vascularization determined by color Doppler flow imaging (CDFI) as a possible approach for monitoring the therapy response after teletherapy of choroidal melanoma. Materials and Methods: A single-center retrospective pilot study of 24 patients was conducted, all of whom had been diagnosed with choroidal neoplasm, treated and followed up. Besides tumor vascularization, the following parameters were collected: age, gender, tumor entity, location, radiation dose, knowledge of relapse, tumor height, radiation-related complications, occurrence of metastases, visual acuity in logMAR. Results: The level of choroidal melanoma vascularization markedly decreased in all included subjects after treatment with the CyberKnife® technology. Initially, the level of vascularization was 2.1 (SD: 0.76 for n = 10); post-therapeutically, it averaged 0.14 (SD: 0.4). Regarding the tumor apex, CDFI sonography also demonstrated a significant tumor regression (mean value pre-therapeutically: 8.35 mm—SD: 3.92 for n = 10; mean value post-therapeutically: 4.86 mm—SD: 3.21). The level of choroidal melanoma vascularization declined in the patient collective treated with ruthenium-106 brachytherapy. The pre-therapeutic level of vascularization of 2 (SD: 0 for n = 2) decreased significantly to a level of 0 (mean: 0—SD: 0). The tumor height determined by CDFI did not allow any valid statement regarding local tumor control. In contrast to these findings, the patient population of the control group without any radiation therapy did not show any alterations in vascularization. Conclusions: Our data suggest that the determination of the tumor vascularization level using CDFI might be a useful and supplementary course parameter in the follow-up care of choroidal melanoma to monitor the success of treatment. This especially applies to robot-assisted radiotherapy using CyberKnife®. Further studies are necessary to validate the first results of this assessment.

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14

Fanelli, M., N. Locopo, D. Gattuso, and G. Gasparini. "Assessment of Tumor Vascularization: Immunohistochemical and Non-Invasive Methods." International Journal of Biological Markers 14, no. 4 (October 1999): 218–31. http://dx.doi.org/10.1177/172460089901400405.

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Growth of solid tumors beyond a certain mass is dependent on the vascular bed from pre-existing host vasculature. The process of angiogenesis is essential not only for primary tumor growth but also for metastasis. The number of microvessels within the invasive component of a primary tumor reflects the degree of tumor angiogenesis. At present the most widely used method to assess neovascularization is the quantitation of intratumoral microvessel density (IMD) by immunohistochemical methods in which specific markers for endothelial cells are employed. In this paper we analyze the different methods used to assess IMD, as well as their advantages and potential methodological pitfalls. Several studies have shown a close correlation between IMD, tumor growth and the occurrence of metastasis, suggesting that IMD is a prognostic indicator of clinical relevance. Furthermore, preliminary studies suggest that determination of angiogenesis may predict responsiveness to some forms of conventional anticancer therapy. Although the histological microvessel density technique is the current gold standard to characterize tumor angiogenesis, it may not be the ideal tool for clinical purposes because it needs to be performed on biopsy material and does not assess the functional pathways involved in the angiogenic activity of tumors. Non-invasive assessment of tumor vascularity is possible in vivo by means of Doppler sonography, dynamic contrast-enhanced magnetic resonance imaging (MRI) and positron emission tomography (PET). These methods may be preferable to histological assay because they are non-invasive, survey the entire tumor, reflect both anatomic and physiologic characteristics, and may be useful to monitor the activity of antiangiogenic therapies.

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15

Munaron, Luca, Tullio Genova, Daniele Avanzato, Susanna Antoniotti, and Alessandra Fiorio Pla. "Targeting Calcium Channels to Block Tumor Vascularization." Recent Patents on Anti-Cancer Drug Discovery 8, no. 1 (November 1, 2012): 27–37. http://dx.doi.org/10.2174/1574892811308010027.

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16

Bussolati, Benedetta, Cristina Grange, and Giovanni Camussi. "Tumor exploits alternative strategies to achieve vascularization." FASEB Journal 25, no. 9 (May 31, 2011): 2874–82. http://dx.doi.org/10.1096/fj.10-180323.

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17

Guo, Chunqing, Annicole Buranych, Devanand Sarkar, Paul B. Fisher, and Xiang-Yang Wang. "Correction: The role of tumor-associated macrophages in tumor vascularization." Vascular Cell 6, no. 1 (2014): 2. http://dx.doi.org/10.1186/2045-824x-6-2.

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18

Upcin, Berin, Erik Henke, Florian Kleefeldt, Helene Hoffmann, Andreas Rosenwald, Ster Irmak-Sav, Huseyin Bertal Aktas, Uwe Rückschloß, and Süleyman Ergün. "Contribution of Adventitia-Derived Stem and Progenitor Cells to New Vessel Formation in Tumors." Cells 10, no. 7 (July 7, 2021): 1719. http://dx.doi.org/10.3390/cells10071719.

