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Journal articles on the topic 'Vessel normalization'

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Author: Grafiati

Published: 11 March 2023

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1

Augustin, Hellmut G., and Gou Young Koh. "Antiangiogenesis: Vessel Regression, Vessel Normalization, or Both?" Cancer Research 82, no. 1 (January 1, 2022): 15–17. http://dx.doi.org/10.1158/0008-5472.can-21-3515.

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2

Coulon, Cathy, Maria Georgiadou, Carmen Roncal, Katrien De Bock, Tobias Langenberg, and Peter Carmeliet. "From Vessel Sprouting to Normalization." Arteriosclerosis, Thrombosis, and Vascular Biology 30, no. 12 (December 2010): 2331–36. http://dx.doi.org/10.1161/atvbaha.110.214106.

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3

Li, Sai, Qi Zhang, and Yupeng Hong. "Tumor Vessel Normalization: A Window to Enhancing Cancer Immunotherapy." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382098011. http://dx.doi.org/10.1177/1533033820980116.

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Hostile microenvironment produced by abnormal blood vessels, which is characterized by hypoxia, low pH value and increasing interstitial fluid pressure, would facilitate tumor progression, metastasis, immunosuppression and anticancer treatments resistance. These abnormalities are the result of the imbalance of pro-angiogenic and anti-angiogenic factors (such as VEGF and angiopoietin 2, ANG2). Prudent use of anti-angiogenesis drugs would normalize these aberrant tumor vessels, resulting in a transient window of vessel normalization. In addition, use of cancer immunotherapy including immune checkpoint blockers when vessel normalization is achieved brings better outcomes. In this review, we sum up the advances in the field of understanding and application of the concept of tumor vessels normalization window to treat cancer. Moreover, we also outline some challenges and opportunities ahead to optimize the combination of anti-angiogenic agents and immunotherapy, leading to improve patients’ outcomes.

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4

Cully, Megan. "Tumour vessel normalization takes centre stage." Nature Reviews Drug Discovery 16, no. 2 (February 2017): 87. http://dx.doi.org/10.1038/nrd.2017.4.

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5

Jones, Bryony. "Early vessel normalization improves glioblastoma outcomes." Nature Reviews Clinical Oncology 11, no. 1 (November 26, 2013): 4. http://dx.doi.org/10.1038/nrclinonc.2013.228.

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Urits, Ivan, Purna Mukherjee, Joshua Meidenbauer, and Thomas N. Seyfried. "Dietary Restriction Promotes Vessel Maturation in a Mouse Astrocytoma." Journal of Oncology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/264039.

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Mature vasculature contains an endothelial cell lining with a surrounding sheath of pericytes/vascular smooth muscle cells (VSMCs). Tumor vessels are immature and lack a pericyte sheath. Colocalization of vascular endothelial growth factor receptor 2 (VEGFR-2) and platelet-derived growth factor receptor beta (PDGF-Rβ) reduces pericyte ensheathment of tumor vessels. We found that a 30% dietary restriction (DR) enhanced vessel maturation in the mouse CT-2A astrocytoma. DR reduced microvessel density and VEGF expression in the astrocytoma, while increasing recruitment of pericytes, positive for alpha-smooth muscle actin (α-SMA). Moreover, DR reduced colocalization of VEGF-R2 and PDGF-Rβ, but did not reduce total PDGF-Rβexpression. These findings suggest that DR promoted vessel normalization by preventing VEGF-induced inhibition of the PDGF signaling axis in pericytes. DR appears to shift the tumor vasculature from a leaky immature state to a more mature state. We suggest that vessel normalization could improve delivery of therapeutic drugs to brain tumors.

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Martin, John, Ryan Lanning, Dai Fukumura, Timothy Padera, and Rakesh Jain. "Abstract LB557: Multiphoton phosphorescence quenching microscopy reveals kinetics of tumor oxygenation during anti-angiogenesis and angiotensin signaling inhibition." Cancer Research 82, no. 12_Supplement (June 15, 2022): LB557. http://dx.doi.org/10.1158/1538-7445.am2022-lb557.

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Abstract Purpose: The abnormal function of tumor blood vessels causes hypoxia fueling disease progression and conferring treatment resistance. The local level of oxygen experienced by a cell will determine its response, making it critical to understand tissue oxygen levels with a spatial resolution on the order of the size of a cell. While microenvironment normalization strategies alleviate global hypoxia, how local oxygen levels change are not known because there are no in vivo techniques to longitudinally assess tumor vessels and interstitial oxygen in tumors with sufficient resolution. Understanding the heterogeneity of oxygen levels after microenvironmental normalization will help improve the efficacy of various normalization strategies. Experimental Design: We developed a multiphoton phosphorescence quenching microscopy system using a low-molecular weight palladium porphyrin probe to measure perfused vessels, oxygen tension and their spatial correlations in vivo in mouse skin, bone marrow, and tumors. Further, we measured the temporal and spatial changes in oxygen and vessel perfusion in tumors in response to microenvironmental normalization. Results: We found that vessel function was highly dependent on tumor type. Although some tumors had vessels with greater oxygen carrying ability than normal skin, most tumors had inefficient vessels. Further, inter-vessel heterogeneity in tumors coincided with heterogeneous response to microenvironmental normalizing agents. Using both vascular and stromal normalizing agents, we show that spatial heterogeneity in oxygen levels persist, even with global reductions in hypoxia. Conclusions: We present the first study to examine the high-resolution spatial and temporal response of tumor vessels to two agents known to improve vascular perfusion globally. Our measurements demonstrate that the heterogeneities in the local imbalance of pro- and anti-angiogenic signaling lead to spatially heterogeneous changes in vessel structure and function. Microscale dynamic vascular changes should be considered in optimizing the dose and schedule of microenvironment normalizing therapies to improve function. Citation Format: John Martin, Ryan Lanning, Dai Fukumura, Timothy Padera, Rakesh Jain. Multiphoton phosphorescence quenching microscopy reveals kinetics of tumor oxygenation during anti-angiogenesis and angiotensin signaling inhibition [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr LB557.

