Colorectal carcinoma growth and progression is dependent on the vasculature of the tumor microenvironment. Tumor-derived endothelial cells differ functionally from their normal counterpart. For this reason we isolated microvascular endothelial cells from human colon cancer tissue (HCTEC) and compared them with endothelial cells from normal colonic tissue (HCMEC) of the same donor. Since hypoxia is a universal hallmark of carcinomas, we examined its effects on HCTEC of five patients in comparison with the corresponding HCMEC, with respect to the secretion of the soluble form of the two important vascular endothelial growth factor (VEGF) receptors, VEGFR-1 and -2. After dissociation by dispase/collagenase of central non-necrotic tumor areas obtained from colon carcinomas, HCTEC were isolated using CD31-coated magnetic beads and cultivated as monolayers. Subsequent characterization studies demonstrated the endothelial phenotype, including VEGFR-1 and -2 mRNA and protein expression as well as E-selectin

Tumor angiogenesis, growth and metastasis are three closely related processes. We therefore investigated the effects of barbigerone on all three in the B16F10 tumor model established in both zebrafish and mouse models, and explored underlying molecular mechanisms. In vitro, barbigerone inhibited B16F10 cell proliferation, survival, migration and invasion and suppressed human umbilical vascular endothelial cell migration, invasion and tube formation in concentration-dependent manners. In the transgenic zebrafish model, treatment with |TEX|$10{\mu}M$|/TEX| barbigerone remarkably inhibited angiogenesis and tumor-associated angiogenesis by reducing blood vessel development more than 90%. In vivo, barbigerone significantly suppressed angiogenesis as measured by H and E staining of matrigel plugs and CD31 staining of B16F10 melanoma tumors in C57BL/6 mice. Furthermore, it exhibited highly potent activity at inhibiting tumor growth and metastasis to the lung of B16F10 melanoma cells injected into C57BL/6

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 ...

Expression of integrin αvβ3 is increased on endothelial cells after exposure to bFGF in vitro (Cheng and Kramer, 1989; Senger et al., 1996; Boudreau et al., 1997) and angiogenic blood vessels in vivo (Brooks et al., 1994a,b, 1995). In addition, integrin αvβ3 expression on chick CAM angiogenic blood vessels has been linked to the ability of bFGF to promote expression of the Hox D3 homeobox gene in these tissues (Boudreau et al., 1997). While αvβ3 was detectable on preexisting blood vessels in 10-d-old chick CAMs, αvβ3 levels were not significantly increased above this baseline level for at least 12 h after bFGF treatment. This suggests that the preexisting levels of αvβ3 are sufficient to initiate this sustained phase of MAP kinase activity in these blood vessels and that the requirement of αvβ3 ligation for the sustained MAP kinase activity in blood vessels within 4 h was independent of an increase in the total expression of αvβ3 protein. To support the model that integrin-mediated ...

The ECM protein Del-1 is one of several novel ECM proteins that accumulate around angiogenic blood vessels in embryonic and tumor tissue and promote angiogenesis in the absence of exogenous growth factors. Del-1 expressed in mouse or rabbit ischemic hind-limb muscle by gene transfer rapidly promotes new blood vessel formation and restores muscle function. This angiogenic ECM protein initiates angiogenesis by binding to integrin αvβ5 on resting endothelium, thereby resulting in expression of the transcription factor Hox D3 and integrin αvβ3. Hox D3 converts resting endothelium to angiogenic endothelium by inducing expression of proangiogenic molecules such as integrin αvβ3. These findings provide evidence for an angiogenic switch that can be initiated in the absence of exogenous growth factors and indicate that the angiogenic matrix protein Del-1 may be a useful tool for the therapy of ischemic disease.. ...

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 ...

