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Results for “Neovascularization, Pathologic”

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PubMedDate not supplied

[Results of laser photocoagulation in diabetic retinopathy with maculopathy].

Examined were 91 eyes with non-proliferative and proliferative retinopathy with coexisting maculopathy in 51 patients in whom segmental or retinal pan-photocoagulation were performed. The period of observation--3 to 4.5 years. Stabilization of the pathological process was observed in 37.3 p.c. of cases, 54.9 p.c. of patients showed further deterioration and 7.6 p.c. loss of vision. The most frequent cause of deterioration was the progression of the macular lesions (72 p.c.), a smaller number of cases (28 p.c.) was due to other changes.

Adult↗

PubMed1986

[Pathologic and adaptive changes in the hemomicrocirculatory system].

General principles of the description and functional evaluation of the morphological changes developing in the hemomicrocirculatory bed under pathological conditions are given. A necessity of dividing vascular, intra- and extravascular (stromal) changes into pathological and adaptive is underlined. A conclusion is made that such an approach to the characteristics of morphological transformations in the microcirculation system will provide a more deep insight into mechanisms of compensation of the terminal hemodynamics disorders and into the causes of a collapse of function of the local adaptive apparatus.

Adaptation, Physiological↗

PubMed1989

Cytokine-mediated proteolysis in tissue remodelling.

Proteolytic enzymes play a key role in a variety of physiological processes in which the degradation of macromolecules is essential: angiogenesis, embryogenesis, bone and tissue remodelling, blood hemostasis and cell migration. The action of these enzymes is also crucial in the development of many pathological conditions such as wound healing, neoplasia, inflammation and arthritic disorders. The activity of proteases is negatively affected by specific protease-inhibitors. Various growth factors and other cytokines modulate the synthesis and secretion of both proteases and protease-inhibitors. The study of this regulation results in a better insight into (patho)physiology at the molecular level and promises to result in alternative treatment strategies.

Animals↗

PubMed2003

VEGF-receptor signal transduction.

The vascular endothelial growth factor (VEGF) family of ligands and receptors has been the focus of attention in vascular biology for more than a decade. There is now a consensus that the VEGFs are crucial for vascular development and neovascularization in physiological and pathological processes in both embryo and adult. This has facilitated a rapid transition to their use in clinical applications, for example, administration of VEGF ligands to enhance vascularization of ischaemic tissues and, conversely, inhibitors of VEGF-receptor function in anti-angiogenic therapy. More recent data indicate essential roles for the VEGFs in haematopoietic cell function and in lymphangiogenesis.

Animals↗

PubMedDate not supplied

Pyogenic granuloma stimulates angiogenesis in the chick embryo chorioallantoic membrane.

Ten samples of pyogenic granuloma and 10 of normal skin from age- and sex-matched controls were grafted onto the chick embryo chorioallantoic membrane (CAM) to investigate their possible angiogenic activity. The angiogenic response in pathological and control implants was assessed on histologic sections by a planimetric point-count method 4 days after grafting. The CAM mast cells were also quantified. The vascular counts in the area underlying the pyogenic granuloma were four times higher than those of normal skin. A higher number of mucosa-like mast cells was detected in the intermediate mesenchyme of the CAM in pathological samples in comparison to controls. Pyogenic granuloma may promote angiogenesis leading to release of several angiogenic factors. The role played in angiogenic response by the inflammatory cells, mainly mast cells, forming the perilesional infiltrate was supported by this study.

Adolescent↗

PubMed2005

Histological observations on the microenvironment of osteolytic bone metastasis by breast carcinoma cell line.