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Slavnoe, N. V., V. V. Markov, N. A. Kovpan, V. M. Rudichenko, and G. N. Terekhova. "Peripheral circulation regulation in patients with the hypothalamic syndrome neuroendocrine metabolic form." Problems of Endocrinology 39, no. 6 (December 15, 1993): 17–20. http://dx.doi.org/10.14341/probl11928.

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Peripheral circulation and regulating hormonal (renin- angiotensin-aldosterone system) and electrolytic (plasma sodium and potassium) factors were studied in 102 patients with the hypothalamic syndrome neuroendocrine metabolic form administered pathogenetic therapy with antiserotonin and dopaminergic drugs as well as routine therapy. Blood plasma sodium vasopressin and aldosterone levels were found increased, arterial vessel reactivity in the forearm reduced, and venous circulation disordered in these patients. Routine therapy failed to normalize electrolytes and hormonal parameters and was conducive to a still more marked reduction of arterial vessel reactivity. Peritol therapy resulted in a reduction of vasopressin concentration and normalization of blood plasma sodium and aldosterone, as well as in improvement of the myogenic mechanisms of vascular tone regulation and normalization of venous circulation parameters. A course of parlodel therapy lead to normalization of blood plasma levels of vasopressin, aldosterone, and sodium but no changes in the regional vessels were observed.

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9

Mpekris, Fotios, James W. Baish, Triantafyllos Stylianopoulos, and Rakesh K. Jain. "Role of vascular normalization in benefit from metronomic chemotherapy." Proceedings of the National Academy of Sciences 114, no. 8 (February 7, 2017): 1994–99. http://dx.doi.org/10.1073/pnas.1700340114.

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Metronomic dosing of chemotherapy—defined as frequent administration at lower doses—has been shown to be more efficacious than maximum tolerated dose treatment in preclinical studies, and is currently being tested in the clinic. Although multiple mechanisms of benefit from metronomic chemotherapy have been proposed, how these mechanisms are related to one another and which one is dominant for a given tumor–drug combination is not known. To this end, we have developed a mathematical model that incorporates various proposed mechanisms, and report here that improved function of tumor vessels is a key determinant of benefit from metronomic chemotherapy. In our analysis, we used multiple dosage schedules and incorporated interactions among cancer cells, stem-like cancer cells, immune cells, and the tumor vasculature. We found that metronomic chemotherapy induces functional normalization of tumor blood vessels, resulting in improved tumor perfusion. Improved perfusion alleviates hypoxia, which reprograms the immunosuppressive tumor microenvironment toward immunostimulation and improves drug delivery and therapeutic outcomes. Indeed, in our model, improved vessel function enhanced the delivery of oxygen and drugs, increased the number of effector immune cells, and decreased the number of regulatory T cells, which in turn killed a larger number of cancer cells, including cancer stem-like cells. Vessel function was further improved owing to decompression of intratumoral vessels as a result of increased killing of cancer cells, setting up a positive feedback loop. Our model enables evaluation of the relative importance of these mechanisms, and suggests guidelines for the optimal use of metronomic therapy.

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10

Yu, Xianzhe, Shan He, Jian Shen, Qiushi Huang, Peng Yang, Lin Huang, Dan Pu, et al. "Tumor vessel normalization and immunotherapy in gastric cancer." Therapeutic Advances in Medical Oncology 14 (January 2022): 175883592211101. http://dx.doi.org/10.1177/17588359221110176.

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Gastric cancer (GC) is a common malignant tumor, and patients with GC have a low survival rate due to limited effective treatment methods. Angiogenesis and immune evasion are two key processes in GC progression, and they act synergistically to promote tumor progression. Tumor vascular normalization has been shown to improve the efficacy of cancer immunotherapy, which in turn may be improved through enhanced immune stimulation. Therefore, it may be interesting to identify synergies between immunomodulatory agents and anti-angiogenic therapies in GC. This strategy aims to normalize the tumor microenvironment through the action of the anti-vascular endothelial growth factor while stimulating the immune response through immunotherapy and prolonging the survival of GC patients.

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11

Maes, Hannelore, Anna Kuchnio, Aleksandar Peric, Stijn Moens, Kris Nys, Katrien De Bock, Annelies Quaegebeur, et al. "Tumor Vessel Normalization by Chloroquine Independent of Autophagy." Cancer Cell 26, no. 2 (August 2014): 190–206. http://dx.doi.org/10.1016/j.ccr.2014.06.025.

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12

Claes, An, and William Leenders. "Vessel normalization by VEGF inhibition: a complex story." Cancer Biology & Therapy 7, no. 7 (July 2008): 1014–16. http://dx.doi.org/10.4161/cbt.7.7.6474.

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13

Brekke, Johan Fredrik, Natalia I. Gokina, and George Osol. "Vascular smooth muscle cell stress as a determinant of cerebral artery myogenic tone." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2210—H2216. http://dx.doi.org/10.1152/ajpheart.00633.2002.