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Blocking tumor vascularization has not yet come to fruition to the extent it was hoped for, as angiogenesis inhibitors have shown only partial success in the clinic. We hypothesized that under-appreciated vascular wall-resident stem and progenitor cells (VW-SPCs) might be involved in tumor vascularization and influence effectiveness of anti-angiogenic therapy. Indeed, in patient samples, we observed that vascular adventitia-resident CD34+ VW-SPCs are recruited to tumors in situ from co-opted vessels. To elucidate this in detail, we established an ex vivo model using concomitant embedding of multi-cellular tumor spheroids (MCTS) and mouse aortic rings (ARs) into collagen gels, similar to the so-called aortic ring assay (ARA). Moreover, ARA was modified by removing the ARs’ adventitia that harbors VW-SPCs. Thus, this model enabled distinguishing the contribution of VW-SPCs from that of mature endothelial cells (ECs) to new vessel formation. Our results show that the formation of capillary-like sprouts is considerably delayed, and their number and network formation were significantly reduced by removing the adventitia. Substituting iPSC-derived neural spheroids for MCTS resulted in distinct sprouting patterns that were also strongly influenced by the presence or absence of VW-SPCs, also underlying the involvement of these cells in non-pathological vascularization. Our data suggest that more comprehensive approaches are needed in order to block all of the mechanisms contributing to tumor vascularization.

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19

Petrov, S. B. "Quantitative characteristics of the microvasculature of cancer tumors." Kazan medical journal 66, no. 2 (April 15, 1985): 98–100. http://dx.doi.org/10.17816/kazmj60732.

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20

Alvernia, Jorge E., and Marc P. Sindou. "Preoperative neuroimaging findings as a predictor of the surgical plane of cleavage: prospective study of 100 consecutive cases of intracranial meningioma." Journal of Neurosurgery 100, no. 3 (March 2004): 422–30. http://dx.doi.org/10.3171/jns.2004.100.3.0422.

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Object. To understand the cause and prevention of postoperative ischemic and/or venous parenchymal infarcts after intracranial meningioma resection, the authors describe the value of neuroimaging in predicting the surgical plane of cleavage. Methods. A prospective study of 100 meningiomas was performed, in which tumor size, absence or presence of peritumoral edema, tumor—parenchyma interface, and types of arterial vascularization (that is, dural—meningeal, pial—cortical, or mixed) were correlated with the type of dissection plane (extrapial, subpial, or mixed) encountered at surgery. A direct correlation was found between the tumor size identified on T1-weighted magnetic resonance (MR) imaging sequences and the degree of subpial (nonextrapial) surgical plane of cleavage (p < 0.00001). A similar correlation was found with the grade of peritumoral edema identified on preoperative computerized tomography (CT) scanning (p < 0.0001) or T2-weighted MR imaging sequences (p < 0.00001) and tumor pial vascularization as seen on angiography (p < 0.0001). Nevertheless, the tumor—parenchyma interface on preoperative T2-weighted MR imaging sequences was not predictive of the surgical plane (p > 0.5). The worst clinical outcome was found in the tumors located in eloquent areas and in which a subpial plane was encountered at surgery (p = 0.03). Conclusions. Peritumoral edema on preoperative CT and MR studies and tumor pial vascularization as seen on selective angiography can be used to predict the surgical plane of cleavage in meningiomas. The association between tumor size and a subpial surgical plane may be explained by a more pial vascularization seen on angiography. Meningiomas with a location in eloquent cortex and a subpial dissection plane should be considered a high-risk group.

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Zielinski, Mark R., Melissa Muenchow, Matthew A. Wallig, Peggy L. Horn, and Jeffrey A. Woods. "Exercise delays allogeneic tumor growth and reduces intratumoral inflammation and vascularization." Journal of Applied Physiology 96, no. 6 (June 2004): 2249–56. http://dx.doi.org/10.1152/japplphysiol.01210.2003.

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This investigation determined whether daily strenuous exercise would alter the progression and regression of an allogeneic lymphoid tumor in mice. We also determined whether exercise would alter the cellular composition and vascularity of the tumor. Female BALB/c mice (age 6–8 wk) were randomly assigned to sedentary control (Con) or daily exercised groups (EXH). EXH mice ran on a treadmill at incremental speeds (20–40 m/min) for 3 h or until fatigue. Each mouse was subcutaneously injected with 20 × 106 EL-4 lymphoma cells immediately after the first exercise bout ( day 1) and run daily. Tumor volume was measured daily with calipers. In some experiments, mice were euthanized on days 5–10, 12, and 14. Tumors were excised and stained with hematoxylin and eosin or for Factor VIII-associated antigen using immunohistochemistry and analyzed in a blinded fashion under a light microscope. There was no significant treatment main effect found for tumor volumes. Interestingly, a significant treatment × time interaction was found, such that there was a 2-day delay in peak tumor volume and a more rapid tumor regression in EXH. Tumors isolated from Con exhibited significantly higher numbers of apoptotic bodies, blood vessels, macrophages, and neutrophils when compared with EXH. Intratumoral lymphocytes were higher in Con early in tumor growth but higher in EXH at peak tumor size. These data indicate that daily strenuous exercise may influence tumor growth by affecting the microenvironment of the tumor, resulting in a delay in tumor growth and a more rapid regression.