Bone tissue, with its dynamic microenvironment featuring osteoclastic bone resorption, angiogenesis and matrix degradation, appears to facilitate proliferation of tumor cells after the onset of bone metastasis. In this study, we examined metastatic lesions in the femora of BALB/c nu/nu mice two weeks after intracardiac injection with human breast carcinoma MDA-231 cells. Histopathological observations showed the metastatic lesions close to the chondro-osseous junction, and revealed MDA-231 cells loosely intermingled with different cell types such as osteoblasts, fibroblastic stromal cells, osteoclasts and endothelial cells. In the metastatic nest, many tartrate resistant acid phosphatase (TRAPase)-positive osteoclasts accumulated in direct contact with or were close to alkaline phosphatase (ALPase)- or receptor activator of NF-kappaB ligand (RANKL)-positive osteoblastic cells. It seems likely that osteoclastogenesis is mediated through cell-to-cell contacts with ALPase- and RANKL-expressing osteoblastic cells. Formation of many capillaries lacking complete basal membranes and pericytes ratified the results of in situ hybridization, which revealed intense expression of VEGF in tumor nests, and therefore, indicated ongoing tumor-induced angiogenesis. The tumor cells possessed matrix metallo-proteinases (MMPs)-1 and -9, and frequently extended their stout cytoplasmic processes into fragmented fibrillar components of the growth plate cartilage, implicating degradation of cartilaginous matrix. Thus, osteolytic bone metastasis has demonstrated pathological features as tumor-induced angiogenesis and degradation of extracellular matrix, in addition to osteoclastogenesis. This complex interplay between tumor cells and host tissues may enable and nourish the establishment of a microenvironment that facilitates tumor progression.

Animals↗

PubMed2000

Characterization of lymphocyte-dependent angiogenesis using a SCID mouse: human skin model of psoriasis.

From a clinical perspective, angiogenesis is an important component of acute and chronic psoriatic skin lesions as they are erythematous and display a tendency to bleed after superficial removal of scale. By routine histology, numerous microscopic vascular abnormalities are also present. The structural expansion of capillaries and distinctive activated phenotype of lesional endothelial cells are believed not only to be clinical and pathologic hallmarks of the disease, but to play a central role in the pathogenesis of psoriatic plaques. Despite over 20 years of research by leading angiogenesis experts and numerous studies, many details regarding the cellular and molecular basis for angiogenesis in psoriasis remain unknown. In this review, 10 different sections are presented to update recent progress in this active field of investigative skin biology. Highlights of this review include the phenotypic characterization of endothelial cells in acute and chronic psoriatic plaques, and a review of a novel animal model of psoriasis using human skin engrafted onto severe combined immunodeficient mice followed by injection of activated immunocytes. This new experimental model represents a reproducible and pharmacologically validated method to trigger neovascularization and bona fide psoriatic plaque formation. In addition, the potential contribution of epidermal keratinocytes and dermal macrophages to the angiogenic tissue reaction is presented, and a series of questions are then posed that can be answered using the severe combined immunodeficient mouse model of psoriasis. Finally, a model is proposed integrating all available data into a coherent multistep reaction schema that includes active participation by multiple cell types including natural killer T cells, keratinocytes, macrophages, and microvascular endothelial cells.

Animals↗

PubMedDate not supplied

Molecular imaging with contrast ultrasound and targeted microbubbles.

There is growing interest in the development of methods for imaging cellular and molecular mediators of cardiovascular diseases. Techniques for imaging molecular and cellular alterations have been explored for essentially all noninvasive cardiac imaging modalities. Molecular imaging with contrast-enhanced ultrasound relies on the detection of novel site-targeted microbubble contrast agents. These microbubbles are retained within regions of a specific disease process, thereby allowing phenotypic characterization of tissue. As microbubbles are pure intravascular tracers, the disease processes assessed must be characterized by antigens that are expressed within the vascular compartment. Accordingly, the pathologic states that have been targeted include inflammation, neoplasms, angiogenesis, and thrombus formation, all of which are mediated in part by molecular events within the vascular space. This review describes (1) different strategies that have been used to target microbubbles to regions of disease, (2) the unique challenges for imaging targeted ultrasound contrast agents, and (3) some of the early experience imaging molecular events in animal models of disease.

Animals↗

PubMed1994

Evolution of soft drusen in age-related macular degeneration.