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Although the level of myogenic tone (MT) varies considerably from vessel to vessel, the regulatory mechanisms through which the actual diameter set point is determined are not known. We hypothesized that a unifying principle may be the equalization of active force at the contractile filament level, which would be reflected in a normalization of wall stress or, more specifically, media stress. Branched segments of rat cerebral arteries ranging from <50 μm to >200 μm in diameter were cannulated and held at 60 mmHg with the objectives of: 1) evaluating the relationship between arterial diameter and the extent of myogenic tone, 2) determining whether differences in MT correlate with changes in cytosolic calcium ([Ca2+]i), and 3) testing the hypothesis that a normalization of wall or media stress occurs during the process of tone development. The level of MT increased significantly as vessel size decreased. At 60 mmHg, vascular smooth muscle [Ca2+]i concentrations were similar in all vessels studied (averaging 230 ± 9.2 nM) and not correlated with vessel size or the extent of tone. Wall tension increased with increasing arterial size, but wall stress and media stress were similar in large versus small arteries. Media stress, in particular, was quite uniform in all vessels studied. Both morphological and calcium data support the concept of equalization of media stress (and, hence, vascular smooth muscle cell stress and force) as an underlying mechanism in determining the level of tone present in any particular vessel. The equalization of active (vascular smooth muscle cell) stress may thus explain differences in MT observed in the different-sized vessels constituting the arterial network and provide a link between arterial structure and function, in both short- and long-term (hypertension) pressure adaptation.

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14

Schadler, Keri L., Nicholas J. Thomas, Peter A. Galie, Dong Ha Bhang, Kerry C. Roby, Prince Addai, Jacob E. Till, et al. "Tumor vessel normalization after aerobic exercise enhances chemotherapeutic efficacy." Oncotarget 7, no. 40 (August 31, 2016): 65429–40. http://dx.doi.org/10.18632/oncotarget.11748.

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15

Tian, Lin, Amit Goldstein, Hai Wang, Hin Ching Lo, Ik Sun Kim, Thomas Welte, Kuanwei Sheng, et al. "Mutual regulation of tumour vessel normalization and immunostimulatory reprogramming." Nature 544, no. 7649 (April 2017): 250–54. http://dx.doi.org/10.1038/nature21724.

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16

Nikmaneshi, Mohammad R., Bahar Firoozabadi, and Lance L. Munn. "Optimizing Vessel Normalization and Chemotherapies to Control Tumor Growth." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.07206.

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17

Murphy, P. A., T. N. Kim, G. Lu, A. W. Bollen, C. B. Schaffer, and R. A. Wang. "Notch4 Normalization Reduces Blood Vessel Size in Arteriovenous Malformations." Science Translational Medicine 4, no. 117 (January 18, 2012): 117ra8. http://dx.doi.org/10.1126/scitranslmed.3002670.

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18

Ehling, Manuel, and Massimiliano Mazzone. "Vessel Normalization in the Spot-LIGHT of Cancer Treatment." Trends in Molecular Medicine 22, no. 2 (February 2016): 85–87. http://dx.doi.org/10.1016/j.molmed.2015.12.009.

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19

Treps, Lucas. "EnLIGHTenment of tumor vessel normalization and immunotherapy in glioblastoma." Journal of Pathology 246, no. 1 (July 5, 2018): 3–6. http://dx.doi.org/10.1002/path.5103.

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20

Prieto-Peña, D., I. Martínez-Rodríguez, B. Atienza-Mateo, O. Cuenca-Vera, F. J. Gomez de la Fuente, A. Sanchez-Salmón, M. A. González-Gay, and R. Blanco. "AB0365 CLINICAL, LABORATORY AND IMAGING OUTCOMES IN TOCILIZUMAB-TREATED PATIENTS WITH LARGE VESSEL-GIANT CELL ARTERITIS ACCORDING TO EARLY ONSET THERAPY." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1208.1–1208. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1733.

