Accumulating evidence shows the emerging roles of the S1P signaling pathway in the regulation of blood vessel functions, including vascular formation, vascular permeability, and the proliferative responses to injury (22, 32). Compared with S1P1, the roles of S1P2 in vascular pathophysiology are relatively poorly understood. In the present investigation, we studied the role of S1P2 in tumor angiogenesis. The present study showed that S1P2 is expressed in both ECs and VSMCs of tumor blood vessels and BMDCs infiltrating in the tumor stroma, as well as in normal blood vessels in a variety of organs. Deletion of host S1P2 resulted in stimulation of tumor angiogenesis with enhanced vascular mural cell recruitment and myeloid cell mobilization, leading to acceleration of tumor cell proliferation and tumor growth. These data collectively suggest that S1P2, which is expressed in ECs and BDMC, is involved in suppression of tumor angiogenesis. The action of S1P2 in tumor angiogenesis contrasts with ... Angiogenesis, the summation of multiple cellular and biologic processes culminating in the propagation of blood vessels, has been the subject of extensive examination in the context of tumor biology over the past 4 decades since it was first proposed by Judah Folkman in 1971 (1). Solid tumor growth and progression is dependent on tumor-associated angiogenesis. Tumor expression and circulating levels of angiogenic factors have been correlated with aggressive tumor growth, predilection for metastasis, and prognosis in a wide array of solid tumors, including lung cancer (2-4). Although many putative regulators of angiogenesis have been identified, 2 secreted factors, VEGF and basic fibroblast growth factor (bFGF), have been, in particular, strongly implicated in tumor-associated angiogenesis (5). VEGF and bFGF interact with distinct families of tyrosine kinase receptors (RTK) on the surface of endothelial cells and activate multiple downstream signaling pathways. Together, these pathways promote ... TY - JOUR. T1 - Prognostic and predictive value of tumour angiogenesis in ovarian carcinomas. AU - Gasparini, Giampietro. AU - Bonoldi, Emanuela. AU - Viale, Giuseppe. AU - Verderio, Paolo. AU - Boracchi, Patrizia. AU - Panizzoni, Gino A.. AU - Radaelli, Umberto. AU - Di Bacco, Alessandra. AU - Guglielmi, Rosa B.. AU - Bevilacqua, Pierantonio. PY - 1996. Y1 - 1996. N2 - Experimental studies suggest that angiogenesis plays an important role in the pathogenesis of ascites and progression of ovarian cancer. To evaluate the association of intratumoral microvessel density (IMD) with the conventional clinicopathologic features and to determine the capability of these factors in predicting responsiveness to platinum-based chemotherapy and overall survival (OS) we studied 112 ovarian carcinomas. IMD was determined using the anti-CD31 antibody and immunocytochemistry. In the entire series, we correlated IMD with the other features. In the subgroup of patients with FIGO stage III-IV (60 cases), we ... There is a very strong link between the vascularization of a tumour and the spread of the disease, both locally and to distant sites (Gimbrone et al., 1974, J. Natl. Cancer Inst. 52, 413-27; Muthukkaruppan et al, 1982, J. Natl. Cancer Inst. 69, 699-704; Ellis & Fiddler, 1995, Lancet 346, 388-9). A tumour becomes vascularized by a process known as angiogenesis. Tumour angiogenesis is initiated by the release of diffusible substances by the tumour, whereby neighbouring capillary vessels are stimulated to grow and eventually penetrate the tumour. Anti-angiogenesis has been proposed as a potential strategy for the treatment of cancer (Folkman, 1995, Nature Med. 1, 21-31; Harris et al, 1996, Breast Cancer Res. Treat. 