License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on how to request permission may be found at: http://www.dovepress.com/permissions.php International Journal of Nanomedicine 2015:1

The secretion of angiogenic factors by vascular endothelial cells is one of the key mechanisms of angiogenesis. to induce angiogenic and proliferative effects (1.340.26 nmol L-1). In conclusion, Up4U is a novel strong human endothelium-derived angiogenic factor. Introduction Vasculature in adult mammals is mainly quiescent; however, new blood vessel formation is required for timely tissue repair and remodeling after injury [1]. The formation of new blood vessels is an essential process in the life of higher organisms. Development, reproduction, wound healing, communication of humoral signals, transport of nutrients and waste products all require angiogenesis [2]. The process of angiogenesis involves migration, proliferation, differentiation, and adhesion of multiple cell types, including endothelial, mural, and inflammatory cells [3], [4]. However, disease processes such as cancer growth [5], diabetic retinopathy or chronic inflammation are also dependent on angiogenesis [6]. Hence, the humoral ...

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 ...

Tumors are composed not only of malignant cells, but also of various types of normal cells, including vascular cells and infiltrating immune cells, which drive tumor development and progression. The tumor vasculature is abnormal and dysfunctional due to sustained tumor angiogenesis driven by high levels of pro-angiogenic factors. Proteins differentially expressed in tumor vessels affect vascular function and the tumor microenvironment and may serve as targets for therapy. The tumor is also a site of sustained chronic inflammation. The recruitment and activation of inflammatory cells significantly influence tumor progression and regression. Targeting molecules regulating tumor angiogenesis and inflammation in the tumor microenvironment is therefore a promising strategy for the treatment of cancer. This thesis is aiming to understand and investigate the molecular regulation of these two processes in tumors.. αB-crystallin is a heat shock protein previously proposed as a target for cancer therapy ...

Tumor neovascularization is highly dependent upon numerous cytokines and signaling events critical for the growth and organization of the vascular tree. A number of agents targeting tumor neovascularization and which interfere with one or several steps in this robust process have demonstrated significant clinical efficacy and have received FDA approval [24]. These include agents which block angiogenesis signaling events by inhibiting various growth factor receptor kinases [25]; interfere with VEGF physical interaction with its receptors such as anti-VEGF antibodies (bevacizumab and ranibizumab) and anti-receptor antibodies (IMC-1121B and DC101) [26, 27]; and strategies that trap growth factor ligands (VEGF-Trap) [28]. These have all shown antitumor efficacy alone and in combination with conventional antitumor modalities [29, 30].. VEGF-A has been shown to play an important role in tube formation of endothelial cells in vitro [31] and in angiogenesis [32]. In the present study, the effect of ...

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 ...

Fluciclatide (GE Healthcare) (AH111585) is a small cyclic peptide containing the RGD tripeptide (figure 1), which preferentially binds with high affinity to α¬vβ3 integrins that are up-regulated in angiogenesis.. The IMP is supplied as a solution for injection, 400 MBq at the reference date and time. Participants will receive one injection of the imaging agent at this dose on 3 occasions ...

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 ...

VEGFs are found at high levels in hypoxic tumors. As major components directing pathologic neovascularization, they regulate stromal reactions. Consequently, novel strategies targeting and inhibiting VEGF overproduction upon hypoxia offer considerable potential for modern anticancer therapies controlling rather than destroying tumor angiogenesis. Here, we report the design of a vector expressing the soluble form of VEGF receptor-2 (sVEGFR2) driven by a hypoxia-responsive element (HRE)-regulated promoter. To enable in vivo imaging by infrared visualization, mCherry and IFP1.4 coding sequences were built into the vector. Plasmid construction was validated through transfection into embryonic human kidney HEK293 and murine B16F10 melanoma cells. sVEGFR2 was expressed in hypoxic conditions only, confirming that the gene was regulated by the HRE promoter. sVEGFR2 was found to bind efficiently and specifically to murine and human VEGF-A, reducing the growth of tumor and endothelial cells as well as ...

The role of bone marrow (BM)-derived precursor cells in tumor angiogenesis is not known. We demonstrate here that tumor angiogenesis is associated with recruitment of hematopoietic and circulating endothelial precursor cells (CEPs). We used the angiogenic defective, tumor resistant Id-mutant mice to …

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 ...

Topolovec, Zlatko and Ćorušić, Ante and Babić, Damir and Mrčela, Milanka and Šijanović, Siniša and Müller-Vranješ, Andrijana and Čuržik, Darko (2010) Vascular endothelial growth factor and intratumoral microvessel density as prognostic factors in endometrial cancer. Collegium Antropologicum, 34 (2). pp. 447-53. ISSN 0350-6134 ...

