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Results for “Neovascularization, Pathologic”

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At least 1,423 records · Page 79Linked to original sources

PubMed2003

High magnification bronchovideoscopy combined with narrow band imaging could detect capillary loops of angiogenic squamous dysplasia in heavy smokers at high risk for lung cancer.

BACKGROUND: We investigated the use of high magnification bronchovideoscopy combined with narrow band imaging (NBI) for the detailed examination of angiogenic squamous dysplasia (ASD). This was carried out in relation to bronchial vascular patterns with abnormal mucosal fluorescence in heavy smokers at high risk for lung cancer. METHODS: Forty eight patients with sputum cytology specimens suspicious or positive for malignancy were entered into the study. Conventional white light and fluorescence bronchoscopic examination was first performed. Observations by high magnification bronchovideoscopy with conventional white light were made primarily at sites of abnormal fluorescence, and then repeated with NBI light to examine microvascular networks in the bronchial mucosa. Spectral features on the RGB (Red/Green/Blue) sequential videoscope system were changed from the conventional RGB broadband filter to the new NBI filter. The wavelength ranges of the new NBI filter were B1: 400-430 nm, B2: 420-470 nm, and G: 560-590 nm. ASD tissues were also examined using a confocal laser scanning microscope equipped with argon-krypton (488 nm) and argon (514 nm) laser sources. RESULTS: The microvessels, vascular networks of various grades, and dotted vessels in ASD tissues were clearly observed in NBI-B1 images. Diameters of the dotted vessels visible on NBI-B1 images agreed with the diameters of ASD capillary blood vessels diagnosed by pathological examination. Capillary blood vessels were also clearly visualised by green fluorescence by confocal laser scanning microscopy. There was a significant association between the frequency of dotted vessels by NBI-B1 imaging and tissues confirmed as ASD pathologically (p=0.002). CONCLUSIONS: High magnification bronchovideoscopy combined with NBI was useful in the detection of capillary blood vessels in ASD lesions at sites of abnormal fluorescence. This may enable the discrimination between ASD and another pre-invasive bronchial lesion.

Adult↗

PubMed2000

Mechanisms of tumor metastasis to bone.

Bone metastases occur in approximately 80% of patients with advanced cancer. They are characterized by cancer cell growth and bone destruction that cause pain, fractures, anemia, and hypercalcemia. At diagnosis, bone metastases are usually incurable owing to their advanced development. However, the early stages in their formation are asymptomatic and begin as single micrometastatic cells from the blood stream. These cells can be detected by molecular analysis of bone marrow in approximately 30% of patients at the time of cancer diagnosis, but not all single micrometastatic cells develop into clinically significant bone metastases. A synergistic relationship exists between the micometastasis and the bone environment creating favorable conditions for the development and growth of disseminated tumor cells. Such bone metastases induce osteolysis or new bone formation, releasing growth factors and cytokines, which in turn amplify this pathological mechanism. The underling hypothesis, first proposed by Paget in 1889, is that the growth of disseminated tumor cells in bone is dependent on the fertility of the soil or bone itself. This article explores the most current opinions in this area of study and presents a comprehensive summary of the major factors involved.

Bone Neoplasms↗

PubMedDate not supplied

Clinical perspectives of tumor angiogenesis in pediatric oncology.

Angiogenesis, the formation of new capillaries from existing blood vessels, is necessary for embryonic growth and development. It is also seen later during the female cycle and wound healing, but is virtually absent otherwise in the healthy adult organism. Angiogenesis is again observed under pathological conditions, like for example in solid pediatric malignancies. Once grown to a diameter of several millimeters, the latter depend on angiogenesis in order to further grow and to metastasize. Recent experimental and clinical evidence suggests 1) that the extent of tumor angiogenesis could serve to predict clinical outcome and 2) that the inhibition of angiogenesis could be a means to improve the conventional therapy of solid pediatric malignancies.

Adult↗

PubMed2000

Autocrine motility factor receptor expression associates with tumor progression in thymoma.

