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Results for “Neovascularization, Pathologic”

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PubMed1993

Inverse relationship between hyaluronan and collagens in development and angiogenesis.

The extracellular matrix plays a vital role in regulating normal tissue development and function--largely via the specific arrangement of macromolecules such as collagens, proteoglycans, glycosaminoglycans and glycoproteins. Previous reports have concentrated on associations between combinations of collagens/proteoglycans, collagens/glycoproteins and proteoglycans/glycosaminoglycans whilst little information is available on associations between collagens and free glycosaminoglycans. In this review, we discuss possible associations between collagens and the glycosaminoglycan hyaluronan; macromolecules which are known to exhibit changes in amount and composition during development and under pathological conditions. We demonstrate two types of collagen/hyaluronan association in vivo: the first, during the formation of extracellular matrix structures where neither collagens nor hyaluronan are degraded, resulting in the regulation of collagen fibrillogenesis, and the second, involving an inverse correlation between collagen synthesis and hyaluronan degradation and vice versa. We suggest that associations between collagens and hyaluronan play an important role in the initiation and maintenance of angiogenesis and put forward a model of cartilage vascularisation which relies on these associations.

Animals↗

PubMed1990

Angiogenic activity of normal and pathologic human thyroid tissue.

Thyroid tissue was collected from 60 patients during operations for various thyroid conditions. The tissue's angiogenic capacity was assessed in a chick chorioallantoic membrane preparation. Angiogenic activity was observed in 22 (85%) of 26 solitary follicular neoplasms, in none of ten papillary carcinomas and in one of seven glands with Graves' disease (all pretreated with propranolol). Of 17 glands with euthyroid multinodular colloid goitre, three (18%) showed angiogenic activity. No angiogenic activity was detected in normal thyroid tissue from 26 patients. Angiogenic activity of diseased human thyroid does not seem to be a marker of thyroid malignancy.

Adult↗

PubMed1993

[Angiogenesis and its regulation].

Angiogenesis (formation of new blood vessels) is essential in embryonal development, female reproduction and wound repair. Under these physiological conditions, angiogenesis is highly regulated by the endogenous angiogenic factor and its inhibitor. However, angiogenic diseases such as rheumatoid arthritis, diabetic retinopathy, solid tumor, hemangioma and psoriasis are driven by persistent unregulated angiogenesis. The angiogenic process consists of such multi-steps as degradation of basement membrane, cell migration and proliferation, and tube formation following activation of vascular endothelial cells by stimulators appearing at the pathological site. Thus, for modulating the pathological conditions, it is most important to elucidate the angiogenic mechanism at the molecular level. It is not sufficiently clear yet as compared with the blood coagulation and hematopoietic systems. On the other hand, there have been advances in the study of new anticancer metastatic agents as a target of activated endothelial cells and they have been found to have promising substances. In this study, the angiogenic factor, its inhibitor, and then the anticancer effect of the angiogenic inhibitor, have been investigated from the standpoint of cancer therapy.

Angiogenesis Inducing Agents↗

PubMedDate not supplied

Interactions between cancer cells and the microvasculature: a rate-regulator for metastasis.

Hematogenous metastasis is a major consideration in the staging, treatment and prognosis of patients with cancer. Key events affecting hematogeneous metastasis occur in the microvasculature. This is a brief, selective review of some interactions involving cancer cells and the microvasculature in pathologic sequence, specifically: (1) intravasation of cancer cells; (2) the arrest of circulating cancer cells in the microvasculature; (3) cancer cell trauma associated with arrest; (4) microvascular trauma; (5) the inflammatory; and (6) the hemostatic coagulative responses associated with arrest, and finally (7) angiogenesis, leading to tumor vascularization. The evidence shows that through a series of complex interactions with cancer cells, the microvasculature acts as a rate-regulator for the metastatic process, in addition to providing routes for cancer cell dissemination and arrest sites for cancer cell emboli.

Cell Adhesion↗

PubMed1989

Role of growth factors in the formation of blood vessels.

The turnover of endothelial cells in the normal human adult male is very low, on the order of years. However, in a number of mainly pathological conditions endothelial cells rapidly proliferate, thereby giving rise to new blood vessels (a process called angiogenesis). Angiogenesis-inducing factors have been purified from normal and tumor tissues. Some of these factors are growth or chemotactic factors for endothelial cells. Others have no effect in vitro and are thought to act via indirect mechanisms. Growth and chemotactic factors are also secreted by endothelial cells themselves and may be involved in the development of the vascular wall. In addition they might play a role in atherosclerosis.