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: ...

β3-Integrin-knockout mice exhibit a complex phenotype that includes enhanced pathological angiogenesis. However, as mentioned above, β3-integrin is expressed by a diverse set of cells, and the described phenotype must arise from the integration of its pattern of expression. Although interesting, this biological integration makes it difficult to distinguish cell autonomous effects of β3-integrin. Our studies have addressed, for the first time to our knowledge, the specific contribution that endothelial β3-integrin makes to tumor growth and angiogenesis. Our findings have profound implications for targeting the endothelial-specific expression of β3-integrin to inhibit tumor angiogenesis, a strategy that is growing in popularity with the maturation of nanotechnology.38. Consistent with our findings in β3-knockout animals,10 the depletion of endothelial β3-integrin did not alter the structure of established tumor vessels (Online Figure IA and Online Figure VIA). Sprouting angiogenesis ...

Significant advances have been made in understanding the role of tumor angiogenesis and its influence on tumor progression in cancer. Based on this knowledge, a series of inhibitors of angiogenesis have been developed and evaluated in preclinical and clinical trials. Since detailed information of tumor progression in response to therapy is important to assess the efficacy of anti-tumor treatment in vivo, noninvasive imaging techniques emerge more and more as important tools to monitor alterations in tumor growth and vessel recruitment, as well as metastatic spread over time. So far, remarkable efforts have been made to improve the technical capability of these imaging modalities based on better resolution, as well as to implement multimodal approaches combining molecular with anatomical information. Advanced imaging techniques not only allow the detection and monitoring of tumor development, but also facilitate a broad understanding of the cellular and molecular events that propagate tumor angiogenesis,

BAY1143269 is an orally bioavailable inhibitor of mitogen-activated protein kinase interacting serine/threonine-protein kinase 1 (MKNK1), with potential antineoplastic activity. Upon oral administration, MKNK1 inhibitor BAY 1143269 binds to MKNK1, thereby preventing its activation and the downstream MKNK1-mediated phosphorylation and activation of eukaryotic translation initiation factor 4E (eIF4E). As eIF4E enhances the synthesis of oncogenic proteins, preventing eIF4E activity inhibits the synthesis of tumor angiogenic factors and leads to both the inhibition of cellular proliferation and apoptosis in susceptible tumor cells.

Current antiangiogenic therapy is limited by its cytostatic property, scarce drug delivery to the tumor, and side toxicity. To address these limitations, we unveiled the role of ZEB1, a tumor endothelium-enriched zinc-finger transcription factor, during tumor progression. We discovered that the patients who had lung adenocarcinomas with high ZEB1 expression in tumor endothelium had increased prevalence of metastases and markedly reduced overall survival after the diagnosis of lung cancer. Endothelial ZEB1 deletion in tumor-bearing mice diminished tumor angiogenesis while eliciting persistent tumor vascular normalization by epigenetically repressing TGF-β signaling. This consequently led to improved blood and oxygen perfusion, enhanced chemotherapy delivery and immune effector cell infiltration, and reduced tumor growth and metastasis. Moreover, targeting vascular ZEB1 remarkably potentiated the anticancer activity of nontoxic low-dose cisplatin. Treatment with low-dose anti-programmed cell ...

Blockade of the glycolytic activator PFKFB3 in cancer cells (using a maximum tolerable dose of 70 mg/kg of the PFKFB3 blocker 3PO) inhibits tumor growth in preclinical models and is currently being tested as a novel anticancer treatment in phase I clinical trials. However, a detailed preclinical analysis of the effects of such maximum tolerable dose of a PFKFB3 blocker on the tumor vasculature is lacking, even though tumor endothelial cells are hyper-glycolytic. We report here that a high dose of 3PO (70 mg/kg), which inhibits cancer cell proliferation and reduces primary tumor growth, causes tumor vessel disintegration, suppresses endothelial cell growth for protracted periods, (model-dependently) aggravates tumor hypoxia, and compromises vascular barrier integrity, thereby rendering tumor vessels more leaky and facilitating cancer cell intravasation and dissemination ...

