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At least 1,153 records · Page 64Linked to original sources
PubMed2005

Tie receptors and their angiopoietin ligands are context-dependent regulators of vascular remodeling.

Angiopoietins are ligands of the Tie2 receptor that control angiogenic remodeling in a context-dependent manner. Tie signaling is involved in multiple steps of the angiogenic remodeling process during development, including destabilization of existing vessels, endothelial cell migration, tube formation and the subsequent stabilization of newly formed tubes by mesenchymal cells. Beyond this critical role in blood vessel development, recent studies suggest a wider role for Tie2 and angiopoietins in lymphangiogenesis and the development of the hematopoietic system, as well as a possible role in the regulation of certain non-endothelial cells. The outcome of Tie signaling depends on which vascular bed is involved, and crosstalk between different VEGFs has an important modulating effect on the properties of the angiopoietins. Signaling through the Tie1 receptor is not well understood, but Tie1 may have both angiopoietin-dependent and ligand-independent functions. Changes in the expression of Tie receptors and angiopoietins occur in many pathological conditions, and mutations in the Tie2 gene are found in familial cases of vascular disease.

Angiopoietins↗
PubMed2001

The role of thrombospondin-1 in tumor progression.

The role of thrombospondin-1 (TSP-1) in tumor progression is both complex and controversial. It is clear from the literature that the function of TSP-1 in malignancy depends on the presence of other factors and the level of TSP-1 expression in the tumor tissue. High levels of TSP-1 secreted by tumors, which were engineered to overexpress TSP-1, inhibit tumor growth, while anti-sense inhibition of TSP-1 production in certain tumors also inhibits growth. Clearly, the presence of other factors in these experimental systems must be important. The role of TSP-1 in angiogenesis also depends on the levels of TSP-1, the presence and level of angiogenic stimulators such as basic fibroblast growth factor (bFGF), and the localization of TSP-1 in the tissue. Matrix-bound TSP-1 promotes capillary tube formation in the rat aorta model of angiogenesis, while TSP-1 inhibits bFGF- induced angiogenesis in the rat cornea model. The inhibitory effect also depends on the proteolytic state of TSP-1 since the amino terminus promotes angiogenesis in the cornea model, while the remaining 140-kDa fragment inhibits bFGF-induced angiogenesis. Both the stimulatory and inhibitory effects of TSP-1 are likely due to upregulation of matrix-degrading enzymes and their inhibitors. These enzymes are critical for maintaining optimal matrix turnover during angiogenesis. These varied TSP-1-dependent mechanisms offer new targets for the development of anti-angiogenic therapeutics for the treatment of a variety of cancers, as well as other pathologies involving inappropriate angiogenesis such as diabetic retinopathy.

Animals↗
PubMed2001

Angiogenesis in the pathogenesis of inflammatory joint and lung diseases.

This paper reviews hypotheses about roles of angiogenesis in the pathogenesis of inflammatory disease in two organs, the synovial joint and the lung. Neovascularisation is a fundamental process for growth and tissue repair after injury. Nevertheless, it may contribute to a variety of chronic inflammatory diseases, including rheumatoid arthritis, osteoarthritis, asthma, and pulmonary fibrosis. Inflammation can promote angiogenesis, and new vessels may enhance tissue inflammation. Angiogenesis in inflammatory disease may also contribute to tissue growth, disordered tissue perfusion, abnormal ossification, and enhanced responses to normal or pathological stimuli. Angiogenesis inhibitors may reduce inflammation and may also help to restore appropriate tissue structure and function.

Arthritis↗
PubMedDate not supplied

[Evaluation of hemodynamic changes in inflammatory hyperplastic processes in the thyroid gland with the aid of ultrasound color mapping].

Ultrasound dopplerography techniques constitute an investigation of highly informative value, designed to study vascularization of pathological states of the thyroid gland. It permits the most effective and comprehensive evaluation of the organ circulation along the periphery of the capsule, in the parenchyma, in all pathological formations. This warrants the use of the method in diagnosing, in identification of the process dissemination beyond the organ into the surrounding tissues or regional lymph nodes. Colour Doppler-mapping of the thyroid gland is a highly sensitive method of investigation of neovascularization of the organ which comes to be changed in cancer depending on the stage of the process.