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Background:Tocilizumab (TCZ) has shown efficacy in large vessel vasculitis (LVV)-Giant Cell Arteritis (LVV-GCA) (1-2). 18F-fluodeoxyglucose positron emission tomography (18F-FDG PET/CT) is useful to assess LVV disease activity (3-5). It is unknown if early treatment with TCZ may have an influence on clinical, laboratory and imaging outcomes.Objectives:To assess clinical, laboratory and PET/CT activity improvement in LVV-GCA patients treated with TCZ according to the time from disease diagnosis to TCZ onset.Methods:Comparative single-center study of 30 LVV-GCA patients treated with TCZ who were divided into 2 groups depending on the time of onset of TCZ: a) early onset (≤ 6 months; n=15) and b) late onset (> 6 months; n=15). All patients had a baseline and a follow-up PET/CT scan. Complete clinical improvement and normalization of laboratory markers (CRP ≤0.5mg/dL and/or ESR ≤ 20 mm/1st hour) was assessed. For imaging evaluation, normalization of total visual score (TVS) was considered when TVS = 0 and normalization of semiquantitative activity if the target to background ratio (TBR) at the thoracic aorta was <1.34.Results:30 patients were included (24 women/6 men); mean age 65.7± 9.8 years. Patients in the TCZ early-onset group were receiving higher doses of prednisone (10.0[5.9-15.0] vs 5.0 [5.0-7.5] mg/day; p< 0.01) and had higher TVS scores (7.0 [4.0-9.0] vs 3.0 [2.0-5.0]; p< 0.01) at baseline (Table 1). Following TCZ initiation, after a mean of 10.8±3.7 months, most patients achieved complete clinical improvement and normalization of ESR and CRP in both groups. Uncoupling with imaging outcomes was observed in both groups. Although non-significant statistical differences were observed, complete TBR normalization (TBR <1.34) and complete TVS normalization (TVS=0) tended to be more frequent in the group of patients who received early-onset TCZ therapy (Figure 1).Table 1.Early-onset TCZ therapy(n= 15)Late-onset TCZ therapy(n=15)pGeneral featuresAge (years), mean ± SD65.8 ± 9.965.5 ± 10.10.94Sex (female), n (%)11 (73.3)13 (86.7)0.65GCA evolution before TCZ onset, median [IQR]2.0 [1.0-5.0]18.0 [9.0-34.0]< 0.01LaboratoryESR (mm/1st hour), mean ± SD34.7 ± 26.330.8 ± 28.70.70CRP (mg/dL), median [IQR]1.1 [0.6-2.3]0.8 [1.8 -2.5]0.28Prednisone dose (mg/day), mean ± SD10.0 [5.9-15.0]5.0 [5.0-7.5]0.01TCZ therapyIntravenous, n (%)10 (66.7)11(73.3)0.99Combined with MTX, n(%)6 (40)8 (53.3)0.46PET /CT activityTBR at thoracic aorta1.86 ± 0.691.54 ± 0.180.09TVS7.0 [4.0-9.0]3.0 [2.0-5.0]< 0.01Complete clinical improvement, n (%)13 (86.7)12 (80)0.99Normalization of ESR and CRP, n (%)15 (100)15 (100)0.99PET/CT improvementComplete TBR normalization6 (40)3 (20)0.23Complete TVS normalization2 (13.3)1 (6.7)0.54CRP: C-reactive protein; ESR: erythrocyte sedimentation rate; TBR: target-to-background ratio. * Normalization of TBR was considered when TBR < 1.34. ** Normalization of TVS was considered when TVS=0.Conclusion:TCZ was effective in patients with LVV-GCA regardless the time from disease diagnosis to TCZ onset. However, complete normalization of vascular activity in PET/CT scans tended to occur more likely in patients who receive early-onset TCZ therapy within the first 6 months of the disease.References:[1]Calderón-Goercke M et al. Semin Arthritis Rheum. 2019; 49:126-135. PMID: 30655091[2]Prieto Peña D et al. Clin Exp Rheumatol. 2020. PMID: 33253103[3]González-Gay MA et al. Expert Rev Clin Immunol. 2018; 14:593-605. PMID: 29877748[4]Martínez-Rodríguez et al. Semin Arthritis Rheum.2018; 47(4): 530-537. PMID: 28967430[5]Prieto-Peña D et al. Semin Arthritis Rheum. 2019; 48:720-727. PMID: 28967430Disclosure of Interests:Diana Prieto-Peña Grant/research support from: UCB Pharma, Roche, Sanofi, Pfizer, AbbVie and Lilly, Isabel Martínez-Rodríguez: None declared, Belén Atienza-Mateo: None declared, Oriana Cuenca-Vera: None declared, Francisco Javier Gomez de la Fuente: None declared, Aida Sanchez-Salmón: None declared, Miguel A González-Gay Grant/research support from: Abbvie, MSD, Jansen and Roche and had consultation fees/participation in company sponsored speaker´s bureau from Abbvie, Pfizer, Roche, Sanofi, Lilly, Celgene and MSD, Ricardo Blanco Grant/research support from: Abbvie, MSD and Roche, and had consultation fees/participation in company sponsored speaker´s bureau from Abbvie, Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma and MSD

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Datta, Meenal, Laura E. Via, Walid S. Kamoun, Chong Liu, Wei Chen, Giorgio Seano, Danielle M. Weiner, et al. "Anti-vascular endothelial growth factor treatment normalizes tuberculosis granuloma vasculature and improves small molecule delivery." Proceedings of the National Academy of Sciences 112, no. 6 (January 26, 2015): 1827–32. http://dx.doi.org/10.1073/pnas.1424563112.

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Tuberculosis (TB) causes almost 2 million deaths annually, and an increasing number of patients are resistant to existing therapies. Patients who have TB require lengthy chemotherapy, possibly because of poor penetration of antibiotics into granulomas where the bacilli reside. Granulomas are morphologically similar to solid cancerous tumors in that they contain hypoxic microenvironments and can be highly fibrotic. Here, we show that TB-infected rabbits have impaired small molecule distribution into these disease sites due to a functionally abnormal vasculature, with a low-molecular-weight tracer accumulating only in peripheral regions of granulomatous lesions. Granuloma-associated vessels are morphologically and spatially heterogeneous, with poor vessel pericyte coverage in both human and experimental rabbit TB granulomas. Moreover, we found enhanced VEGF expression in both species. In tumors, antiangiogenic, specifically anti-VEGF, treatments can “normalize” their vasculature, reducing hypoxia and creating a window of opportunity for concurrent chemotherapy; thus, we investigated vessel normalization in rabbit TB granulomas. Treatment of TB-infected rabbits with the anti-VEGF antibody bevacizumab significantly decreased the total number of vessels while normalizing those vessels that remained. As a result, hypoxic fractions of these granulomas were reduced and small molecule tracer delivery was increased. These findings demonstrate that bevacizumab treatment promotes vascular normalization, improves small molecule delivery, and decreases hypoxia in TB granulomas, thereby providing a potential avenue to improve delivery and efficacy of current treatment regimens.

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22

Du, Shi, Hui Xiong, Cheng Xu, Yun Lu, and Jing Yao. "Attempts to strengthen and simplify the tumor vascular normalization strategy using tumor vessel normalization promoting nanomedicines." Biomaterials Science 7, no. 3 (2019): 1147–60. http://dx.doi.org/10.1039/c8bm01350k.

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23

Arjaans, Marlous, Sjoukje F. Oosting, Carolina P. Schröder, and Elisabeth G. E. de Vries. "Bevacizumab-Induced Vessel Normalization Hampers Tumor Uptake of Antibodies—Response." Cancer Research 73, no. 23 (November 21, 2013): 7147–48. http://dx.doi.org/10.1158/0008-5472.can-13-2532.

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24

Ganss, Ruth. "Tumour vessel normalization and immune checkpoint blockade: a new synergism." Immunology & Cell Biology 95, no. 6 (May 23, 2017): 497–98. http://dx.doi.org/10.1038/icb.2017.30.