Tumor progression depends on sequential events, including a switch to the angiogenic phenotype (i.e., initial recruitment of blood vessels). Failure of a microscopic tumor to complete one or more early steps in this process may lead to delayed clinical manifestation of the cancer. Microscopic human …

We investigated whether the angiogenic profile, which is based on the local expression and systemic levels of angiogenic growth factors (VEGF, Ang-1, Ang-2, and the corresponding receptors), differs between rheumatoid arthritis (RA) and osteoarthritis (OA) patients. We determined the expression of VEGF, Ang-1, and Ang-2 together with its receptors (VEGFR-1/-2 ...

The Dermaroller is a cylindrical shaped drum studded with very fine needles. It is a medical device used in micro needling to break down old scar tissue & to stimulate skin cells to proliferate. This cell multiplication results in the formation of new tissue layers of elastin and collagen fibres (neo-collagenesis) as well as in new capillaries for an improved blood supply (neo-angiogenesis). The procedures are called Scar Reduction Therapy (SRT) & Collagen Induction Therapy (CIT).. ...

Oral cancer is common among men in the developed world and among the most difficult neoplasms to treat. The growth and metastasis of all solid tumors requires i...

My research has focused on several basic and translational aspects of cancer biology. From a basic science perspective, my lab cloned NOL7, a novel gene that induces an anti-angiogenic phenotype and suppresses in vivo tumor growth. NOL7 acts as a master regulator of angiogenesis by modulating the expression of angiogenesis-associated mRNAs via both steady-state downregulation and posttranscriptional upregulation. NOL7 itself is positively regulated by the retinoblastoma (Rb) gene, supporting the paradigm shift that Rb can act as a positive regulator of gene transcription. Our long-term goal is to understand how transcriptional and posttranscriptional regulation of angiogenesis-related mRNAs contributes to the expression of the phenotype and to leverage this knowledge to develop novel therapeutic approaches. Our central hypothesis is that Rb positively regulates NOL7 expression and that loss of NOL7 protein expression results in decreased regulation of NOL7 target mRNA transcripts, the gain of ...

Angiogenesis is the formation of new blood vessels from pre-existing blood vessels. Angiogenesis may take place in two ways - endothelial sprouting or non-sprouting (intussusceptive).

Angiogenesis (angiogenesis) -- the growth of new blood vessels -- is an important natural process occurring in the body, both in health and in disease. Angiogenesis occurs in the healthy body for healing wounds and for restoring blood flow to tissues after injury or insult. In females, angiogenesis also occurs during the monthly reproductive cycle (to rebuild the uterus lining, to mature the egg during ovulation) and during pregnancy (to build the placenta, the circulation between mother and fetus ...

One of us predicted previously that the cytoplasmic conclude of CHL1 protein may interact with the cytoskeleton and might induce/control filopodia formation driving tumor cell migration and invasion. CHL1 behavior in CYT387 cancer is as a result strikingly equivalent to L1 and LOX which both perform by way of the actin network. This examine suggested that CHL1 may possibly add to cancer invasive growth and metastasis. It might act possibly as a tumorsuppressor or oncogene. CHL1 consequently could belong to the new rapidly developing category of most cancers genes that could operate possibly as TSGs or oncogenes. For the duration of initial progress CHL1 is not expressed in tumor cells to aid in situ tumor expansion. Re-expression of CHL1 on the edge of the tumor mass and all around tumor vessels could encourage migration and nearby invasive expansion and furthermore enable initiating the metastatic approach. As a result, our final results along with the results that CHL1 was a mutated applicant ...

Angiogenesis (also known as neovascularization) is the generation of new blood vessels from pre-existing vasculature. It is a normal process in growth and development and is required for the formation of arteries, veins, and capillaries in an embryo. Proliferation of new blood vessels also takes place in adults and is essential for the repair or regeneration of tissue during wound healing ...

BACKGROUND AND PURPOSE: Quantifying MVA rather than MVD provides better correlation with survival in HGG. This is attributed to a specific glomeruloid vascular pattern, which is better characterized by vessel area than number. Despite its prognostic value, MVA quantification is laborious and clinically impractical. The DSC-MR imaging measure of rCBV offers the advantages of speed and convenience to overcome these limitations; however, clinical use of this technique depends on establishing accurate correlations between rCBV, MVA, and MVD, particularly in the setting of heterogeneous vascular size inherent to human HGG. ...