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Merickel, Joshua L., G. Elizabeth Pluhar, Aaron Rendahl, and M. Gerard O’Sullivan. "Prognostic histopathologic features of canine glial tumors." Veterinary Pathology 58, no. 5 (July 5, 2021): 945–51. http://dx.doi.org/10.1177/03009858211025795.

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Gliomas are relatively common tumors in aged dogs (especially brachycephalic breeds), and the dog is proving to be useful as a translational model for humans with brain tumors. Hitherto, there is relatively little prognostic data for canine gliomas and none on outcome related to specific histological features. Histologic sections of tumor biopsies from 33 dogs with glioma treated with surgical resection and immunotherapy and 21 whole brains obtained postmortem were reviewed. Tumors were diagnosed as astrocytic, oligodendroglial, or undefined glioma using Comparative Brain Tumor Consortium criteria. Putative features of malignancy were evaluated, namely, mitotic counts, glomeruloid vascularization, and necrosis. For biopsies, dogs with astrocytic tumors lived longer than those with oligodendroglial or undefined tumor types (median survival 743, 205, and 144 days, respectively). Dogs with low-grade gliomas lived longer than those with high-grade gliomas (median survival 734 and 194 days, respectively). Based on analysis of tumor biopsies, low mitotic counts, absence of glomeruloid vascularization, and absence of necrosis correlated with increased survival (median 293, 223, and 220 days, respectively), whereas high mitotic counts, glomeruloid vascularization, and necrosis correlated with poor survival (median 190, 170, and 154 days, respectively). Mitotic count was the only histological feature in biopsy samples that significantly correlated with survival ( P < .05). Whole-brain analyses for those same histologic features had similar and more robust correlations, and were statistically significant for all features ( P < .05). The small size of biopsy samples may explain differences between biopsy and whole-brain tumor data. These findings will allow more accurate prognosis for gliomas.

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23

Krawczyk, Marek, Bogna Ziarkiewicz-Wróblewska, Tadeusz Wróblewski, Joanna Podgórska, Jakub Grzybowski, Beata Gierej, Piotr Krawczyk, et al. "PEComa—A Rare Liver Tumor." Journal of Clinical Medicine 10, no. 8 (April 18, 2021): 1756. http://dx.doi.org/10.3390/jcm10081756.

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PEComa (perivascular epithelioid cell tumor) is a rare liver tumor. Decisions regarding patient management are currently based on a few small case series. The aim of this study was to report the clinicopathological features of PEComa in order to provide guidance for management, complemented by our own experience. This retrospective observational study included all patients with PEComa who underwent surgical treatment in two departments between 2002 and 2020. A total of 20 patients were diagnosed with PEComa following histopathological examination. The age of the patients ranged from 21 to 73 years. The majority of patients were women (85%). In most patients, the tumors were incidental. In diagnostic studies, PEComas with high arterial vascularization have been described. Liver resection was the treatment of choice. There was only one postoperative complication. During histopathological evaluation, tumors were composed mostly of epithelioid cells, rarely with spindle cell components, thick-walled vessels, and adipocytes in different proportions. Melanocytic markers (HMB45, MelanA) and at least one smooth muscle marker were expressed in all tumors. Features suggestive of malignancy were found in three cases. In conclusion, PEComa is a rare liver tumor that is usually diagnosed incidentally. In radiological studies, tumors with high arterial vascularization are observed. Liver resection is the treatment of choice.

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Chang, Claudia V., Andre C. Felicio, Andrea Cecilia Toscanini, Manoel Jacobsen Teixeira, and Malebranche Berardo Carneiro da Cunha-Neto. "Pituitary tumor apoplexy." Arquivos de Neuro-Psiquiatria 67, no. 2a (June 2009): 328–33. http://dx.doi.org/10.1590/s0004-282x2009000200033.

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Pituitary tumor apoplexy is a medical emergency due to acute infarction or hemorrhage in the pituitary gland. In this review, the authors discuss the sellar anatomy, the pituitary gland and adenomas' vascularization and the general aspects of the syndrome such as its ethiopatogenesis, predisposing factors, clinical features, treatment and prognosis.

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Chantrain, Christophe F., Yves A. DeClerck, Susan Groshen, and George McNamara. "Computerized Quantification of Tissue Vascularization Using High-resolution Slide Scanning of Whole Tumor Sections." Journal of Histochemistry & Cytochemistry 51, no. 2 (February 2003): 151–58. http://dx.doi.org/10.1177/002215540305100203.