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Kim, S. J., J. Kyung Hee, S. Mi Kwon, L. Joo Han, and H. Soon-Sun. "Synergistic anticancer effects through tumor vessel normalization by PI3K inhibitors." European Journal of Cancer 69 (December 2016): S129. http://dx.doi.org/10.1016/s0959-8049(16)32983-5.

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26

Bhattarai, Pravin, Sadaf Hameed, and Zhifei Dai. "Recent advances in anti-angiogenic nanomedicines for cancer therapy." Nanoscale 10, no. 12 (2018): 5393–423. http://dx.doi.org/10.1039/c7nr09612g.

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Yu, Shao Rong, Yi Hui Yin, and Bing Xu. "Blast Pressure Analysis of a Pressure Vessel." Advanced Materials Research 295-297 (July 2011): 2417–21. http://dx.doi.org/10.4028/www.scientific.net/amr.295-297.2417.

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The sensitivity of blast pressure of a pressure vessel to the material strength, the effective welding depth and the relative radius is studied by finite element simulations and single-factor sensitivity analyses. And the sensitivity coefficients are obtained by normalization procession. Furthermore, a three-factor regression model is obtained by multi-factor numerical experiments. The investigation of this paper provides guidelines for further researches of relating problems.

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Ma, Yuliang, Xue Li, Xiaopeng Duan, Yun Peng, and Yingchun Zhang. "Retinal Vessel Segmentation by Deep Residual Learning with Wide Activation." Computational Intelligence and Neuroscience 2020 (October 10, 2020): 1–11. http://dx.doi.org/10.1155/2020/8822407.

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Purpose. Retinal blood vessel image segmentation is an important step in ophthalmological analysis. However, it is difficult to segment small vessels accurately because of low contrast and complex feature information of blood vessels. The objective of this study is to develop an improved retinal blood vessel segmentation structure (WA-Net) to overcome these challenges. Methods. This paper mainly focuses on the width of deep learning. The channels of the ResNet block were broadened to propagate more low-level features, and the identity mapping pathway was slimmed to maintain parameter complexity. A residual atrous spatial pyramid module was used to capture the retinal vessels at various scales. We applied weight normalization to eliminate the impacts of the mini-batch and improve segmentation accuracy. The experiments were performed on the DRIVE and STARE datasets. To show the generalizability of WA-Net, we performed cross-training between datasets. Results. The global accuracy and specificity within datasets were 95.66% and 96.45% and 98.13% and 98.71%, respectively. The accuracy and area under the curve of the interdataset diverged only by 1%∼2% compared with the performance of the corresponding intradataset. Conclusion. All the results show that WA-Net extracts more detailed blood vessels and shows superior performance on retinal blood vessel segmentation tasks.

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Deng, Liwei, Shanshan Liu, Xiaofei Wang, Guofu Zhao, and Jiazhong Xu. "Particle Swarm Optimization and Salp Swarm Algorithm for the Segmentation of Diabetic Retinal Blood Vessel Images." Computational Intelligence and Neuroscience 2022 (August 23, 2022): 1–14. http://dx.doi.org/10.1155/2022/1936482.

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In recent years, the incidence of diabetes has been increasing year by year. Since most of the fundus lesions are located near blood vessels, the image information is complex, and the end vessels are difficult to identify. So, a new segmentation method of diabetic retinal vessel images based on particle swarm optimization and salp swarm algorithm is proposed. This paper uses a Gaussian filter to enhance the main blood vessels, and a top-bot hat transform is used to strengthen the end vessels. The preprocessing process is completed by combining and reconstructing the two images through a normalization operation. The improved particle swarm optimization and salp swarm algorithms perform multi-threshold segmentation on the preprocessed vessel images. The best fit value, Structural Similarity Index Measure, Peak Signal to Noise Rati, feature similarity index measure, sensitivity, accuracy, regional consistency, Dice coefficient, Jaccard similarity, and Shannon entropy are selected for comprehensive evaluation and analysis. The results showed that this paper’s improved particle swarm-salp swarm algorithm for segmenting diabetic retinal blood vessel images is more efficient, and the threshold is better. The vascular segmentation method in this paper is applied in medical image processing, which improves the accuracy of medical image processing and reduces the computational effort.

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JIANG, AIXIANG, WEI PAN, LIMING C. MILBAUER, YU SHYR, and ROBERT P. HEBBEL. "A PRACTICAL QUESTION BASED ON CROSS-PLATFORM MICROARRAY DATA NORMALIZATION: ARE BOEC MORE LIKE LARGE VESSEL OR MICROVASCULAR ENDOTHELIAL CELLS OR NEITHER OF THEM?" Journal of Bioinformatics and Computational Biology 05, no. 04 (August 2007): 875–93. http://dx.doi.org/10.1142/s0219720007002989.

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Since the available microarray data of BOEC (human blood outgrowth endothelial cells), large vessel, and microvascular endothelial cells were from two different platforms, a working cross-platform normalization method was needed to make these data comparable. With six HUVEC (human umbilical vein endothelial cells) samples hybridized on two-channel cDNA arrays and six HUVEC samples on Affymetrix arrays, 64 possible combinations of a three-step normalization procedure were investigated to search for the best normalization method, which was selected, based on two criteria measuring the extent to which expression profiles of biological samples of the same cell type arrayed on two platforms were indistinguishable. Next, three discriminative gene lists between the large vessel and the microvascular endothelial cells were achieved by SAM (significant analysis of microarrays), PAM (prediction analysis for microarrays), and a combination of SAM and PAM lists. The final discriminative gene list was selected by SVM (support vector machine). Based on this discriminative gene list, SVM classification analysis with best tuning parameters and 10,000 times of validations showed that BOEC were far from large vessel cells, they either formed their own class, or fell into the microvascular class. Based on all the common genes between the two platforms, SVM analysis further confirmed this conclusion.