Global Tumor Blood Testing Market Report 2020 has complete details about market of Tumor Blood Testing industry, Tumor Blood Testing analysis and current trends. Global Tumor Blood Testing Market Report 2020 Full Report: 2350 USD Multi License (Section): 4700 USD Section Price: As below Page: 115 Chart and Figure: 124 Publisher: BisReport Delivery Time: 24 hour At the beginning of 2020, COVID-19 disease began to spread around the world, millions of people worldwide were infected with COVID-19 disease, .

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].

Angiogenesis Modulators Industry Description Angiogenesis Modulators & Therapeutics Market report studies the impact of Inhibitors and Stimulators on

Angiogenesis is the process which enables a tumor to proliferate into a cancerous tumor that has the ability to grow and spread to the other parts of the body. Knowing the ...

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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 ...

Regulation of Bone Marrow Angiogenesis by Osteoblasts during Bone Development and Homeostasiss profile, publications, research topics, and co-authors

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 ...

The approval of the first antiangiogenic agent for clinical use in patients with colorectal carcinoma has taught us many lessons, the most important of which is that these agents must be used in combination with agents that target cancer cells to have an appreciable impact on patient survival. Increasing the dose of antiangiogenic agent may harm normal tissues and destroy too much of the tumor vasculature, leading to hypoxia and poor drug delivery in the tumor and to toxicity in normal tissues. However, optimal doses and schedules of these reagents tailored to the angiogenic profile of tumors can normalize tumor vasculature and microenvironment without harming normal tissue.. At least three major challenges must be met before therapies based on this vascular normalization model can be successfully translated to the clinic. The first challenge is to determine which other direct or indirect antiangiogenic therapies lead to vascular normalization. In principle, any therapy that restores the balance ...

The treatment of the most common cancers (colon, breast, lung, liver and kidney) has recently added a new therapeutic class known as the anti-angiogenic. It was born from a better understanding of tumor growth requires the development of neo-vessels. These new vessels are of major importance for the viability of the tumor but also the birth of metastases. This neo-angiogenesis is complex and results from an imbalance between pro-angiogenic factors and anti-angiogenic factors. Growth factor VEGF and its receptors (VEGFR-1, VEGFR-2 and VEGFR-3) are a way of survival of endothelial cells required for tumor neoangiogenesis. The anti-angiogenic drugs currently available on the market are bevacizumab (Avastin ®), sunitinib (Sutent ®) and sorafenib (Nexavar ®). The mechanism of anti-angiogenic action of these three main drugs are pharmacological inhibition of the VEGF pathway.. These new anti-angiogenic therapies, however, have significant adverse effects are common and some other more serious but ...

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 ...

Tumor-induced angiogenesis is of major interest for oncology research. Vascular endothelial growth factor (VEGF) is the most potent angiogenic factor characterized so far. VEGF blockade was shown to be sufficient for angiogenesis inhibition and subsequent tumor regression in several preclinical tumor models. Bevacizumab was the first treatment targeting specifically tumor-induced angiogenesis through VEGF blockade to be approved by the Food and Drugs Administration (FDA) for cancer treatment. However, after very promising results in preclinical evaluations, VEGF blockade did not show the expected success in patients. Some tumors became resistant to VEGF blockade. Several factors have been accounted responsible, the over-expression of other angiogenic factors, the noxious influence of VEFG blockade on normal tissues, the selection of hypoxia resistant neoplastic cells, the recruitment of hematopoietic progenitor cells and finally the transient nature of angiogenesis inhibition by VEGF blockade. ...