Adolescent↗
PubMed2006

Selective occlusion of tumor blood vessels by targeted delivery of an antibody-photosensitizer conjugate.

The irregular vasculature and high interstitial pressure of solid tumors hinder the delivery of cytotoxic agents to cancer cells. As a consequence, the doses of chemotherapy necessary to achieve complete tumor eradication are associated with unacceptably high toxicities. The selective thrombosis of tumor blood vessels has been postulated as an alternative avenue for combating cancer, depriving tumors of nutrients and oxygen and causing an avalanche of tumor cell deaths. The human antibody L19, specific to the EDB domain of fibronectin, a marker of angiogenesis, is capable of selective in vivo localization around tumor blood vessels and is thus a suitable agent for delivering toxic payloads to the tumor neovasculature. Here we show that a chemical conjugate of the L19 antibody with the photosensitizer bis(triethanolamine)Sn(IV) chlorin e(6), after intravenous injection and irradiation with red light, caused an arrest of tumor growth in mice with subcutaneous tumors. By contrast, a photosensitizer conjugate obtained with an antibody of identical pharmacokinetic properties but irrelevant specificity did not exhibit a significant therapeutic effect. These results confirm that vascular targeting strategies, aimed at the selective occlusion/disruption of tumor blood vessels, have a significant anticancer therapeutic potential and encourage the use of antibody-photosensitizer conjugates for the therapy of superficial tumors and possibly other angiogenesis-related pathologies.

Adenocarcinoma↗
PubMed1992

Angiogenesis and angiogenesis inhibitors in paediatric diseases.

Angiogenesis, the generation of new capillaries from existing blood vessels, is rarely observed in the healthy organism, but can present during various paediatric diseases. In this review, we describe recent progress in the understanding of pathological angiogenesis and approaches for an improved therapy of angiogenic childhood diseases.

Angiogenesis Inducing Agents↗
PubMed2003

Atherosclerotic plaque rupture and intraplaque hemorrhage do not correlate with symptoms in carotid artery stenosis.

OBJECTIVE: Previously we failed to demonstrate a correlation between plaque type and symptoms in 165 carotid endarterectomy specimens. The purpose of this study was to analyze the relation between the anatomy of the carotid plaques and the presence of symptoms in 281 carotid endarterectomy specimens. METHODS: The patients were 213 men (mean age, 68 years) and 68 women (mean age, 68.7 years), with symptomatic disease (n = 133) or asymptomatic disease (n = 148). Specimens were processed for histologic analysis and immunohistochemistry. RESULTS: Plaques were categorized as complicated or noncomplicated, and ruptured or nonruptured. Risk factors could not be correlated with any pathologic or immunohistochemical findings or between plaque type and clinical symptoms. CONCLUSIONS: Almost 70% of plaque specimens demonstrated thrombus, intraplaque hemorrhage, or both. Thrombosis was observed in one fourth of specimens, and intraplaque hemorrhage in almost two thirds of specimens. Sixty four percent of plaques demonstrated neovascularization. It was not possible to demonstrate that complicated plaques (plaque rupture, thrombosis, intraplaque hemorrhage) are associated with symptoms, and it appears that such plaques may occur at any time, irrespective of symptoms.

Adult↗
PubMed2005

Tumstatin, the NC1 domain of alpha3 chain of type IV collagen, is an endogenous inhibitor of pathological angiogenesis and suppresses tumor growth.