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Assessment of tissue vascularization using immunohistochemical techniques for microvessel detection has been limited by difficulties in generating reproducible quantitative data. The distinction of individual blood vessels and the selection of microscopic fields to be analyzed remain two factors of subjectivity. In this study, we used imaging analysis software and a high-resolution slide scanner for measurement of CD31-immunostained endothelial area (EA) in whole sections of human neuroblastoma xenograft and murine mammary adenocarcinoma tumors. Imaging analysis software provided objective criteria for analysis of sections of different tumors. The use of the criteria on images of entire tumor section acquired with the slide scanner constituted a rapid method to quantify tumor vascularization. Compared with previously described methods, the “hot spot” and the “random fields” methods, EA measurements obtained with our “whole section scanning” method were more reproducible with 8.6% interobserver disagreement for the “whole section scanning” method vs 42.2% and 39.0% interobserver disagreement for the “hot spot” method and the “random fields,” respectively. Microvessel density was also measured with the whole section scanning method and provided additional data on the distribution and the size of the blood vessels. Therefore, this method constitutes a time efficient and reproducible method for quantification of tumor vascularization.

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Бучарская, А. Б., Г. Н. Маслякова, М. Л. Чехонацкая, Н. Б. Захарова, Г. С. Терентюк, Н. А. Наволокин, Б. Н. Хлебцов, et al. "К вопросу об эффективности плазмонной фототермической терапии экспериментальных опухолей." Журнал технической физики 128, no. 6 (2020): 846. http://dx.doi.org/10.21883/os.2020.06.49419.34-20.

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The aim of the study was to study the prognostic factors of the effectiveness of plasmon photothermal therapy (PPT) in rats with transplanted liver cancer based on an assessment of the degree of tumor vascularization. Prior to any exposure, rats with transplanted liver cancer RS-1 underwent a doppler ultrasonography to assess the degree of vascularization of the transplanted tumors. Half of the animals with transplanted tumors were removed from the experiment after dopplerography to determine the content of vascular factors in blood serum by immunoassay and immunohistochemical methods in tumor tissue. After triple intravenous administration of gold nanorods (GNRs) coated with polyethylene glycol at a dose of 0.4 mg/ml, the transplanted tumors were irradiated percutaneously with infrared laser radiation at a wavelength of 808 nm and a thermography of local tumor heating was conducted. After 24 hours, the animals were removed from the experiment and samples of tumor tissue were taken for histological examination. It was found that the accumulation of gold in the tumor tissue and the effectiveness of PPT after repeated intravenous administration of GNRs are determined by the presence of a formed vasculature in the tumor.

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Ballmer-Hofer, Kurt. "Vascular Endothelial Growth Factor, from Basic Research to Clinical Applications." International Journal of Molecular Sciences 19, no. 12 (November 26, 2018): 3750. http://dx.doi.org/10.3390/ijms19123750.

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Judah Folkman’s landmark discovery in the 1970s showing that tumors, growing beyond a few millimeters in diameter, depend on de novo vascularization triggered by specific growth factors released by tumor cells encountering hypoxia [...]

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Patenaude, Alexandre, Jeremy Parker, and Aly Karsan. "Involvement of endothelial progenitor cells in tumor vascularization." Microvascular Research 79, no. 3 (May 2010): 217–23. http://dx.doi.org/10.1016/j.mvr.2010.01.007.

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Wilson, YuShan, Robert Suriano, Shilpi Rajoria, Raj Tiwari, and Stimson Schantz. "Role of Estrogen in Thyroid Tumor Neo-Vascularization." Otolaryngology–Head and Neck Surgery 141, no. 2_suppl (September 2009): P57—P58. http://dx.doi.org/10.1016/j.otohns.2009.06.172.

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Hori, Katsuyoshi, Maroh Suzuki, Shigeru Tanda, and Sachiko Saito. "In vivoAnalysis of Tumor Vascularization in the Rat." Japanese Journal of Cancer Research 81, no. 3 (March 1990): 279–88. http://dx.doi.org/10.1111/j.1349-7006.1990.tb02562.x.

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De, S., O. Razorenova, N. P. McCabe, T. O'Toole, J. Qin, and T. V. Byzova. "VEGF-integrin interplay controls tumor growth and vascularization." Proceedings of the National Academy of Sciences 102, no. 21 (May 16, 2005): 7589–94. http://dx.doi.org/10.1073/pnas.0502935102.

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Weingärtner, K., P. J. Barth, E. W. Gerharz, R. Bonfig, A. Bittinger, and H. Riedmiller. "Morphometric assessment of tumor vascularization in prostate cancer." Journal of Cancer Research and Clinical Oncology 121, S1 (January 1995): A39. http://dx.doi.org/10.1007/bf02572119.

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Zheng, Ruiqi, Feifan Li, Fengcen Li, and Aihua Gong. "Targeting tumor vascularization: promising strategies for vascular normalization." Journal of Cancer Research and Clinical Oncology 147, no. 9 (June 19, 2021): 2489–505. http://dx.doi.org/10.1007/s00432-021-03701-8.

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Jones, Lee W., Benjamin L. Viglianti, Jessica A. Tashjian, Sejal M. Kothadia, Stephen T. Keir, Stephen J. Freedland, Michael Q. Potter, et al. "Effect of aerobic exercise on tumor physiology in an animal model of human breast cancer." Journal of Applied Physiology 108, no. 2 (February 2010): 343–48. http://dx.doi.org/10.1152/japplphysiol.00424.2009.