We assessed the autocrine motility factor receptor (AMFR/gp78) expression in thymoma. AMFR/gp78 antigen was identified in tumor cells in 16 out of 51 (31.4%) thymomas. The AMFR/gp78 expression was closely associated with the stage (I/II vs. III/IV, p<0.0001), pathological subtypes (epithelial vs. other types, p=0.0214), and enhanced expression of alpha-smooth-muscle actin within stroma (p<0. 0001). The outcome of the patients with AMFR/gp78 expression was significantly worse than for those without it (p<0.01). All initial tumors with recurrence expressed AMFR/gp78. The AMFR/gp78 appears to be involved in tumor progression in thymoma.

Actins↗

PubMed1994

[Vascular endothelial system--from the pathological aspects].

Endothelial functions have been paid much attention in the interaction between blood and vascular wall and their functional aterations play an important role in the development and progression of thrombosis and atherosclerosis. In this paper two topics in these fields, namely, the in vivo expression of tissue factor by endothelial cells as well as macrophages in hepatic sinusoids of rats and rabbits with endotoxemia, and the angiogenic mechanism in atherosclerotic intima of human coronary arteries and its pathophysiological significance, would be reviewed mainly based on our data obtained by immunohistochemical and biochemical examinations and molecular analyses.

Animals↗

PubMed2004

Prognostic significance of anaplasia and angiogenesis in childhood medulloblastoma: a pediatric oncology group study.

The purpose of this study was to investigate whether quantitative assessment of cytologic anaplasia and angiogenesis may predict the clinical prognosis in medulloblastoma and stratify the patients to avoid both undertreatment and overtreatment. Medulloblastomas from 23 patients belonging to the Pediatric Oncology Group were evaluated with respect to some prognostic variables, including histologic assessment of nodularity and desmoplasia, grading of anaplasia, measurement of nuclear size, mitotic cell count, quantification of angiogenesis, including vascular surface density (VSD) and microvessel number (NVES), and immunohistochemical scoring of vascular endothelial growth factor (VEGF) expression. Univariate and multivariate analyses for prognostic indicators for survival were performed. Univariate analysis revealed that extensive nodularity was a significant favorable prognostic factor, whereas the presence of anaplasia, increased nuclear size, mitotic rate, VSD, and NVES were significant unfavorable prognostic factors. Using multivariate analysis, increased nuclear size was found to be an independent unfavorable prognostic factor for survival. Neither the presence of desmoplasia nor VEGF expression was significantly related to patient survival. Although care must be taken not to overstate the importance of the results of this single-institution preliminary report, pathologic grading of medulloblastomas with respect to grading of anaplasia and quantification of nodularity, nuclear size, and microvessel profiles may be clinically useful for the treatment of medulloblastomas. Further validation of the independent prognostic significance of nuclear size in stratifying patients is required.

Adolescent↗

PubMed1996

[Radical treatment by the surgeon and reality of the pathologist].

The aim of the radical resection of lung tumors is curative treatment. However, in each lung tumor of more than 2 cm in diameter an angioinvasion of tumor cells could be proved by morphological means. Frequently, the existence of lymph nodes and especially hematogenic dissemination is underestimated at the time of resection. By pathological-anatomical means in 33% of T1/T2-N2 and 60% of T1/T2-N3 lung tumors, disseminated tumor cells or organoid metastasis in the bone marrow can be demonstrated. Therefore, the demand for radicalness of the surgeon does not agree with a curative tumor therapy in more advanced tumor stages. Actually, the course of the disease following a local radical resection is predominantly predetermined by the individual hematogenic metastatic spread.

Humans↗

PubMed2001

The role of matrix metalloproteinases in tumor angiogenesis and tumor metastasis.

Although a considerable amount of effort has been placed on discovering the etiologies of cancer, the majority of the basic cancer research existing today has focused on understanding the molecular mechanism of tumor formation and metastasis. Metastatic spread of tumors continues to be a major obstacle to successful treatment of malignant tumors. Approximately 30% of those patients diagnosed with a solid tumor have a clinically detectable metastasis and for the remaining 70%, metastases are continually being formed throughout the life of the tumor. Even after the tumor is excised, the threat of death is attributable to the metastasis that may occur through the remaining tumor cells. In addition, treating the metastasis often proves futile since metastasis often vary in size, composition, and anatomical location. New treatments blocking the formation of metastasis will provide greater chances of survival for cancer patients. One family of enzymes that has been shown over the years to play a role in tumor progression is the matrix metalloproteinase (MMP) family. The main function of MMPs, also known as matrixins, is degradation of the extracellular matrix physiologic function involving MMPs include wound healing, bone resorption and mammary involution. MMPs, however, also contribute to pathological conditions including rheumatoid arthritis, coronary artery disease, and cancer. Tumor cells are believed to utilize the matrix degrading capability of these enzymes to spread to distant sites. In addition, MMPs also are thought to promote the growth of these tumor cells once they have metastasized. This review will discuss the role of MMPs and their inhibitors in tumor invasion, angiogenesis and metastasis with special emphasis on the gelatinases, MMP-2 and MMP-9.