Angiogenesis, the formation of new blood vessels, is required for physiological development of vertebrates and repair of damaged tissue, but in the pathological setting contributes to progression of cancer. During tumor growth, angiogenesis is supported by up-regulation of angiogenic stimulators (pro-angiogenic) and down-regulation of angiogenic inhibitors (anti-angiogenic). The switch to the angiogenic phenotype (angiogenic switch) allows the tumors to grow and facilitate metastasis. The bioactive NC1 domain of type IV collagen alpha3 chain, called tumstatin, imparts anti-tumor activity by inducing apoptosis of proliferating endothelial cells. Tumstatin binds to alphaVbeta3 integrin via a mechanism independent of the RGD-sequence recognition and inhibits cap-dependent protein synthesis in the proliferating endothelial cells. The physiological level of tumstatin is controlled by matrix metalloproteinase-9, which most effectively cleaves it from the basement membrane and its physiological concentration in the circulation keeps pathological angiogenesis and tumor growth in check. These findings suggest that tumstatin functions as an endogenous inhibitor of pathological angiogenesis and functions as a novel suppressor of proliferating endothelial cells and growth of tumors.

Angiogenesis Inhibitors↗
PubMed2004

Vaso-occlusive and prothrombotic mechanisms associated with tumor hypoxia, necrosis, and accelerated growth in glioblastoma.

Glioblastoma (GBM) has explosive biologic properties with rapid clinical progression leading to death. Its distinguishing pathologic features, necrosis with surrounding pseudopalisades and microvascular hyperplasia, are believed to be instrumental to its accelerated growth. Microvascular hyperplasia arises in response to the secretion of proangiogenic factors by hypoxic pseudopalisades and allows for peripheral neoplastic expansion. Mechanisms underlying necrosis and hypoxia remain obscure, but vaso-occlusive and prothrombotic contributions could be substantial. Recent investigations on the origin of pseudopalisades suggest that this morphologic phenomenon is created by a tumor cell population actively migrating away from a central hypoxic region and that, in at least a significant subset, hypoxia-induced migration appears due to vaso-occlusion caused by intravascular thrombosis. Both vascular endothelial growth factor induced vascular permeability to plasma coagulation factors and the increased neoplastic expression of tissue factor likely contribute to a prothrombotic state favoring intravascular thrombosis. In addition to prothrombotic mechanisms, vaso-occlusion could also result from angiopoietin-2-mediated endothelial cell apoptosis and vascular regression, which follows neoplastic co-option of native vessels in animal models of gliomas. Vaso-occlusive and prothrombotic mechanisms in GBM could readily explain the presence of pseudopalisades and coagulative necrosis in tissue sections, the emergence of central contrast enhancement and its rapid peripheral expansion on neuroimaging, and the dramatic shift to an accelerated rate of clinical progression. Since the hypoxic induction of angiogenesis appears to support further neoplastic growth, therapeutic targeting of the underlying vascular pathology and thrombosis could provide a new means to prolong time to progression.

Blood Vessels↗
PubMed1999

Prostate biopsy 1999: strategies and significance of pathological findings.

Needle biopsy of the prostate plays a pivotal role in the diagnosis of prostate cancer and prediction of outcome. Strategies for sampling the prostate are being refined, which is increasing the diagnostic yield. In combination with other clinical factors, the pathological findings obtained from the biopsy specimen will provide enhanced predictive accuracy for stage and individual outcome.

Biopsy, Needle↗
PubMed2002

Vascular endothelial growth-permeability factor in granulation tissue of chronic subdural haematomas.

BACKGROUND: Vascular Endothelial Growth/Permeability Factor (VEG/PF) has been correlated with angiogenesis and vascular leakage in diverse pathological conditions of the brain. On the other hand, neoformation of capillaries and vascular hyperpermeability have been related to progressive enlargement of chronic subdural haematomas (CSDH). The purpose of the present study is to verify the presence of VEG/PF in tissue of CSDH, with the hypothesis that neovascularization and vascular hyperpermeabitity in CSDH can be related to the presence of this cytokine. METHODS: Immunohistochemical studies and Reverse Transcription Polymerase Chain Reaction (RT-PCR) analysis were performed in the neomembranes of 12 CSDH to verify presence of VEG/PF in this tissue. FINDINGS: Strong expression of VEG/PF was immunohistochemically disclosed in neomembranes of CSDH, as well as in inflammatory cells currently infiltrating this tissue. Furthermore, RT-PCR studies showed the presence of VEG/PF in all the studied samples. INTERPRETATION: These findings suggest a role for inflammatory cells, currently present in the granulation tissue of CSDH, in the release of VEG/PF and in the enlargement of these lesions, stating the possibility of a new therapeutic approach to CSDH, based on blocking the physiological effects of VEG/PF.