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Lee, Eun-Ah, Beom Yong Park, Nuri Kang, Cheon Ho Park, and Weon Sup Lee. "Abstract 5970: Tumor vessel normalization by a novel anti-TIE2 antibody PMC-403 enhances the effectiveness of radiation therapy on cancer therapy." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5970. http://dx.doi.org/10.1158/1538-7445.am2022-5970.

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Abstract Purpose: The delivery of drugs and immune cells into the tumor microenvironment is limited due to abnormal tumor vessel which is characterized as low oxygen concentration, low perfusion rate and leakage. It leads to diminish the efficacy radiation therapy. Traditional anti-angiogenesis strategies attempt to reduce the tumor vascular supply, but their success is restricted by insufficient efficacy or development of resistance. To solve the problem, we try to using PMC-403, which can normalize the abnormal condition of tumor vessel. Experimental procedures: Target selectivity: It was measured by Surface Plasmon Resonance (SPR) assay. Human TIE2 Cho-K1 cells or mouse TIE2 Cho-K1 cells were tested for species cross-reactive assay based on flow cytometry (FACS).In vitro studies: Human umbilical vein endothelial cells (HUVEC) were used for TIE2 signal pathway analysis with western blot assay and efficacy analysis with VEGF-induced vessel permeability assay.In vivo study: Glioblastoma model mice were employed for the assessment of tumor vessel normalizing activity of 1 mg/mouse PMC-403. CT26 colon cancer model mice were used to evaluate the anti-tumor efficacy of PMC403 (10 mg/kg) in combination with radiation therapy. Hypoxyprobe was used to measure the improvement of hypoxic conditions in tumor tissue. Summary of data: PMC-403 has a nanomolar range of affinity for both human or mouse TIE2 expressing cells. This contributed to dose-dependent ANG1-like TIE2 and FOXO1 phosphorylation and inhibited VEGF-induced vascular leakage, thereby contributing to ANG1-like vascular normalization. Moreover, similar to ANG-1, p-VEGFR2 and p-VE-Cadherin levels were significantly reduced by PMC-403, suggesting that PMC-403 can normalize blood vessels. In addition, PMC-403 stabilized abnormal tumor blood vessels in the glioblastoma mouse model and significantly reduced tumor growth and tumor hypoxia in the combination treatment (PMC-403 + radiation therapy) compared to radiation therapy alone, although the antitumor effect of PMC-403 alone was not effective in the same condition model. Conclusions: PMC-403, an anti-TIE2 monoclonal antibody, is a novel tumor vessel stabilizer. PMC-403 improved tumor microenvironment hypoxic condition that synergized with radiotherapy when it combined together for the anticancer therapy. These data strongly support the notion that PMC-403 can effectively treat tumors even with low doses of radiation by stabilizing tumor blood vessels. Citation Format: Eun-Ah Lee, Beom Yong Park, Nuri Kang, Cheon Ho Park, Weon Sup Lee. Tumor vessel normalization by a novel anti-TIE2 antibody PMC-403 enhances the effectiveness of radiation therapy on cancer therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5970.

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Yang, Jun, Chengde Liao, Yifan Liu, Guangjun Yang, Tengfei Ke, Yingying Ding, and Qinqing Li. "MR imaging biomarkers evaluating vascular normalization window after anti-vessel treatment." Oncotarget 9, no. 15 (November 21, 2017): 11964–76. http://dx.doi.org/10.18632/oncotarget.22600.

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Hellmann, Kurt. "Recognition of tumor blood vessel normalization as a new antiangiogenic concept." Nature Medicine 10, no. 4 (April 1, 2004): 329. http://dx.doi.org/10.1038/nm0404-329a.

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Magrini, Elena, Alessandra Villa, Francesca Angiolini, Andrea Doni, Giovanni Mazzarol, Noemi Rudini, Luigi Maddaluno, et al. "Endothelial deficiency of L1 reduces tumor angiogenesis and promotes vessel normalization." Journal of Clinical Investigation 124, no. 11 (November 3, 2014): 5085. http://dx.doi.org/10.1172/jci79236.

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Magrini, Elena, Alessandra Villa, Francesca Angiolini, Andrea Doni, Giovanni Mazzarol, Noemi Rudini, Luigi Maddaluno, et al. "Endothelial deficiency of L1 reduces tumor angiogenesis and promotes vessel normalization." Journal of Clinical Investigation 124, no. 10 (August 26, 2014): 4335–50. http://dx.doi.org/10.1172/jci70683.

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Fleming, A. D., S. Philip, K. A. Goatman, J. A. Olson, and P. F. Sharp. "Automated microaneurysm detection using local contrast normalization and local vessel detection." IEEE Transactions on Medical Imaging 25, no. 9 (September 2006): 1223–32. http://dx.doi.org/10.1109/tmi.2006.879953.

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Manzoor ali, Qamar un nisa. "Contrast Normalization Filtering Modules for Segmentations of Retinal Blood Vessels from Color Retinal Fundus Images." Sukkur IBA Journal of Emerging Technologies 5, no. 1 (June 30, 2022): 64–77. http://dx.doi.org/10.30537/sjet.v5i1.1025.

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Vision loss is one of the main complications of eye disease, especially diabetic retinopathy (DR), because DR is a silent disease affecting the retina of the eye and resulting in loss of vision. Manual observation of eye disease takes time and delays effective treatment, so computerized methods are used to diagnose eye disease by extracting their features such as blood vessels, optic disc, and other abnormalities. Many computerized methods are proposed but it is still lacking to obtain small vessels. To overcome this problem, we have proposed methods based on image processing techniques for detection of retinal vessels. The proposed method is based on the elimination of uneven illumination using morphological tactics and principal component analysis. These initial steps are known as the preprocessing module, and our post-processing module contains the vessel coherence and the double threshold binarization method to obtain an image of the segmented vessels. Our proposed method obtained comparable results (average results (sensitivity: 0.78, specificity: 0.95 and precision: 0.951)) compared to the existing methods on the DRIVE and STARE databases.