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Recent epidemiologic studies report that regular exercise may be associated with substantial reductions in cancer-specific and all-cause mortality following a breast cancer diagnosis. The mechanisms underlying this relationship have not been identified. We investigated the effects of long-term voluntary wheel running on growth and progression using an animal model of human breast cancer. We also examined effects on the central features of tumor physiology, including markers of tumor blood perfusion/vascularization, hypoxia, angiogenesis, and metabolism. Athymic female mice fed a high-fat diet were orthotopically (direct into the mammary fat pad) implanted with human breast cancer cells (MDA-MB-231 at 1 × 106) into the right dorsal mammary fat pad and randomly assigned (1:1) to voluntary wheel running ( n = 25) or a nonintervention (sedentary) control group ( n = 25). Tumor volume was measured every three days using digital calipers. All experimental animals were killed when tumor volume reached ≥1,500 mm3. Kaplan-Meier (KM) analysis indicated that tumor growth (survival) was comparable between the experimental groups (exercise 44 days vs. control 48 days; KM proportional hazard ratio = 1.41, 95% confidence interval, 0.77–2.58, P = 0.14). However, tumors from exercising animals had significantly improved blood perfusion/vascularization relative to the sedentary control group ( P < 0.05). Histological analyses indicated that intratumoral hypoxia levels (as assessed by hypoxia-inducible factor 1) were significantly higher in the exercise group relative to sedentary control ( P < 0.05). Aerobic exercise can significantly increase intratumoral vascularization, leading to “normalization” of the tissue microenvironment in human breast tumors. Such findings may have important implications for inhibiting tumor metastasis and improving the efficacy of conventional cancer therapies.

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Tilan, Jason, and Joanna Kitlinska. "Sympathetic Neurotransmitters and Tumor Angiogenesis—Link between Stress and Cancer Progression." Journal of Oncology 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/539706.

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Recent evidence supports a longstanding hypothesis that chronic stress can influence tumor growth and progression. It has been shown that sympathetic neurotransmitters, such as catecholamines and neuropeptides, can affect both cancer cell growth and tumor vascularization. Depending on neurotransmitter and type of tumor, these effects can be both stimulatory and inhibitory. Norepinephrine (NE) and epinephrine (E) are potent stimulators of vascularization, acting both by inducing the release of angiogenic factors from tumor cells and directly on endothelial cell (EC) functions. As a result, activation of the adrenergic system increases growth of various types of tumors and has been shown to mediate stress-induced augmentation of tumor progression. Dopamine (DA), on the other hand, interferes with VEGF signaling in endothelial cells, blocks its angiogenic functions and inhibits tumor growth. Another sympathetic neurotransmitter coreleased with NE, neuropeptide Y (NPY), directly stimulates angiogenesis. However, proangiogenic actions of NPY can be altered by its direct effect on tumor cell proliferation and survival. In consequence, NPY can either stimulate or inhibit tumor growth, depending on tumor type. Hence, sympathetic neurotransmitters are powerful modulators of tumor growth and can become new targets in cancer therapy.

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36

Muhammad, Syamel, and Nindya Rahmadita. "Correlation of Tumor Vascularization Using Spectral Pulse Wave Doppler with Neoadjuvant Chemotherapy Response in IB2 and IIA2 stages of Cervical Cancer." JOURNAL OBGIN EMAS 4, no. 2 (July 6, 2020): 145–54. http://dx.doi.org/10.25077/aoj.4.2.145-154.2020.

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Cervical cancer is an abnormal growth or cell changes in the cervical wall, which is the 4th rank in the most common cancer among female and the 2nd most common cancer in female aged fifteen until fourty four years old worldwide. Neovascularization becomes an important step in determining the onset and progressive cancer. Neoadjuvant chemotherapy has been evaluated as a treatment strategy in the stages IB2 and IIA2. The use of chemotherapy drug becomes more effective in adjacent and regular vascularization, and it allows the blood flow to the organs more quickly. This study aims to determine the correlation of tumor vascularization using Spectral Pulse Wave Doppler with neoadjuvant chemotherapy response in IB2 and IIA2 stages of cervical cancer. This research is a cohort analytic study which involves thirty six of patient in IB2 and IIA2 stages. The sampling is selected by using consecutive sampling technique. The data includes the result of ultrasound examination and were analyzed by using the Chi-square test. The results of the research on good and poor tumor vascularization had a good response to thirty of patient (83.3%) who were given neoadjuvant chemotherapy. There was no significant effect between tumor vascularization using Spectral Pulse Wave Doppler to the responses of neoadjuvant chemotherapy in IB2 and IIA2 stages of cervical cancer.Keywords: tumor vascularization using Spectral Pulse Wave Doppler, responses of neoadjuvant chemotherapy, IB2 and IIA2 stages of cervical cancer

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Muhammad, Syamel, and Nindya Rahmadita. "Correlation of Tumor Vascularization Using Spectral Pulse Wave Doppler with Neoadjuvant Chemotherapy Response in IB2 and IIA2 stages of Cervical Cancer." JOURNAL OBGIN EMAS 4, no. 2 (July 6, 2020): 176–85. http://dx.doi.org/10.25077/aoj.4.2.176-185.2020.