Aged↗
PubMed2004

Determination of tumour prognosis based on angiogenesis-related vascular patterns measured by fractal and syntactic structure analysis.

AIMS: Intratumoural micro-vessel density (IMD) has recently been shown to be a valuable prognostic tool in many tumours. Yet, IMD does not take into account the spatial arrangement of the vessels, therefore only partly reflecting the angiogenic situation. In order to describe contextual vascular relationships more accurately, we have used fractal and syntactic structure analysis (SSA) based on computerised image processing to quantify micro-vascular hot spots. MATERIALS AND METHODS: The parametric performance in prediction of patients' outcome was evaluated by univariate analysis and compared with manually obtained IMDs, whereas an automated K-nearest-neighbour (KNN) classifier searched most discriminative parametric combinations. The method is based on analysis of vascular 'hot-spots' of paraffin-embedded tissue sections of invasive cervical carcinoma, colorectal carcinoma and malignant mesothelioma. RESULTS: For all three cancers, prediction of prognosis based on SSA yielded in general much higher recognition scores compared with IMD or fractal dimension. Survival of cervical carcinoma was mostly correlated with clinical data, with the vascular permeation being the only parameter with independent value. Prognosis of colorectal carcinoma is best described by SSA, completed with IMD, indicating an inverse correlation of survival time with a more irregular pattern and a slight increase in vessel number. For mesothelioma, we found a strong correlation with SSA and patients' outcome, with two SSA-parameters having independent prognostic value. CONCLUSIONS: The more accurate angiogenic description obtained with SSA may be useful for further exploitation as a prognosticator in a general diagnostic pathology service.

Belgium↗
PubMed2004

Attenuation of vascularity by preoperative radiosurgery facilitates total removal of a hypervascular hemangioblastoma at the cerebello-pontine angle: case report.

BACKGROUND: The surgical removal of solid, large, and deep-seated hemangioblastomas remains challenging because it is difficult to control bleeding during the procedure. We used preoperative radiosurgery in a solid, highly vascular hemangioblastoma at the left cerebello-pontine angle and present our angiographic, operative, and histologic findings. CASE DESCRIPTION: A 37-year-old paraplegic woman with multiple hemangioblastomas was re-admitted to our clinic with cerebellar ataxia 6 years after resection of a tumor at the fourth ventricle. A vertebral artery angiogram revealed that the 3.5 cm diameter hemangioblastoma at the left cerebello-pontine angle was highly vascular and fed by the left anterior inferior cerebellar artery and posterior inferior cerebellar artery. Nine months before surgical removal it was treated with stereotactic radiosurgery (gamma knife, margin dose 28 Gy) to inhibit tumor progression and to reduce its vascularity. The tumor was totally removed via the left lateral suboccipital approach; bleeding was well controlled and there were no complications. Pathologic examination of the content of the excised tumor revealed coagulation necrosis with hyaline degeneration of the tumor vessels, resulting in a marked decrease in its vascularity. CONCLUSION: Preoperative radiosurgery led to a marked reduction in the vascularity of this hypervascular hemangioblastoma and was useful for controlling bleeding from the tumor during resection. We succeeded to remove the vascular-rich hemangioblastma after the intentional preoperative radiosurgery. The pathologic changes induced by radiotherapy were confirmed by operative finding.

Adult↗
PubMed1999

Stimulation of angiogenesis through cathepsin B inactivation of the tissue inhibitors of matrix metalloproteinases.