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Mpekris, Fotios, Chrysovalantis Voutouri, James W. Baish, Dan G. Duda, Lance L. Munn, Triantafyllos Stylianopoulos, and Rakesh K. Jain. "Combining microenvironment normalization strategies to improve cancer immunotherapy." Proceedings of the National Academy of Sciences 117, no. 7 (February 3, 2020): 3728–37. http://dx.doi.org/10.1073/pnas.1919764117.

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Advances in immunotherapy have revolutionized the treatment of multiple cancers. Unfortunately, tumors usually have impaired blood perfusion, which limits the delivery of therapeutics and cytotoxic immune cells to tumors and also results in hypoxia—a hallmark of the abnormal tumor microenvironment (TME)—that causes immunosuppression. We proposed that normalization of TME using antiangiogenic drugs and/or mechanotherapeutics can overcome these challenges. Recently, immunotherapy with checkpoint blockers was shown to effectively induce vascular normalization in some types of cancer. Although these therapeutic approaches have been used in combination in preclinical and clinical studies, their combined effects on TME are not fully understood. To identify strategies for improved immunotherapy, we have developed a mathematical framework that incorporates complex interactions among various types of cancer cells, immune cells, stroma, angiogenic molecules, and the vasculature. Model predictions were compared with the data from five previously reported experimental studies. We found that low doses of antiangiogenic treatment improve immunotherapy when the two treatments are administered sequentially, but that high doses are less efficacious because of excessive vessel pruning and hypoxia. Stroma normalization can further increase the efficacy of immunotherapy, and the benefit is additive when combined with vascular normalization. We conclude that vessel functionality dictates the efficacy of immunotherapy, and thus increased tumor perfusion should be investigated as a predictive biomarker of response to immunotherapy.

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Zhou, Jing, Yaocheng Li, Xuejing Shi, Shulan Hao, Fupeng Zhang, Zhi Guo, Yu Gao, Hao Guo, and Likun Liu. "Oridonin inhibits tumor angiogenesis and induces vessel normalization in experimental colon cancer." Journal of Cancer 12, no. 11 (2021): 3257–64. http://dx.doi.org/10.7150/jca.55929.

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Yang, Jun, Chengde Liao, Yifan Liu, Guangjun Yang, Tengfei Ke, Yingying Ding, and Qinqing Li. "Correction: MR imaging biomarkers evaluating vascular normalization window after anti-vessel treatment." Oncotarget 13, no. 1 (January 1, 2022): 641. http://dx.doi.org/10.18632/oncotarget.28217.

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Carmeliet, Peter, and Rakesh K. Jain. "Principles and mechanisms of vessel normalization for cancer and other angiogenic diseases." Nature Reviews Drug Discovery 10, no. 6 (June 2011): 417–27. http://dx.doi.org/10.1038/nrd3455.

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Claes, An, Pieter Wesseling, Judith Jeuken, Cathy Maass, Arend Heerschap, and William P. J. Leenders. "Antiangiogenic compounds interfere with chemotherapy of brain tumors due to vessel normalization." Molecular Cancer Therapeutics 7, no. 1 (January 2008): 71–78. http://dx.doi.org/10.1158/1535-7163.mct-07-0552.

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Kim, Soo Jung, Kyung Hee Jung, Mi Kwon Son, Jung Hee Park, Hong Hua Yan, Zhenghuan Fang, Yeo Wool Kang, Boreum Han, Joo Han Lim, and Soon-Sun Hong. "Tumor vessel normalization by the PI3K inhibitor HS-173 enhances drug delivery." Cancer Letters 403 (September 2017): 339–53. http://dx.doi.org/10.1016/j.canlet.2017.06.035.

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Lv, Jie, Jin-feng Cao, Yan Cai, Yu Zhou, Quan Long, Wei Yao, and Shi-xiong Xu. "Numerical Simulation of Solid Tumor Blood Perfusion and Drug Delivery during the “Vascular Normalization Window” with Antiangiogenic Therapy." Journal of Applied Mathematics 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/190371.

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To investigate the influence of vascular normalization on solid tumor blood perfusion and drug delivery, we used the generated blood vessel network for simulations. Considering the hemodynamic parameters changing after antiangiogenic therapies, the results show that the interstitial fluid pressure (IFP) in tumor tissue domain decreases while the pressure gradient increases during the normalization window. The decreased IFP results in more efficient delivery of conventional drugs to the targeted cancer cells. The outcome of therapies will improve if the antiangiogenic therapies and conventional therapies are carefully scheduled.

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Goel, Shom, Dan G. Duda, Lei Xu, Lance L. Munn, Yves Boucher, Dai Fukumura, and Rakesh K. Jain. "Normalization of the Vasculature for Treatment of Cancer and Other Diseases." Physiological Reviews 91, no. 3 (July 2011): 1071–121. http://dx.doi.org/10.1152/physrev.00038.2010.