The pathways by which soft drusen are formed are illustrated by representative clinical and clinicopathological cases. One type is derived from small hard drusen which first tend to aggregate into clusters and then fuse, forming larger deposits termed hard clusters. Breakdown of the hard drusen results in varying degrees of softening and confluence. These soft clusters may appear in middle age and, like the preceding hard drusen, remain a focal pathology. Soft clusters commonly lead to the atrophic form of age-related macular degeneration. Another type of soft drusen is formed from membranous debris as part of a diffuse disturbance of the retinal pigment epithelium. These membranous soft drusen first appear in the seventh decade and are commonly associated with choroidal neovascularisation.

Adult↗

PubMed2003

Renal cell carcinoma: new prognostic factors?

PURPOSE OF REVIEW: There are limited independent predictors of survival in patients with renal cell carcinoma. Factors related to the tumor, host and treatment may help us to predict prognosis to a certain extent. Prognostic indicators would enable selection of patients who can benefit from adjuvant therapy and thus should be enrolled in clinical trials. This review highlights developments in the identification of current prognosticators for patients with renal cell carcinoma. RECENT FINDINGS: Tumor stage, grade and patient-performance status are the known prognostic indicators in renal cell carcinoma. Besides these parameters, many molecular and cytogenetic markers were evaluated recently. Unfortunately, none of these parameters appear to be a better predictive prognostic factor than the usual staging and grading. Therefore, efforts to identify new markers for tumor proliferation and progression are still ongoing. It was recently reported that low carbonic anhydrase 9 staining may be an independent poor prognostic factor in patients with renal cell carcinoma. Moreover, there is increasing interest in prognostic indices and predictive algorithms for survival. Staging systems that combine the pathological features with additional prognostic variables have been constructed to predict outcome. The UCLA Integrated Staging System seems to be superior to staging alone in differentiating patients' survival. SUMMARY: Although the literature reviewed contains numerous promising clinical, histological, molecular and cytogenetic parameters, none of them has yet been shown to have an independent prognostic value

Adult↗

PubMed2002

Magnetic resonance of the breast: correlation between enhancement patterns and microvessel density in malignant tumors.

The continuous growth of a solid tumor is contingent upon the induction and formation of new vascular structures (angiogenesis). Several studies have established a close correlation between the microvessel density (MVD) of a tumor and its growth capacity. Therefore, a non-invasive method to accurately assess tumor MVD in vivo would be clinically useful. We studied 20 consecutive patients (age range: from 39 to 78 yrs; average age: 58.9 yrs), with malignant breast neoplasms using dynamic MR examinations with a paramagnetic contrast agent and post-operative pathological evaluation. We found that the differences in dynamic MRI enhancement are a direct consequence of microvascular distribution within the neoplasm. This study did not yield a statistically significant correlation between high microcirculation neo-formation and high aggressiveness of the neoplasm, but did indicate that further studies with a larger study populations are necessary.

Adult↗

PubMed1989

Hyaluronan and angiogenesis.

Remodelling tissues, in both normal and pathological situations, show a greatly increased synthesis and turnover of hyaluronan. An essential part of these processes is new blood vessel formation. Whereas native hyaluronan has been reported to inhibit angiogenesis in vivo, partial degradation products (4-25 disaccharide units) have been found to stimulate angiogenesis in several in vivo systems. Examination of the effect of hyaluronan and its oligosaccharides on cultured cells suggests that these effects are due to the direct action of hyaluronan on endothelial cells. Native HA inhibits endothelial cell proliferation and disrupts cell-cell/cell-substrate interactions at physiological concentration. Angiogenic oligosaccharides induce both endothelial proliferation and migration, possibly via a receptor-mediated mechanism. Thus the metabolic state of hyaluronan could have profound effects on tissue neovascularization.

Animals↗

PubMed2003

Influence of transarterial chemoembolization on angiogenesis and expression of vascular endothelial growth factor and basic fibroblast growth factor in rat with Walker-256 transplanted hepatoma: an experimental study.