38, 97-108). In this paper, a mathematical model of the development of the tumour vasculature is presented. By suitable manipulation of the model parameters, we simulate various anti-angiogenesis strategies and we examine the roles that haptotaxis and chemotaxis may play during the ... The present study demonstrated the validity and superiority of CD105 as a marker of angiogenesis in NSCLC; the CD105-IMVD was more closely correlated with the expression of VEGF than the CD34-IMVD. Kumar et al. (11 , 13 , 15, 16, 17, 18) and others have demonstrated that anti-CD105 antibodies preferentially react with activated ECs in tissues participating in angiogenesis, such as tumor tissues, and that antibodies against pan-ECs, such as anti-CD34 antibodies, react with normal vessels, as well as activated vessels. According to the hypothesis, we tried to define the CD34-IMVD-CD105-IMVD as the baseline IMVD. As a result, the baseline IMVD proved not at all to be correlated with VEGF expression, suggesting the baseline IMVD was not a measurement of angiogenesis but a measurement of vessels just trapped within tumor tissues. Of course, it should be noted that angiogenesis is not influenced only by VEGF but also other angiogenic factors and antiangiogenic factors, such as angiostatin. Comparative ... Angiogenesis, the process of new blood vessel formation from existing vessels, plays an important role in normal physiology (Tonnesen et al., 2000), as well as in many pathological conditions including cancer (Folkman, 1971; Papetti and Herman, 2002), macular degeneration (Ahmad et al., 2011), and various vascular diseases (Khurana et al., 2005). Strikingly, increased angiogenesis is observed in many types of human cancers (Bergers and Benjamin, 2003; Dvorak, 2003), whereas angiogenesis is decreased in age-associated vascular diseases (Ungvari et al., 2010). Therefore, diseases that are associated with increased angiogenesis, such as human cancers, can be treated by inhibiting angiogenesis (Folkman, 2007). In contrast, stimulation of angiogenesis could be beneficial in the treatment of coronary artery disease and other vascular diseases characterized by insufficient blood flow to target organs as a result of blocked or damaged blood vessels (Khan et al., 2002; Al Sabti, 2007). Many factors that ... Now, Barbara Ranscht, Ph.D., and Robert Oshima, Ph.D., at Burnham have led a team that developed the first living model to study this proteins effect on tumor angiogenesis by creating a strain of mice that develops spontaneous mammary gland tumors in the absence of T-cadherin. Their results appeared March 1 in Cancer Research.. "Evidence of T-cadherins role in vascularization has been somewhat controversial," explains Dr. Ranscht, senior author of the study, which includes Drs. Lionel Hebbard and Michèle Garlatti from the Burnham Institute as equally contributing first authors and Drs. Robert Cardiff and Lawrence Young as collaborators from the University of California, Davis. "But our knockout model clearly shows that T-cadherin plays a role in promoting tumor vascularization, with implications for tumor growth and animal survival.". The tumor model developed in Dr. Ranschts laboratory shows that loss of T-cadherin slows down tumor growth and improves survival compared to controls where ... For the paper by Seiichiro Takahashi, Markus Moser, Eloi Montanez, Takanari Nakano, Makoto Seo, Steffen Backert, Ikuo Inoue, Takuya Awata, Sigehiro Katayama, Tsugikazu Komoda, and Reinhard Fässler (The fibronectin RGD motif is required for multiple angiogenic events during early embryonic development. Arterioscler Thromb Vasc Biol. 2009 August 27 [Epub ahead of print]; DOI: 10.1161/ATVBAHA.108.181164), after an investigation by the Saitama Medical University Internal Investigation Committee, the Committee concluded that it was unethical for Dr. Takahashi to publish this paper for the following reasons: ... Sigma-Aldrich offers abstracts and full-text articles by [Bing Yan, Long Liu, Ying Zhao, Li-Juan Xiu, Da-Zhi Sun, Xuan Liu, Ye Lu, Jun Shi, Yin-Cheng Zhang, Yong-Jin Li, Xiao-Wei Wang, Yu-Qi Zhou, Shou-Han Feng, Can Lv, Pin-Kang Wei, Zhi-Feng Qin]. TY - JOUR. T1 - A catechin nanoformulation inhibits WM266 melanoma cell proliferation, migration and associated neo-angiogenesis. AU - di Leo, Nicoletta. AU - Battaglini, Matteo. AU - Berger, Liron. AU - Giannaccini, Martina. AU - Dente, Luciana. AU - Hampel, Silke. AU - Vittorio, Orazio. AU - Cirillo, Giuseppe. AU - Raffa, Vittoria. N1 - This work was supported