Humans↗

PubMed2004

Moyamoya-like vasculopathy (moyamoya syndrome) in children.

INTRODUCTION: A large variety of inherited or acquired childhood disorders and conditions may present in conjunction with progressive bilateral stenosis and/or occlusion of the terminal segments of the internal carotid artery. In addition, the development of pathological collateral vessels can be observed in the vicinity of the steno-occlusive changes in these patients. This condition is known as moyamoya-like (MML) vasculopathy. The natural history, the angiographic appearance, and the pathology of MML vasculopathy probably differ from those of definite moyamoya disease. Adequate cerebral vascular imaging should be considered in all pediatric patients with inherited or acquired systemic disorders and symptoms attributable to cerebral ischemia. CASES AND DISCUSSION: We present four pediatric cases of MML vasculopathy, and outline the etiology, the current classification, and the therapeutic approaches for this heterogeneous disease entity.

Brain Neoplasms↗

PubMed2006

Pulmonary venous drainage through a highly vascularized left atrial tumor.

We present a patient with symptomatic congestive heart failure due to a left atrial sarcoma infiltrating and apparently occluding the left pulmonary veins. The tumor was highly vascularized and enabled attenuated blood drainage from the left upper and lower pulmonary veins despite intra-operative appearance as completely obliterative, thus avoiding persistent left lung pulmonary edema. The tumor was partially removed and the pathologic findings showed advanced angiogenesis. Malignant tumors may occlude large blood vessels and thus may result in the development of a collateral flow. However, we suggest that highly vascularized tumors (macroscopic totally occlusive) may serve as a sponge and enable attenuated blood flow through the tumor and hence may avoid a complete cut off in blood supply or drainage.

Aged, 80 and over↗

PubMed1999

Pathological angiogenesis in a murine model of human Wilms' tumor.

BACKGROUND/PURPOSE: Pathological vascular architecture is a feature of neoangiogenic processes such as diseases of the retina and tumor growth. The authors hypothesized that experimental human Wilms' tumors would display a vascular architecture similar to retinal diseases that are driven by vascular endothelial growth factor (VEGF). METHODS: Human Wilms' tumors were established in the right kidneys of nude mice. After 4.5 weeks of tumor growth, fluorescein angiograms were performed before death. Representative sections of tumors and contralateral, control kidneys were evaluated by fluorescent microscopy. RESULTS: Fluorescein angiograms demonstrated a characteristic pathological architecture. Vascular tortuosity, capillary tufting, and hemorrhage were noted. These features were not present in normal kidneys. CONCLUSIONS: Vascular architecture of Wilms' tumor displays the specific features previously described in diseases of the retina, which have been shown to be driven by VEGF, suggesting that neoangiogenesis in this model is also VEGF driven.

Animals↗

PubMed1999

Predictive factors in prostate cancer: current concepts from the 1999 College of American Pathologists Conference on Solid Tumor Prognostic Factors and the 1999 World Health Organization Second International Consultation on Prostate Cancer.

Many clinically important predictive factors in prostate cancer are derived from light microscopic examination of tissue specimens by the pathologist. Two separate international consensus conferences held in 1999 addressed the contemporary status of such prognostic factors, sponsored by the College of American Pathologists (CAP) and the World Health Organization (WHO). Both conferences concluded that the following factors are recommended for routine use based on evidence from multiple published trials: TNM stage, histological grade using the Gleason system, surgical margin status, and serum prostate-specific antigen concentration. The WHO conference additionally recommended use of WHO nuclear grade, location of cancer within the prostate, and pathological effects of treatment. Other factors were categorized as promising or of unproven utility, including a wide variety of histopathologic and genetic markers. Standards are needed for analysis and quantitation of methods of tissue analysis, particularly for immunohistochemical studies and genotypic studies. This report describes the recommendations and conclusions of these two conferences.