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Cervical cancer is an abnormal growth or cell changes in the cervical wall, which is the 4th rank in the most common cancer among female and the 2nd most common cancer in female aged fifteen until fourty four years old worldwide. Neovascularization becomes an important step in determining the onset and progressive cancer. Neoadjuvant chemotherapy has been evaluated as a treatment strategy in the stages IB2 and IIA2. The use of chemotherapy drug becomes more effective in adjacent and regular vascularization, and it allows the blood flow to the organs more quickly. This study aims to determine the correlation of tumor vascularization using Spectral Pulse Wave Doppler with neoadjuvant chemotherapy response in IB2 and IIA2 stages of cervical cancer. This research is a cohort analytic study which involves thirty six of patient in IB2 and IIA2 stages. The sampling is selected by using consecutive sampling technique. The data includes the result of ultrasound examination and were analyzed by using the Chi-square test. The results of the research on good and poor tumor vascularization had a good response to thirty of patient (83.3%) who were given neoadjuvant chemotherapy. There was no significant effect between tumor vascularization using Spectral Pulse Wave Doppler to the responses of neoadjuvant chemotherapy in IB2 and IIA2 stages of cervical cancer.Keywords: tumor vascularization using Spectral Pulse Wave Doppler, responses of neoadjuvant chemotherapy, IB2 and IIA2 stages of cervical cancer

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38

Kuhn, Susanne Antje, Tobias Kratzsch, Viktor Gruenwald, and Hannes Haberl. "Factor Xa: PAR-1 growth loop is blocked by low-molecular weight heparins—A new perioperative and adjuvant concept in glioblastoma." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 2038. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.2038.

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2038 Background: Glioblastoma patients suffer from thromboembolism, aggravating the disease. Recently, increased activity was shown for coagulation factors II, VIII, IX, X, XI, and XII in patient peripheral blood. In vitro, the high potential of FXa-PAR1-loop as growth factor system and significant effects of its blockade were proven. Methods: Patient samples (n=108) were analyzed for FXa and PAR-1. In immunodeficient mice, glioblastoma xenografts were established and treated with low-molecular weight heparins (LMWH) (30mg/kg SC daily for 3 wks). Phosphate buffered saline served as control. Tumor growth rates, final tumor size, tumor proliferation (Ki67), and tumor vascularization (CD31) were determined. Results: Human glioblastomas overexpressed FXa and PAR-1 in the compact tumor center (FXa: p<.001; PAR-1: p<.001) and in the invasion zone (FXa: p=.006; PAR-1: p=.005). Neoangiogenic endothelial cells disproportionately high expressed FXa and PAR-1 with rising intensity in the invasion zone (FXa: p<.001; PAR-1: p<.001), and the compact tumor mass. (FXa: p<.001; PAR-1: p<.001). Growth curves of LMWH-treated tumors slowed (p<.001). Final tumor size was reduced (s.c.: p<.001; i.c.: p<.05). Tumor cell proliferation was massively inhibited in situ (tinzaparin: p<.001; enoxaparin: p<.001) as was the number of CD31 positive endothelial cells ((tinzaparin: p<.001; enoxaparin: p<.001) and the tumor vascularization (p<.001 each). Conclusions: Glioblastoma patients display abnorm activation of coagulation factors in peripheral blood and show high levels of FXa and PAR-1 in the tumor center, invasion zone and angiogenic endothelia. LMWH caused tumor growth retardation and size reduction with blockade of proliferation and vascularization. FXa inhibition should be considered as continuous thrombosis prophylaxis and adjuvant glioblastoma treatment.

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Egners, Antje, Maryam Rezaei, Aleksandar Kuzmanov, David Poitz, Doreen Streichert, Thomas Mueller-Reichert, Ben Wielockx, and Georg Breier. "PHD3 Acts as Tumor Suppressor in Mouse Osteosarcoma and Influences Tumor Vascularization via PDGF-C Signaling." Cancers 10, no. 12 (December 6, 2018): 496. http://dx.doi.org/10.3390/cancers10120496.

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Cancer cell proliferation and insufficient blood supply can lead to the development of hypoxic areas in the tumor tissue. The adaptation to the hypoxic environment is mediated by a transcriptional complex called hypoxia-inducible factor (HIF). HIF protein levels are tightly controlled by oxygen-dependent prolyl hydroxylase domain proteins (PHDs). However, the precise roles of these enzymes in tumor progression and their downstream signaling pathways are not fully characterized. Here, we study PHD3 function in murine experimental osteosarcoma. Unexpectedly, PHD3 silencing in LM8 cells affects neither HIF-1α protein levels, nor the expression of various HIF-1 target genes. Subcutaneous injection of PHD3-silenced tumor cells accelerated tumor progression and was accompanied by dramatic phenotypic changes in the tumor vasculature. Blood vessels in advanced PHD3-silenced tumors were enlarged whereas their density was greatly reduced. Examination of the molecular pathways underlying these alterations revealed that platelet-derived growth factor (PDGF)-C signaling is activated in the vasculature of PHD3-deficient tumors. Silencing of PDGF-C depleted tumor growth, increased vessel density and reduced vessel size. Our data show that PHD3 controls tumor growth and vessel architecture in LM8 osteosarcoma by regulating the PDGF-C pathway, and support the hypothesis that different members of the PHD family exert unique functions in tumors.