Nitric oxide (NO) has been strongly implicated in glioma progression and angiogenesis. The endogenous inhibitors of NO synthesis, asymmetric dimethylarginine (ADMA) and N-monomethyl-L-arginine (L-NMMA), are metabolized by dimethylarginine dimethylaminohydrolase (DDAH), and hence, DDAH is an intracellular factor that regulates NO. However, DDAH may also have an NO-independent action. We aimed to investigate whether DDAH I has any direct role in tumour vascular development and growth independent of its NO-mediated effects, in order to establish the future potential of DDAH inhibition as an anti-angiogenic treatment strategy. A clone of rat C6 glioma cells deficient in NO production expressing a pTet Off regulatable element was identified and engineered to overexpress DDAH I in the absence of doxycycline. Xenografts derived from these cells were propagated in the presence or absence of doxycycline and susceptibility magnetic resonance imaging used to assess functional vasculature in vivo. ...

The Ohio State University College of Pharmacy Division of Pharmacology Assistant Professor Nam Lee has received a $1.6 million grant from the National Institute of Healths National Cancer Institute (NIH NCI) to study therapeutics that target pathways essential for tumor angiogenesis (i.e., how tumors recruit new blood vessels for growth). NIH NCIs grant will fund the project for five years.. While many strategies exist for inhibiting tumor angiogenesis, Food and Drug Administration approved drugs like Avastin (bevacizumab) have yielded mixed results. Lees project aims to understand the basic mechanisms by which another potential vascular target, endoglin (CD105), a protein located on cell surfaces, promotes tumor-associated angiogenesis.. My lab is going to look at several treatment options to better determine what ways we can improve and make current drugs more effective in fighting angiogenesis, said Lee. There is still so much we can learn about the subject.. Part of Lees study will ...

Definition of angiogenesis factor in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is angiogenesis factor? Meaning of angiogenesis factor as a legal term. What does angiogenesis factor mean in law?

Considerable interest is focusing on a treatment approach targeting inhibition of microvessel formation and/or function within atherosclerotic plaque. More than 300 potential inhibitors of angiogenesis have been identified, of which 80 are currently being tested in clinical trials (58). Their mechanisms of action are varied, affecting aspects of angiogenesis such as endothelial cell proliferation, the availability or production of endothelial cell growth factors, the signaling of tyrosine kinase receptors on endothelial cells, and the activity of metalloprotease enzymes. Although significant differences in efficacy between agents may not be apparent in a heterogeneous patient group, it is possible that subpopulations such as diabetics may ultimately benefit from tailored therapy that takes account of specific signaling or other molecular defects of angiogenesis known to be more prevalent in these patients (59). Combination therapy using 2 or more inhibitors with differing mechanisms of action ...

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 ...

A promising strategy to overcome the chemoresistance is the tumor blood vessel normalization, which restores the physiological perfusion and oxygenation of tumor vasculature. Thalidomide (Thal) has been shown to increase the anti-tumor effect of chemotherapy agents in solid tumors. However, it is not yet known whether the synergistic effect of Thal combined with other cytotoxic drugs is attributable to tumor vascular normalization. We used two homograft mice models (4 T1 breast tumor model and CT26 colorectal tumor model) to investigate the effect of Thal on tumor growth, microvessel density, vascular physiology, vascular maturity and function, drug delivery and chemosensitivity. Immunofluorescence, immunohistochemistry and scanning electron microscopy were performed to determine the vessel changes. Protein array assay, qPCR and western blotting were used to detect the molecular mechanism by which Thal regulates tumor vascular. Here we report that Thal potently suppressed tumor growth, angiogenesis,

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

Metastatic potential. Tumor angiogenesis is closely related to lymphangiogenesis in the spread of cancer cells from the primary neoplasm to other tissues and organs and usually first occur via the sentinel lymph node.36 Nevertheless, melanoma tumor cells can bypass the lymph-node system and metastasize to distant organs by gaining direct access to blood circulation. Depending on the angiogenic potential of the tumor cells trapped in secondary organ capillary beds, metastatic tumor growth can be favored by increased induction of neovascularization.37 Some authors therefore suggest that tumor angiogenesis is associated with poor prognostic outcome and increased rate of relapse in melanoma.38-40 Pro-angiogenic factors such as VEGF-A, IL-8, PDEGF, bFGF, Ang-2 and MMP, necessary for tumor angiogenesis can be generated in part by melanoma cells.41,42 Therefore, the clinical utility of VEGF serum determination in melanoma patients has been under investigation as circulating serum levels of VEGF in some ...