Apoptosis↗

PubMed2006

Preclinical evaluation of an anti-alpha5beta1 integrin antibody as a novel anti-angiogenic agent.

Integrin alpha5beta1, the principal fibronectin receptor, is an important survival factor, playing a key role in angiogenesis. Angiogenesis is critical for tumor growth, and anti-angiogenic therapies have met clinical success. To validate the therapeutic potential of an anti-alpha5beta1 strategy, we generated volociximab (M200) a chimeric human IgG4 version of the alpha5beta1 function-blocking murine antibody IIA1; and F200, the Fab derivative. Volociximab, F200 and IIA1 showed similar activity by ELISA (EC50= 0.2nM), Biacore (Kd= 0.1-0.4nM) and inhibition of fibronectin binding (IC50= 2-3nM). The inhibitory potential of alpha5beta1 antibodies was compared to HuMV833, an anti-VEGF antibody. Both volociximab and HuMV833 inhibited HUVEC proliferation (IC50 of volociximab = 0.2-0.5nM; IC50 of HuMV833 = 45nM). However, IIA1, volociximab and F200 were also potent inhibitors of an in vitro model of angiogenesis (HUVEC tube formation assay), unlike HuMV833. Additionally, volociximab inhibited in vitro tube formation induced by VEGF and/or bFGF, suggesting a mechanism of action independent of growth factor stimulus. In fact, inhibition of alpha5beta1 function by volociximab induced apoptosis of actively proliferating, but not resting, endothelial cells. Volociximab does not cross-react with rodent alpha5beta1, therefore in vivo validation of an anti-alpha5beta1 approach was conducted in a cynomolgus model of choroidal revascularization. Volociximab and F200 were potent inhibitors of neovessel formation in this model. These data demonstrate that volociximab has therapeutic potential in diseases in which new vessel formation is a component of the pathology.

Angiogenesis Inhibitors↗

PubMed1996

The relationship between vascularity and cell proliferation in human normal and pathological lesions of the oral cheek epithelium.

The present study investigates relationships between neovascularisation and PCNA cell proliferation markers in different pathological lesions of the oral cheek mucosa. All specimens were fixed in 10% formalin and routinely processed for histology. Six normal (N) samples were taken from resection margins of benign lesions. The pathological lesions consisted of chronic inflammation (n = 10), lichen planus (n = 7), fibrous hyperplasia (n = 11), dysplasia (n = 5), squamous cell carcinoma (n = 22) and epithelium adjacent to carcinoma (n = 6). Adjacent 5 microns sections were stained with monoclonal antibodies against vimentin (clone no. V9) for identification of stromal blood vessels and against proliferating nuclear antigen (PCNA/PC10) using ABC immunoperoxidase techniques. Point counting was used to obtain the primary morphometric data using a Zeiss VIDAS image analyser. No attempt was made to classify the different types of blood vessels. The morphometric blood vessel parameters estimated were volume density, number per unit area, length per unit volume and mean transverse sectional area. PCNA indices were determined by estimating the percentage frequency of PCNA positive nuclei in basal and spinous strata. Generally, there were significant increases in all PCNA indices and blood vessel parameters between the N group and the different pathological lesions. A highly positive correlation was detected between all PCNA indices and blood vessel parameters. These data suggest that increased vascularity and angiogenesis occur in support of actively proliferating and transforming oral epithelial cells in order to permit growth. PCNA indices and blood vessel parameters may have a potential application as diagnostic and prognostic indicators.

Adolescent↗

PubMed2001

Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions.