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Bhujwalla, Zaver M., Dmitri Artemov, and James Glockner. "Tumor Angiogenesis, Vascularization, and Contrast-Enhanced Magnetic Resonance Imaging." Topics in Magnetic Resonance Imaging 10, no. 2 (April 1999): 92–103. http://dx.doi.org/10.1097/00002142-199904000-00002.

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41

Lee, K., H. Zhang, D. Z. Qian, S. Rey, J. O. Liu, and G. L. Semenza. "Acriflavine inhibits HIF-1 dimerization, tumor growth, and vascularization." Proceedings of the National Academy of Sciences 106, no. 42 (October 1, 2009): 17910–15. http://dx.doi.org/10.1073/pnas.0909353106.

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42

Breyer, B., and A. Kurjak. "Tumor vascularization, Doppler measurements and chaos: what to do?" Ultrasound in Obstetrics and Gynecology 5, no. 3 (March 1, 1995): 209–10. http://dx.doi.org/10.1046/j.1469-0705.1995.05030209.x.

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Saxena, Vishal, Ignacio Gonzalez-Gomez, and Walter E. Laug. "A noninvasive multimodal technique to monitor brain tumor vascularization." Physics in Medicine and Biology 52, no. 17 (August 16, 2007): 5295–308. http://dx.doi.org/10.1088/0031-9155/52/17/013.

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Rupertus, Kathrin, Gudrun C. Y. Haberl, Claudia Scheuer, Michael D. Menger, Martin K. Schilling, and Otto Kollmar. "Bone Marrow Suppression by c-Kit Blockade Enhances Tumor Growth of Colorectal Metastases through the Action of Stromal Cell-Derived Factor-1." Journal of Oncology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/196957.

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Background. Mobilization of c-Kit+hematopoietic cells (HCs) contributes to tumor vascularization. Whereas survival and proliferation of HCs are regulated by binding of the stem cell factor to its receptor c-Kit, migration of HCs is directed by stromal cell-derived factor (SDF)-1. Therefore, targeting migration of HCs provides a promising new strategy of anti-tumor therapy.Methods. BALB/c mice () were pretreated with an anti-c-Kit antibody followed by implantation of CT26.WT-GFP colorectal cancer cells into dorsal skinfold chambers. Animals () additionally received a neutralizing anti-SDF-1 antibody. Animals () treated with a control antibody served as controls. Investigations were performed using intravital fluorescence microscopy, immunohistochemistry, flow cytometry and western blot analysis.Results. Blockade of c-Kit significantly enhanced tumor cell engraftment compared to controls due to stimulation of tumor cell proliferation and invasion without markedly affecting tumor vascularization. C-Kit blockade significantly increased VEGF and CXCR4 expression within the growing tumors. Neutralization of SDF-1 completely antagonized this anti-c-Kit-associated tumor growth by suppression of tumor neovascularization, inhibition of tumor cell proliferation and reduction of muscular infiltration.Conclusion. Our study indicates that bone marrow suppression via anti-c-Kit pretreatment enhances tumor cell engraftment of colorectal metastases due to interaction with the SDF-1/CXCR4 pathway which is involved in HC-mediated tumor angiogenesis.

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Senger, Sebastian, Otto Kollmar, Michael D. Menger, and Kathrin Rupertus. "Darbepoetin-α Promotes Cell Proliferation in Established Extrahepatic Colorectal Tumors after Major Hepatectomy." European Surgical Research 56, no. 1-2 (December 18, 2015): 49–60. http://dx.doi.org/10.1159/000442384.

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Background: The glycoprotein hormone erythropoietin and its analogue darbepoetin-α (DPO) have been shown to reduce the risk of acute liver failure after major hepatectomy. However, previous experimental studies have also shown that DPO significantly enhances neovascularization and tumor cell proliferation in established colorectal liver metastasis in hepatectomized and nonhepatectomized mice. The present study now analyzes whether DPO influences cell proliferation and migration as well as vascularization and growth of established colorectal metastasis at extrahepatic sites after major hepatectomy. Methods: GFP-transfected CT26.WT colorectal cancer cells were implanted into dorsal skinfold chambers of syngeneic BALB/c mice. Five days after tumor cell implantation, the animals received a single dose of DPO (10 µg/kg body weight) or phosphate-buffered saline solution (PBS) intravenously. Additional animals received a 70% hepatectomy and DPO or PBS treatment. Tumor vascularization and growth as well as tumor cell migration, proliferation and apoptosis were studied repetitively over 14 days using intravital fluorescence microscopy, histology and immunohistochemistry. Results: DPO did not influence tumor cell migration and apoptosis. In addition, DPO did not stimulate tumor cell infiltration or vascularization; however, significantly increased tumor cell proliferation was detected in hepatectomized animals. Conclusion: DPO increases cell proliferation in established extrahepatic colorectal metastases after major hepatectomy. Thus, DPO may not be recommended to stimulate regeneration of the remnant liver after major hepatectomy for colorectal liver metastasis.