The tissue inhibitors of matrix metalloproteinases (MMPs), TIMP-1 and TIMP-2, are also angiogenesis inhibitors. Cathepsin B and MMPs are found at sites of neovascularization in pathologies such as cancer and osteoarthritis. Treatment of TIMP-1, TIMP-2, and of a mixture of both inhibitors from human articular chondrocytes with cathepsin B resulted in their fragmentation, whereby they lost their MMP-inhibitory and anti-angiogenic activities. Our data suggest that, besides directly participating in tissue destruction, cathepsin B can be harmful for two further reasons: it raises the activity of the MMPs also in the absence of mechanisms up-regulating these enzymes, and it stimulates angiogenesis. This is a prerequisite for blood vessel invasion in a variety of pathological situations of which cancer and osteoarthritis are prominent examples.

Cartilage, Articular↗
PubMed2006

The changes in angiogenic gene expression in recurrent multiple chorioangiomas.

OBJECTIVES: To assess the messenger ribonucleic acid expression in placental tissue of growth factors, cytokines, angiogenic and anti-angiogenic factors in one case of recurrent multiple chorioangiomas. METHODS: Complementary deoxyribonucleic acid array analysis was performed on the affected placentae and on normal placentaes (controls) to compare messenger ribonucleic acid levels of 96 genes involved in angiogenesis. RESULTS: Eleven genes presented more than two-fold alteration in expression levels: undetectable (angiopoietin 1, osteonectin, tyrosine kinase endothelial, neuropilin 1), decreased (transcription growth factor beta receptor 3, tissue inhibitor of metalloproteinase type 2, EGF receptor, integrin-alpha V, tyrosine kinase vascular endothelial growth factor receptor 2), increased (angiopoietin 2, osteopontin). CONCLUSIONS: We illustrated the complexity of angiogenic disruption in recurrent multiple chorioangiomas leading to the difficulty to propose a single candidate gene to explain this pathology.

Adult↗
PubMed2001

Vascular endothelial growth factor signaling pathway as an emerging target in hematologic malignancies.

Angiogenesis is important in a variety of physiologic and pathologic disorders. It is a central element in embryogenesis, ovulation, wound healing, diabetic retinopathy, and rheumatoid arthritis and in the establishment and spread of malignant tumors. Angiogenic factors include direct angiogens, indirect angiogens, and integrins. Direct angiogens stimulate the formation of new blood vessels directly. Indirect angiogens promote neovascular formation by paracrine stimulation of direct angiogens. Integrins mediate interactions between the developing vessels and components of the extracellular matrix. Vascular endothelial growth factor (VEGF) is a principal direct angiogen. By binding to 1 of 3 receptors (VEGFR-1, -2, or -3), it influences vasculogenesis during embryogenesis, physiologic and neoplastic angiogenesis, and lymphangiogenesis. Although the importance of angiogenesis in solid tumors has been recognized for some time, its exact significance in hematologic malignancies is less clear. Evidence now suggests that VEGF has a major role in the development and progression of hematologic malignancies such as acute leukemia, chronic leukemia, myelodysplasia, non-Hodgkin's lymphoma, and multiple myeloma. Potential therapeutic interventions to interrupt the VEGF signaling pathway of malignancy include antibodies that neutralize the growth factor and small molecules that inhibit the receptor tyrosine kinase activity of VEGF receptors.

Endothelial Growth Factors↗
PubMedDate not supplied

Tumor-associated angiogenesis in prostate cancer.

All solid tumors require the induction of new blood vessels to grow. To begin to study this phenomenon in prostate cancer, we investigated the intensity of tumor associated angiogenesis in prostate non malignant and malignant tissue. Angiogenesis was measured by quantitating microvessels in a total of 67 patients: 23 non malignant biopsy specimens, and 34 malignant specimens from patients who had undergone prostatectomy. Angiogenic activity in prostatic cancer (prostatectomy) tissue (utilizing Factor VIII staining) was then correlated with pathological staging (Whitmore-Jewitt). Overall there appeared to be a trend of increasing microvessel count (MVC) from benign through the advancing stages of prostate cancer. Based on mean microvessel counts we were able to distinguish stage D from all other pathological stages (p = 0.004 between stages C and D). There was, however, no statistically significant difference between stage B and C. We conclude that tumor associated angiogenesis in prostate cancer may have both clinical and pathological significance in prostate cancer.

Humans↗