AIM: After transarterial chemoembolization (TACE), the residual cancer cells are under extensive hypoxic or even anoxic environment. Hypoxia can lead to adaptive responses. For example, angiogenesis will help these cells survive. In this study, we examined the effect of TACE on angiogenesis and expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (b-FGF) and to assess their relevance to Walker-256 transplanted hepatoma. METHODS: Male Wistar rats were inoculated with Walker-256 tumor in the left lobe of liver. Angiography and transarterial chemoembolization were performed at d14 after transplantation. Sixty rats bearing walker-256 transplanted hepatoma were randomly divided into control group, arterial infusion group and TACE group. Each group consisted of twenty rats. Normal saline, 5-Fu, 5-Fu and lipiodol were infused through hepatic artery respectively. Two weeks after the infusion, staining of factor VIII, VEGF and b-FGF was performed by immunohistochemistry method in routine paraffin-embedded sections. Microvessel density (MVD) was counted in endothelial cells with positive factor VIII. Their expression levels were analyzed in conjunction with the pathologic features. RESULTS: While a smaller tumor volume was found in TACE group (F=37.818, P<0.001), no statistical differences between MVD and expression of VEGF and b-FGF were found among the 3 groups. MVD of the control group, chemotherapy group and chemoemoblization group was 80.84+/-24.24, 83.05+/-20.29 and 85.20+/-23.91 (F=0.193, P=0.873), respectively. The positive expression of VEGF and b-FGF was 75%, 75%, 85% (chi2=0.449, P=0.799) and 30%, 25%, 30% (chi2=0.141, P=0.922), respectively. Statistical analysis revealed a positive correlation between the expression of VEGF and MVD (r=0.552, P<0.001). CONCLUSION: There has been little influence of lipiodol chemoembolization on the formation of tumor angiogenesis, but the development of neovascularization and expression of VEGF play important roles in establishment of collateral circulation and reconstruction of blood supply of residual cancer tissue.

Animals↗

PubMed2002

p53 and microvessel density in primary resection specimens of superficial bladder cancer.

PURPOSE: p53 Regulates angiogenesis in fibrosarcoma and correlative studies suggest a similar role for muscle invasive bladder cancer. We evaluated the associations of p53 status and microvessel density with pathological features and clinical outcomes in a large population of patients with superficial bladder cancer. In addition, we assessed the correlation of p53 status with microvessel density, which would suggest the regulation of angiogenesis by p53. MATERIALS AND METHODS: We stained 84 primary bladder resection specimens, including 55 stage pTa, 29 stage pT1, 27 grade 1, 35 grade 2 and 22 grade 3 samples, for p53, CD31 and CD34. The relationships of p53 or microvessel density and tumor stage-grade or clinical recurrence-progression were analyzed by analysis of variance and pairwise comparison analysis for least significant difference, and Pearson correlation coefficients. Only patients with no previous biopsy were included in analysis to preclude interference by granulation tissue related neovascularization. The 4 samples with significant inflammation were also excluded from study. RESULTS: At a mean followup of 33 months (range 1 to 93) 34 of 84 patients (40.4%) experienced 1 or more tumor recurrences and 10 (11.9%) had stage and/or grade progression. Statistically significant associations were observed of p53 immunostaining and microvessel density with tumor stage and grade (p <0.05). However, the association of p53 status with microvessel density was weak and not statistically significant. Similar results were observed for the CD31 and CD34 based estimates of microvessel density. Neither p53 status nor microvessel density correlated with recurrence or progression. CONCLUSIONS: Our study confirms the strong association of p53 and microvessel density with the well established prognostic factors of grade and stage in superficial bladder cancer, supporting other evidence of an important role for p53 and angiogenesis in the tumor biology of this disease. However, our data argue against a primary role of p53 in the regulation of angiogenesis in superficial bladder cancer. This study, which to our knowledge is the first to focus on primary resection specimens, suggests that other genetic or environmental factors may contribute to the regulation of angiogenesis in superficial bladder cancer.

Humans↗

PubMed2004

Histological and microscopy FT-IR imaging study on the proliferative activity and angiogenesis in head and neck tumours.

Micro Fourier transform infrared spectroscopy enables one to study small samples because of the high quality spectra that can be obtained. Biochemical and morphological changes between control and pathological tissues of head and neck tumours have been monitored drawing three-dimensional chemical maps of the main vibrational modes in the regions of interest. Comparison between spectral and histological data shows a satisfactory degree of accordance. Among all, proliferating and regressive states of the tumours can be identified.