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Eisinger, Silke, Dhifaf Sarhan, Vanessa F. Boura, Itziar Ibarlucea-Benitez, Sofia Tyystjärvi, Ganna Oliynyk, Marie Arsenian-Henriksson, et al. "Targeting a scavenger receptor on tumor-associated macrophages activates tumor cell killing by natural killer cells." Proceedings of the National Academy of Sciences 117, no. 50 (November 23, 2020): 32005–16. http://dx.doi.org/10.1073/pnas.2015343117.

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Tumor-associated macrophages (TAMs) can have protumor properties, including suppressing immune responses, promoting vascularization and, consequently, augmenting tumor progression. To stop TAM-mediated immunosuppression, we use a novel treatment by injecting antibodies specific for scavenger receptor MARCO, which is expressed on a specific subpopulation of TAMs in the tumor. We now report the location of this TAM as well as the pleiotropic mechanism of action of anti-MARCO antibody treatment on tumor progression and further show that this is potentially relevant to humans. Using specific targeting, we observed decreased tumor vascularization, a switch in the metabolic program of MARCO-expressing macrophages, and activation of natural killer (NK) cell killing through TNF-related apoptosis-inducing ligand (TRAIL). This latter activity reverses the effect of melanoma cell-conditioned macrophages in blocking NK activation and synergizes with T cell-directed immunotherapy, such as antibodies to PD-1 or PD-L1, to enhance tumor killing. Our study thus reveals an approach to targeting the immunosuppressive tumor microenvironment with monoclonal antibodies to enhance NK cell activation and NK cell-mediated killing. This can complement existing T cell-directed immunotherapy, providing a promising approach to combinatorial immunotherapy for cancer.

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Rosińska, Sara, and Julie Gavard. "Tumor Vessels Fuel the Fire in Glioblastoma." International Journal of Molecular Sciences 22, no. 12 (June 17, 2021): 6514. http://dx.doi.org/10.3390/ijms22126514.

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Glioblastoma, a subset of aggressive brain tumors, deploy several means to increase blood vessel supply dedicated to the tumor mass. This includes typical program borrowed from embryonic development, such as vasculogenesis and sprouting angiogenesis, as well as unconventional processes, including co-option, vascular mimicry, and transdifferentiation, in which tumor cells are pro-actively engaged. However, these neo-generated vascular networks are morphologically and functionally abnormal, suggesting that the vascularization processes are rather inefficient in the tumor ecosystem. In this review, we reiterate the specificities of each neovascularization modality in glioblastoma, and, how they can be hampered mechanistically in the perspective of anti-cancer therapies.

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Limoge, Michelle, Alfiya Safina, Amy Beattie, Lauren Kapus, Alexander M. Truskinovsky, and Andrei V. Bakin. "Tumor-fibroblast interactions stimulate tumor vascularization by enhancing cytokine-driven production of MMP9 by tumor cells." Oncotarget 8, no. 22 (March 8, 2017): 35592–608. http://dx.doi.org/10.18632/oncotarget.16022.

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Giampietri, Claudia, Simonetta Petrungaro, Silvia Conti, Antonio Facchiano, Antonio Filippini, and Elio Ziparo. "Cancer Microenvironment and Endoplasmic Reticulum Stress Response." Mediators of Inflammation 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/417281.

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Different stressful conditions such as hypoxia, nutrient deprivation, pH changes, or reduced vascularization, potentially able to act as growth-limiting factors for tumor cells, activate the unfolded protein response (UPR). UPR is therefore involved in tumor growth and adaptation to severe environments and is generally cytoprotective in cancer. The present review describes the molecular mechanisms underlying UPR and able to promote survival and proliferation in cancer. The critical role of UPR activation in tumor growth promotion is discussed in detail for a few paradigmatic tumors such as prostate cancer and melanoma.

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Perisic, Mirjana, Vladimir Jurisic, and Mirko Kerkez. "Doppler ultrasonography of hepatic artery in malignant liver tumors." Archive of Oncology 16, no. 3-4 (2008): 46–48. http://dx.doi.org/10.2298/aoo0804046p.

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Hepatic artery is dominant compared to portal vein in liver tumor vascularization. Malignant tumors have uncontrolled growth and spread onto neighbouring tissues through a tumor vascular network. Based on this we discussed the use arterial flow parameters including systolic and diastolic speed, Doppler perfusion index, and resistance index for early detection of liver metastasis. We also discussed possibility to make differential diagnosis from other disease such as arterial stenosis, liver cirrhosis, steatosis using these parameters in better diagnosis confirmation.

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