by the EU (Marie Curie programme), by Fondazione Veronesi, by Fondazione Arpa, by Fondazione Pisa, and by the Italian "Ministero dellIstruzione, dellUniversità e della Ricerca" (PRA, progetti di ricerca di ateneo).. PY - 2017/5. Y1 - 2017/5. N2 - We validated the anticancer potential of a nanoformulation made by (+)-catechin, gelatin and carbon nanotubes in terms of inhibition of cancer cell proliferation, migration and associated neo-angiogenesis. Gelatin was selected to stabilize the catechin without compromising its anti-oxidant potential and the carbon nanotubes were used to increase its intracellular bioavailability. The ... TY - JOUR. T1 - Targeting tumor neoangiogenesis via targeted adenoviral vector to achieve effective cancer gene therapy for disseminated neoplastic disease. AU - Lee, Myungeun. AU - Lu, Zhi Hong. AU - Li, Jie. AU - Kashentseva, Elena A.. AU - Dmitriev, Igor P.. AU - Mendonca, Samir A.. AU - Curiel, David T.. PY - 2020/3. Y1 - 2020/3. N2 - The application of cancer gene therapy has heretofore been restricted to local, or locoregional, neoplastic disease contexts. This is owing to the lack of gene transfer vectors, which embody the requisite target cell selectivity in vivo required for metastatic disease applications. To this end, we have explored novel vector engineering paradigms to adapt adenovirus for this purpose. Our novel strategy exploits three distinct targeting modalities that operate in functional synergy. Transcriptional targeting is achieved via the hROBO4 promoter, which restricts transgene expression to proliferative vascular endothelium. Viral binding is modified by incorporation ... In the early 1970s (1) , Folkman hypothesized that solid tumor growth and metastasis are critically dependent on angiogenesis, the formation of new blood vessels from preexisting vasculature. Over the past few decades, many mediators of angiogenesis have been characterized, providing new and important targets for drug discovery research. Considerable effort has been directed toward the development of pharmacological agents that modulate specific pathways associated with angiogenesis.. Among the many known triggers of tumor angiogenesis, VEGF6 has emerged as a relatively specific effector (2 , 3) . In fact, VEGF expression has been observed in many human tumor types (4, 5, 6, 7, 8, 9, 10) , is up-regulated in response to hypoxia (11 , 12) , and has been specifically linked with tumor neovascularization (13, 14, 15) . Tumor cells engineered to express VEGF constitutively exhibit enhanced tumor growth and angiogenic phenotypes (16) . Conversely, treatments with anti-VEGF monoclonal antibodies have ... TY - JOUR. T1 - Angiogenesis as targeted breast cancer therapy. AU - Hayes, Daniel F.. AU - Miller, Kathy. AU - Sledge, George. PY - 2007. Y1 - 2007. N2 - Neo-angiogenesis appears to be a critical feature of tumor growth, migration, and metastasis. Therefore, inhibition of angiogenesis is an appealing strategy for treatment of cancer. Since angiogenesis is the result of several mechanistic processes, controlled by numerable pro- and anti-angiogenic factors and their receptors, multiple possibilities to prevent or reverse tumor-induced neo-vascularization have been proposed. Of these, currently, the most promising approach has been the use of bevacizumab, a humanized monoclonal antibody directed against the most potent pro-angiogenic factor, vascular endothelial growth factor (VEGF). Bevacizumab has been shown to be active in several malignancies, in particular colo-rectal cancer. Although early studies of bevacizumab in far-advanced metastatic breast cancer were disappointing, the results of a ... Angiogenesis is defined as the formation of new blood vessels from pre-existing vasculature. Angiogenesis is relevant not just to disease tumors and to non-neoplastic diseases most notably macular degeneration, psoriasis, endometriosis, {and,as well as arthritis. The development {and,because well as metastasis of tumors tend to be really critically dependent upon angiogenesis. Therefore, the inhibition of angiogenesis grew to become {an,a particular,a few sort of,some