University of Pittsburgh scientists have shown that triggering an anti-tumor immune response significantly potentiates the effects of the anti-angiogenic drug endostatin in animal models, leading to permanent and complete regression...

TY - THES. T1 - Preclinical and clinical studies on the co-regulation of tumor-induced angiogenesis and dendritic cell suppression. AU - van Cruijsen, H.. N1 - Naam instelling promotie: S.l.. PY - 2009. Y1 - 2009. M3 - Research VU University Amsterdam, graduation VU University Amsterdam. SN - 9789090240251. PB - s.n.. CY - S.l.. ER - ...

The data of the present study demonstrate that S1P can induce eNOS phosphorylation and NO production by way of the PI3K/Akt pathway in cultured ECs and that NO plays a critical role in S1P-induced angiogenesis in vitro and in vivo. Platelets contain many angiogenic factors, and the angiogenic activity of those released by platelets plays an important role in initiating angiogenesis in injured tissue, especially in wound healing and tumor angiogenesis. It seems likely that S1P, which is known to be abundantly stored in platelets and released on their activation,17 may contribute to platelet-induced angiogenesis in wound repair, because it was demonstrated that S1P is the major EC chemoattractant released into serum by platelets during blood clotting.18 Therefore, it is suggested that the angiogenic activity of S1P may account for the important role of platelet interaction with ECs in angiogenesis at sites of injury. Interestingly, previous studies have demonstrated the crucial role of NO in wound ...

CANSSUFIVE is also based on the technology platform of angiogenesis screening assays. These unique assays screen for angiogenesis which is the process of new blood vessels formation from pre-existing blood vessels. Angiogenesis is an essential natural process in the body for healing and reproduction. The human body produces a precise balance of growth and inhibitory factors in healthy tissues to control angiogenesis. When this balance is altered, the result is either excessive or insufficient angiogenesis. The abnormal angiogenesis is a common denominator in many conditions including cancer, Alzheimers disease, diabetic blindness, wet age related macula degeneration, obesity and rheumatoid arthritis ...

Vascular endothelial growth factor (VEGF) is a key regulator of physiological angiogenesis during embryogenesis, skeletal growth and reproductive functions. VEGF has also been implicated in pathological angiogenesis associated with tumors, intraocular neovascular disorders and other conditions. The biological effects of VEGF are mediated by two receptor tyrosine kinases (RTKs), VEGFR-1 and VEGFR-2, which differ considerably in signaling properties. Non-signaling co-receptors also modulate VEGF RTK signaling. Currently, several VEGF inhibitors are undergoing clinical testing in several malignancies. VEGF inhibition is also being tested as a strategy for the prevention of angiogenesis, vascular leakage and visual loss in age-related macular degeneration.

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 ...

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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 ...

3 hours publish DMXAA remedy, ectopic MCA tumors showed 6 fold better induction of DPP-4 compared to orthotopic MCA tumors. No statistically significant distinction in intratumoral ranges of VEGF had been observed in between untreated ectopic and orthotopic MCA tumors.. Even so, higher levels of VEGF have been seen in orthotopic tumors than ectopic tumors following DMXAA treatment method. The host microenvironment is critically involved in tumor angiogenesis via a complex network of interactions in between tumor cells, endothelial cells and host cells. It is as a result important to assess and interpret the preclinical RAD001 activity of VDAs within the context of the tumor kind and its microenvironment. In the present examine, non invasive MMCM MRI was utilized to investigate the influence of the host microenvironment on tumor angiogenesis and response to DMXAA. The outcomes show the usefulness of MMCM MRI in characterizing vascular variations between ectopic and orthotopic tumors and offer ...