Vascular endothelial growth factor (VEGF) stimulates angiogenesis by activating VEGF receptor-2 (VEGFR-2). The role of its homolog, placental growth factor (PlGF), remains unknown. Both VEGF and PlGF bind to VEGF receptor-1 (VEGFR-1), but it is unknown whether VEGFR-1, which exists as a soluble or a membrane-bound type, is an inert decoy or a signaling receptor for PlGF during angiogenesis. Here, we report that embryonic angiogenesis in mice was not affected by deficiency of PlGF (Pgf-/-). VEGF-B, another ligand of VEGFR-1, did not rescue development in Pgf-/- mice. However, loss of PlGF impaired angiogenesis, plasma extravasation and collateral growth during ischemia, inflammation, wound healing and cancer. Transplantation of wild-type bone marrow rescued the impaired angiogenesis and collateral growth in Pgf-/- mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow-derived cells. The synergism between PlGF and VEGF was specific, as PlGF deficiency impaired the response to VEGF, but not to bFGF or histamine. VEGFR-1 was activated by PlGF, given that anti-VEGFR-1 antibodies and a Src-kinase inhibitor blocked the endothelial response to PlGF or VEGF/PlGF. By upregulating PlGF and the signaling subtype of VEGFR-1, endothelial cells amplify their responsiveness to VEGF during the 'angiogenic switch' in many pathological disorders.

Animals↗

PubMed2006

Molecular genetics of familial cerebral cavernous malformations.

Cerebral cavernous malformations (CMs) are angiographically occult neurovascular lesions that consist of enlarged vascular channels without intervening normal parenchyma. Cavernous malformations can occur as sporadic or autosomal- dominant inherited conditions. Approximately 50% of Hispanic patients with cerebral CMs have the familial form, compared with 10 to 20% of Caucasian patients. There is no difference in the pathological findings or presentation in the sporadic and familial forms. To date, familial CMs have been attributed to mutations at three different loci: CCM1 on 7q21.2, CCM2 on 7p15-p13, or CCM3 on 3q25.2-q27. The authors summarize the current understanding of the molecular events underlying familial CMs.

Animals↗

PubMedDate not supplied

Serum levels of angiogenin (ANG) in invasive cervical cancer and in cervical intraepithelial neoplasia (CIN).

BACKGROUND: The propensity of malignant tumors to increase in size, to invade locally and to metastasize is dependent on angiogenesis, which is induced by a variety of proteins including the family of fibroblast growth factors, vascular endothelial growth factor and angiogenin (ANG). The aim of the present study was to measure the serum levels of ANG in patients with CIN and invasive cervical cancer and to evaluate a possible correlation between ANG and various clinicopathologic parameters. MATERIALS AND METHODS: Blood was collected from 62 patients with invasive cervical cancer and 47 patients with CIN. Serum samples of 30 age-matched healthy women acting as a control group were obtained. Determination of serum levels of ANG was performed using a quantitative human ANG immunoassay. RESULTS: The overall median ANG serum level was 272.0 pg/ml (range 101.6-869.2). The median serum levels of ANG were 248.9 (range 101.6-307.2) for healthy female controls, 246.8 (range 169.7-468.1) for patients with CIN and 308.1 pg/ml (range 180.1-869.2) for patients with invasive cervical cancer. Serum levels of ANG were significantly elevated in patients with invasive cervical cancer compared with patients with CIN (p < 0.05) as well as healthy female controls (p < 0.05). No difference was found between ANG serum levels in women with CIN, and healthy controls (p < 0.05). No correlations were found between serum levels of ANG and clinico-pathologic parameters (p > 0.05). CONCLUSIONS: Our data indicate the important role of ANG in tumor angiogenesis in invasive cervical cancer as ANG serum levels were significantly elevated in these patients. However, elevated ANG serum levels seem to occur only after the transformation from pre-invasive to invasive lesions.

Adenocarcinoma↗

PubMed1999

Tumor cells utilize multiple pathways to down-modulate apoptosis. Lessons from a mouse model of islet cell carcinogenesis.

Apoptosis, the process of programmed cell death, plays a critical role in many normal and pathological (disease) processes. In normal tissues, apoptosis functions in the homeostatic maintenance of proper tissue and organ size by eliminating aged cells to offset the birth of new cells that arise by mitosis. In disease, apoptosis can affect the pathological process is two disparate ways. There are diseases that have too much apoptosis such as autoimmune diabetes and Alzheimer's, or those that have too little apoptosis, such as cancer. This review will focus on the latter and, more specifically, detail and summarize some important lessons learned about apoptosis and cancer from studying a transgenic mouse model of islet cell carcinoma, RIP-Tag, as outlined below.

Animals↗