of important therapeutic approach for cancer. Although the existing anti-angiogenesis options have been stated to have less toxicity than conventional chemo {or, alternatively perhaps radiotherapy, they are frequently connected with clinical side impacts, {and,since well also limited tumor regression. Therefore, there has become {an,a particular,a bunch of type of,a few of increased focus towards development of novel angiogenesis inhibitors {and,also as book approaches to improve the anti-angiogenic options .. Human apolipoprotein ... Title:Cytokine Network: New Targeted Therapy for Pancreatic Cancer. VOLUME: 18 ISSUE: 17. Author(s):Yoichi Matsuo, Hiromitsu Takeyama and Sushovan Guha. Affiliation:Department of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, Kawasumi 1, Mizuho-cho, Mizuho-ku, Nagoya, 4678601, Japan.. Keywords:Pancreatic cancer, cytokine, angiogenesis, targeted therapy. Abstract:Increasing evidence has shown that cytokines have a role in tumor biology. The role of chemokines in tumor biology is important because these peptides may influence tumor growth, invasion, angiogenesis, and metastasis. In this review, we demonstrated the role of cytokines (Interleukin-1α, hepatocyte growth factor, Interleukin-8, stromal cell-derived factor-1 and CXC-chemokines/CXCR2 biological axis) in pancreatic cancer angiogenesis, especially from the standpoint of the interaction between tumor and its microenvironments. The cytokines are intimately related with cancer angiogenesis. Blocking ... Synonyms for angiogenesis factor in Free Thesaurus. Antonyms for angiogenesis factor. 37 synonyms for factor: element, thing, point, part, cause, influence, item, aspect, circumstance, characteristic, consideration, component, determinant.... What are synonyms for angiogenesis factor? Health, ...The beneficial effects of anti-angiogenesis drugs in the treatment of ... Our findings suggest that antiangiogenesis therapy can increase patie...Cediranib inhibits the potent angiogenesis factor VEGF which is known... We frequently see beneficial effects from drugs in patients without f...,Angiogenesis,inhibitor,improves,brain,tumor,survival,by,reducing,edema,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news The sprouting and development of blood vessels affects numerous processes in the body, and excessive or insufficient angiogenesis can exacerbate a variety of disease states. Therefore, precise regulation of angiogenesis is crucial to an organisms survival. Studies knocking down Dicer and Drosha implicated miRNAs in regulation of angiogenesis, and subsequent studies revealed roles for miR-126, the miR17~92 cluster, miR378, miR-210, miR-296, and others in various settings such as neoangiogenesis in response to injury, developmental angiogenesis, and tumor angiogenesis. (1, 5). Over the past year, significant progress has been made in discovering which miRNAs drive this process in both normal physiology and in various disease states. Due to these studies and others, a clearer picture of the miRNA network governing angiogenesis is starting to emerge. This review spans some of the most significant recent discoveries that have contributed to our understanding of "angiomiR" function in vascular ... TY - JOUR. T1 - Modeling three-dimensional invasive solid tumor growth in heterogeneous microenvironment under chemotherapy. AU - Xie, Hang. AU - Jiao, Yang. AU - Fan, Qihui. AU - Hai, Miaomiao. AU - Yang, Jiaen. AU - Hu, Zhijian. AU - Yang, Yue. AU - Shuai, Jianwei. AU - Chen, Guo. AU - Liu, Ruchuan. AU - Liu, Liyu. PY - 2018/10. Y1 - 2018/10. N2 - A systematic understanding of the evolution and growth dynamics of invasive solid tumors in response to different chemotherapy strategies is crucial for the development of individually optimized oncotherapy. Here, we develop a hybrid three-dimensional (3D) computational model that integrates pharmacokinetic model, continuum diffusion-reaction model and discrete cell automaton model to investigate 3D invasive solid tumor growth in heterogeneous microenvironment under chemotherapy. Specifically, we consider the effects of heterogeneous environment