Endometriosis, the presence of endometrium-like tissue outside of the uterine cavity, is a common disease among women of reproductive age. Typical symptoms include abdominal pain and painful menstruation. In addition, endometriosis is associated with reduced fertility. Current treatment modalities, the surgical removal of endometriotic lesions and the hormonal suppression of estrogen are associated with significant morbidity, side-effects and recurrence rates. Despite uncertainties about the pathophysiology of the disease it has recently become apparent that angiogenesis plays a pivotal role in endometriosis. This review focuses on a multitude of factors involved in the angiogenic phenotype of endometriosis demonstrating that many biological systems such as the immune system and steroid hormones are closely connected to angiogenic pathways in this disease. In addition, experimental and clinical data are discussed that concentrate on the inhibition of angiogenesis as a novel therapeutic approach for

Sigma-Aldrich offers abstracts and full-text articles by [Ngoc-Quynh-Nhu Nguyen, Karolien Castermans, Sarah Berndt, Stephanie Herkenne, Sebastien P Tabruyn, Silvia Blacher, Michelle Lion, Agnes Noel, Joseph A Martial, Ingrid Struman].

The angiogenic switch, a rate-limiting step in tumor progression, has already occurred by the time most human tumors are detectable. The angiogenic switch is not limited at earliest stages, but occurs also at different stages of tumor progression (2). Antiangiogenic therapy is a promising alternative for treatment of cancer, and may also be used as a maintenance therapy to prevent the metastasis or recurrence (4). Therapy with endogenous angiogenic inhibitors such as endostatin and angiostatin may reverse the angiogenic switch by preventing growth of tumor vasculature. Angiostatin can maintain metastases in a dormant state in laboratory animals when administered exogenously (34). In transgenic mice overexpressing endostatin, a small increase of circulating endostatin (approximately 1.6-fold) is sufficient to confer dramatic protection against tumor growth (11). In individuals with Down syndrome, a similar small increase of circulating endostatin is associated with a remarkably low incidence of ...

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 ...

Tumors are composed not only of malignant cells, but also of various types of normal cells, including vascular cells and infiltrating immune cells, which drive tumor development and progression. The tumor vasculature is abnormal and dysfunctional due to sustained tumor angiogenesis driven by high levels of pro-angiogenic factors. Proteins differentially expressed in tumor vessels affect vascular function and the tumor microenvironment and may serve as targets for therapy. The tumor is also a site of sustained chronic inflammation. The recruitment and activation of inflammatory cells significantly influence tumor progression and regression. Targeting molecules regulating tumor angiogenesis and inflammation in the tumor microenvironment is therefore a promising strategy for the treatment of cancer. This thesis is aiming to understand and investigate the molecular regulation of these two processes in tumors.. αB-crystallin is a heat shock protein previously proposed as a target for cancer therapy ...

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 ...

Over the last few years the paradigm of how to approach cancer therapy has shifted from solely trying to mitigate cancer cell proliferation to incorporating targeting agents against the production of new vessels, which allow the cancerous cells to thrive. Current anti-angiogenic therapies focus on the earliest steps in these signaling cascades and try to prevent angiogenic molecules like vascular endothelial growth factor from reaching endothelial cells or hinder the activation of their endothelial cell receptors. One or more of the downstream signaling steps might be a signaling ...

Results: In vitro and in vivo angiogenesis assays showed inhibition of capillary-like network formation of microvascular endothelial cells and neovascularization under dorsal skin of nude mice, respectively. We observed inhibition of intracerebral tumorigenesis and s.c. solid tumor formation in nude mice after treatment with combination of hTERT siRNA and IFN-γ. Western blotting of solid tumor samples showed significant downregulation of the molecules that regulate cell invasion, angiogenesis, and tumor progression ...

Tumor angiogenesis is the process through which certain tumors stimulate the growth of the microvascular network in the surrounding tissue. This capillary network is remarkable in that the growth is...

Antibodies for proteins involved in regulation of sprouting angiogenesis pathways, according to their Panther/Gene Ontology Classification

TY - JOUR. T1 - Regulation of tumor angiogenesis by organ-specific cytokines. AU - Singh, R. K.. AU - Fidler, I. J.. PY - 1996/5/22. Y1 - 1996/5/22. UR - http://www.scopus.com/inward/record.url?scp=0029888971&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0029888971&partnerID=8YFLogxK. M3 - Review article. C2 - 9053286. AN - SCOPUS:0029888971. VL - 213 II. SP - 1. EP - 11. JO - Current Topics in Microbiology and Immunology. JF - Current Topics in Microbiology and Immunology. SN - 0070-217X. ER - ...

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