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New vessel formation (angiogenesis) is an essential physiological process for embryologic development, normal growth, and tissue repair. Angiogenesis is tightly regulated at the molecular level. Dysregulation of angiogenesis occurs in various pathologies and is one of the hallmarks of cancer. The imbalance of pro- and anti-angiogenic signaling within tumors creates an abnormal vascular network that is characterized by dilated, tortuous, and hyperpermeable vessels. The physiological consequences of these vascular abnormalities include temporal and spatial heterogeneity in tumor blood flow and oxygenation and increased tumor interstitial fluid pressure. These abnormalities and the resultant microenvironment fuel tumor progression, and also lead to a reduction in the efficacy of chemotherapy, radiotherapy, and immunotherapy. With the discovery of vascular endothelial growth factor (VEGF) as a major driver of tumor angiogenesis, efforts have focused on novel therapeutics aimed at inhibiting VEGF activity, with the goal of regressing tumors by starvation. Unfortunately, clinical trials of anti-VEGF monotherapy in patients with solid tumors have been largely negative. Intriguingly, the combination of anti-VEGF therapy with conventional chemotherapy has improved survival in cancer patients compared with chemotherapy alone. These seemingly paradoxical results could be explained by a “normalization” of the tumor vasculature by anti-VEGF therapy. Preclinical studies have shown that anti-VEGF therapy changes tumor vasculature towards a more “mature” or “normal” phenotype. This “vascular normalization” is characterized by attenuation of hyperpermeability, increased vascular pericyte coverage, a more normal basement membrane, and a resultant reduction in tumor hypoxia and interstitial fluid pressure. These in turn can lead to an improvement in the metabolic profile of the tumor microenvironment, the delivery and efficacy of exogenously administered therapeutics, the efficacy of radiotherapy and of effector immune cells, and a reduction in number of metastatic cells shed by tumors into circulation in mice. These findings are consistent with data from clinical trials of anti-VEGF agents in patients with various solid tumors. More recently, genetic and pharmacological approaches have begun to unravel some other key regulators of vascular normalization such as proteins that regulate tissue oxygen sensing (PHD2) and vessel maturation (PDGFRβ, RGS5, Ang1/2, TGF-β). Here, we review the pathophysiology of tumor angiogenesis, the molecular underpinnings and functional consequences of vascular normalization, and the implications for treatment of cancer and nonmalignant diseases.

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Ollauri-Ibáñez, Claudia, Blanca Ayuso-Íñigo, and Miguel Pericacho. "Hot and Cold Tumors: Is Endoglin (CD105) a Potential Target for Vessel Normalization?" Cancers 13, no. 7 (March 28, 2021): 1552. http://dx.doi.org/10.3390/cancers13071552.

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Tumors are complex masses formed by malignant but also by normal cells. The interaction between these cells via cytokines, chemokines, growth factors, and enzymes that remodel the extracellular matrix (ECM) constitutes the tumor microenvironment (TME). This TME can be determinant in the prognosis and the response to some treatments such as immunotherapy. Depending on their TME, two types of tumors can be defined: hot tumors, characterized by an immunosupportive TME and a good response to immunotherapy; and cold tumors, which respond poorly to this therapy and are characterized by an immunosuppressive TME. A therapeutic strategy that has been shown to be useful for the conversion of cold tumors into hot tumors is vascular normalization. In this review we propose that endoglin (CD105) may be a useful target of this strategy since it is involved in the three main processes involved in the generation of the TME: angiogenesis, inflammation, and cancer-associated fibroblast (CAF) accumulation. Moreover, the analysis of endoglin expression in tumors, which is already used in the clinic to study the microvascular density and that is associated with worse prognosis, could be used to predict a patient’s response to immunotherapy.

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Jain, Rakesh K. "Reply to 'Recognition of tumor blood vessel normalization as a new antiangiogenic concept'." Nature Medicine 10, no. 4 (April 1, 2004): 329–30. http://dx.doi.org/10.1038/nm0404-329b.

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Dettori, D., M. Mazzone, R. Leite-de-Oliveira, J. Aragones, B. Jonckx, A. Luttun, S. Vinckier, B. Jordan, B. Gallez, and P. Carmeliet. "Heterozygous deficiency of the oxygen sensor PHD2 prevents metastasis by inducing vessel normalization." European Journal of Cancer Supplements 6, no. 9 (July 2008): 16. http://dx.doi.org/10.1016/s1359-6349(08)71235-7.

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Zheng, Xichen, Naidong Zhang, Long Qian, Xuexiang Wang, Peng Fan, Jiajie Kuai, Siyang Lin, et al. "CTLA4 blockade promotes vessel normalization in breast tumors via the accumulation of eosinophils." International Journal of Cancer 146, no. 6 (December 28, 2019): 1730–40. http://dx.doi.org/10.1002/ijc.32829.

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Ayuso-Íñigo, Blanca, Lucía Méndez-García, Miguel Pericacho, and José M. Muñoz-Félix. "The Dual Effect of the BMP9–ALK1 Pathway in Blood Vessels: An Opportunity for Cancer Therapy Improvement?" Cancers 13, no. 21 (October 28, 2021): 5412. http://dx.doi.org/10.3390/cancers13215412.

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The improvement of cancer therapy efficacy, the extension of patient survival and the reduction of adverse side effects are major challenges in cancer research. Targeting blood vessels has been considered a promising strategy in cancer therapy. Since the tumor vasculature is disorganized, leaky and triggers immunosuppression and tumor hypoxia, several strategies have been studied to modify tumor vasculature for cancer therapy improvement. Anti-angiogenesis was first described as a mechanism to prevent the formation of new blood vessels and prevent the oxygen supply to tumor cells, showing numerous limitations. Vascular normalization using low doses of anti-angiogenic drugs was purposed to overcome the limitations of anti-angiogenic therapies. Other strategies such as vascular promotion or the induction of high endothelial venules are being studied now to improve cancer therapy. Bone morphogenetic protein 9 (BMP9) exerts a dual effect through the activin receptor-like kinase 1 (ALK1) receptor in blood vessel maturation or activation phase of angiogenesis. Thus, it is an interesting pathway to target in combination with chemotherapies or immunotherapies. This review manuscript explores the effect of the BMP9–ALK1 pathway in tumor angiogenesis and the possible usefulness of targeting this pathway in anti-angiogenesis, vascular normalization or vascular promotion therapies.

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