Antigens, CD34↗

PubMedDate not supplied

Determination of angiogenesis in human neoplasms: current prognostic and therapeutic implications.

The growth of solid tumours beyond a certain mass is strictly dependent on the formation of a vascular bed from a pre-existing host vasculature. This process has been termed OangiogenesisO and its importance in the process of tumour growth and metastasis has recently gained wide acceptance. Studies have been reported in several kinds of human cancers in which the number of microvessels in the most intense areas of neo-vascularisation (Ohot spotsO) have been shown to be strictly related to the development and progression of the tumour. In the majority of these studies highly vascularised tumours showed a poor prognosis and the influence of tumour angiogenesis proved to be independent of conventional prognostic indicators. The evaluation of tumour angiogenesis by quantitative pathology may represent an important prognostic indicator in human cancers and will be increasingly important in the investigation of new therapies directed to inhibiting angiogenesis or targeting tumour vasculature. This review will briefly summarise the current knowledge on the prognostic impact of tumour angiogenesis in human cancers with a final reference to angiogenesis inhibitors which are currently used in phase I/II and III clinical trials.

Antineoplastic Agents↗

PubMed2004

Determination of molecular marker expression can predict clinical outcome in colon carcinomas.

PURPOSE: Conventional staging procedures are often unable to precisely predict prognosis in colorectal cancer (CRC). In this study, we set out to investigate the possible role of molecular/structural indicators involved in cell cycle regulation (p27 and p53), apoptosis (p53 and p27), and tumor neoangiogenesis [p53, vascular endothelial growth factor (VEGF), and microvessel count] in predicting tumor behavior and clinical outcome in CRC patients EXPERIMENTAL DESIGN: Analysis of the above indicators was performed by immunohistochemistry on 104 CRC patient samples and 25 normal colon mucosa specimens. RESULTS: Intense p27 nuclear staining was found in normal colon mucosa, with p53 nuclear staining and VEGF cytoplasmic accumulation <10%, and low microvessel count. In contrast, in CRC samples, p27 was down-regulated in 53.8%, p53 protein was overexpressed in 52%, and VEGF stained positive in 67.3% of the cases, respectively. Multiple regression analysis showed that molecular markers were strongly correlated. In patients treated with curative surgery, a significant relationship was seen between p27 down-regulation and Dukes' stage, nodal status, and the presence of distant metastases. VEGF overexpression correlated significantly with Dukes' stage, tumor (t) and metastasis (m) parameters, and left site. Stepwise regression selected p27, p53, VEGF, and Dukes' stage as the best combination of variables capable of predicting both disease-specific and disease-free survival. CONCLUSIONS: The investigated indicators may be useful for the prediction of outcome and recurrence rate in curatively treated CRC patients. In conjunction with clinical and pathological staging, they may provide a stronger indication of clinical outcome than staging alone and help better select therapeutic options in CRC patients.

Adult↗

PubMed1986

Fibroblast radiosensitivity and intraocular fibrovascular proliferation following radiotherapy for bilateral retinoblastoma.

A 5-day-old female patient was found to have large hereditary retinoblastomas in the posterior pole of each eye. The patient received radiation treatment over a 39-day period, with each retina receiving 4600 rad. Two weeks after the complete treatment the tumours had regressed to approximately one-quarter of their original size. By 14 weeks following completion of radiotherapy the patient had developed in each eye extensive iris neovascularisation with progressive closure of the filtration angles, secondary glaucoma, and retinal detachments resulting from fibrovascular proliferation on the retinal surface. Radiosensitivity studies were from separate conjunctival biopsies obtained before and after radiation. These showed a D0 (calculated survival curve parameters, defined in the Methods section) in the exponential growth phase of 110 prior to radiation and a postirradiation exponential growth phase D0 of 70. Karotype studies showed several chromosomal abnormalities following radiotherapy. The clinical course and pathology findings are thought to represent an unusually severe orbital and ocular response to radiation therapy. These findings are consistent with our hypothesis that some patients with hereditary retinoblastoma may have a defect in the accumulation repair of x-irradiation induced DNA damage.

Cell Survival↗