on drug diffusion, tumor growth, invasion and the drug-tumor interaction on individual cell level. We ... Inflammatory angiogenesis is the pathogenic mechanism of various sight-threatening eye diseases, among them corneal neovascularization. Current treatment options include steroids which have undesirable side effects, or anti-VEGF which has only limited efficacy. In an inflammatory environment, however, angiogenesis can be stimulated by numerous factors not directly targeted by anti-VEGF therapy. The aim of this study was to induce corneal inflammation leading to angiogenesis, and investigate the early, differential effects of steroid and anti-VEGF therapy at the cellular, tissue, and gene expression levels. Fifty-two Wistar rats received a single intrastromal corneal suture to induce a controlled inflammatory angiogenic response. Rats were subsequently treated with dexamethasone, rat specific anti-VEGF, or goat IgG (control), topically 4 times daily for 7 days. In vivo confocal microscopy of the cornea was performed longitudinally from 5 h up to 7 d to investigate morphology at the cellular and ... Treatment with certain anti-cancer agents, particularly taxanes and sunitinib, can lead to mobilization of pro-angiogenic factors and an acute mobilization of endothelial progenitor cells (EPCs) and other stromal cells, which migrate to the viable tumor rim where they can enhance tumor vascularization, invasion and metastasis. This phenomenon has been linked to rapid tumor regrowth following chemotherapy or treatment with specific angiogenesis inhibitors and may thus diminish the long-term efficacy of the treatment. Stromal cells like EPCs are mobilized in response to circulating growth factors and chemokines (VEGFR, FGF, G-CSF, IL-6, SDF1α, etc.) that are induced by the drug or the progressing tumor. Many of these factors contain heparin binding domains for their anchorage to proteoglycans on cell surfaces or the extracellular matrix. We tested a novel heparan sulfate mimetic, M402, for its ability to inhibit EPC mobilization as well as tumor vascularization and invasion. Mice bearing ... TY - JOUR. T1 - A vascular targeted pan phosphoinositide 3-kinase inhibitor prodrug, SF1126, with antitumor and antiangiogenic activity. AU - Garlich, Joseph R.. AU - De, Pradip. AU - Dey, Nandini. AU - Jing, Dong Su. AU - Peng, Xiaodong. AU - Miller, Antoinette. AU - Murali, Ravoori. AU - Lu, Yiling. AU - Mills, Gordon B.. AU - Kundra, Vikas. AU - Shu, H. K.. AU - Peng, Qiong. AU - Durden, Donald L.. PY - 2008/1/1. Y1 - 2008/1/1. N2 - PTEN and the pan phosphoinositide 3-kinase (PI3K) inhibitor 2-(4-morpholinyl)-8-phenyl-4H-1benzopyran-4-one (LY294002) exert significant control over tumor-induced angiogenesis and tumor growth in vivo. The LY294002 compound is not a viable drug candidate due to poor pharmacologic variables of insolubility and short half-life. Herein, we describe the development and antitumor activity of a novel RGDS-conjugated LY294002 prodrug, termed SF1126, which is designed to exhibit increased solubility and bind to specific integrins within the tumor compartment, resulting ... In the present work, we show that short-term cortisol exposure alters the expression of a number of cardiac remodelling markers in a time-dependent manner and in support of previous work (Johansen et al., 2017), we show that cortisol treatment increases RVM. Moreover, markers of pro-hypertrophic signalling (i.e. smlc2, vmhc, anp and bnp) were upregulated by the cortisol treatment in a time-dependent manner. Both the proliferation marker pcna and the angiogenesis marker vegf were downregulated during the course of cortisol treatment, indicating that cortisol suppresses myocardial cell proliferation and angiogenesis at an early stage of cortisol exposure. Further, there was a clear tendency for autoregulation of the cortisol receptor mr in the cardiac tissue early in the course of exposure, perhaps serving to reduce tissue responsiveness to excess cortisol. Since the observed downregulation of mr was not maintained throughout the treatment period, we speculate that such a potentially protective ...