Angiogenesis Inducing Agents↗

PubMed1994

Does the transcription factor c-ets1 take part in the regulation of angiogenesis and tumor invasion?

The c-ets1 proto-oncogene encodes a transcription factor that binds a GGAA/T purine rich core DNA sequence. During normal as well as pathological development, the expression of c-ets1 is associated with the occurrence of invasive processes, either in invading cells or in the invaded tissue. Cellular regulatory sequences responsive to the c-Ets1 proteins include a urokinase-type plasminogen activator (u-PA) gene enhancer, the stromelysin-1 and the collagenase-1 gene promoters. Since invasive processes are thought to require the remodeling of the extra-cellular matrix, we investigate the relationships between c-Ets1 and the expression pattern of transcripts encoding these matrix degrading proteases, in embryos and in solid tumors.

Neovascularization, Pathologic↗

PubMed1985

Tumor angiogenesis.

The hypothesis that tumors are angiogenesis dependent has, in the past decade, generated new investigations designed to elucidate the mechanism of angiogenesis itself. Many laboratories are now engaged in this pursuit. Some are studying angiogenesis that occurs in physiological situations, whereas others are interested in angiogenesis that dominates pathological conditions. These efforts have led to (1) the development of bioassays for angiogenesis; (2) the partial purification and, in one case, the complete purification of angiogenic factors from neoplastic and non-neoplastic cells; (3) the development of new polymer technology for the sustained release of these factors and other macromolecules in vivo; (4) the cloning and long-term culture of capillary endothelial cells; (5) the demonstration of the role of nonendothelial cells, such as mast cells in modulating angiogenesis; (6) the discovery of angiogenesis inhibitors; and (7) the demonstration that certain animal tumors will regress when angiogenesis is inhibited. The effects of angiogenesis inhibitors provide perhaps the most compelling evidence for the role of angiogenesis in tumor growth. It is conceivable that the original effort to understand the role of angiogenesis in tumor growth will also lead to the use of angiogenesis inhibitors as a new class of pharmacologic agents in a variety of non-neoplastic diseases such as arthritis, psoriasis, and ocular neovascularization. However, much work remains to be done before it will be possible to understand (1) the regulatory systems that govern capillary density in normal tissues; (2) the factors that maintain the viability of microvascular endothelium; (3) the development of the vascular system itself; and (4) the mechanism by which vascular regression occurs, both in the embryo and in the postnatal organism. A knowledge of the mechanisms which underlie these normal processes may help to enlarge our comprehension of tumor angiogenesis.

Angiogenesis Inducing Agents↗

PubMed1995

[Angiogenesis is induced by growth factors. The molecular mechanisms are not yet known].

Angiogenesis, the formation of new vessels from the vessel bed, is crucially involved in physiological and pathological processes. Angiogenesis may be regarded as a series of cellular events--e g, basement membrane degradation, and the migration, proliferation and differentiation of endothelial cells. Several different growth factors trigger one or more of these events both in vivo and in vitro, though the underlying mechanisms are still largely unknown. Elucidation of the function of growth factor receptors in angiogenesis, and their propagation of intracellular signals eventually resulting in angiogenesis is an important task for research. In all likelihood, such studies will give rise to clinically useful tools for the regulation of angiogenesis, which might be of importance in such disease as diabetes and cancer.

Collateral Circulation↗

PubMed1994

Pathology from hydroxyapatite deposits in periarticular tissues. First conclusions on etiopathogenesis.

Biopsies of periarticular tissues from patients with episodes of chronic periarthritis were examinated by histological, ultrastructural and chemico-crystallographic methods. In all samples the mineralogical observations at the optical microscope, showed aggregates of microcrystalline incrustations, whose ultrastructural morphology has been characterized by SEM. The histological observations showed necrosis of collagen fibres and microcrystallization process in cavities and in metaplastic fibrocartilage. The HA deposits in the periarticular tissues, in the next stage of the process, are surrounded and demolished by macrophages and multinucleated giant cells. At the same time granulation tissue carries out the repair process, that begins with the formation of thin parallel collagen fibers interposed with many fibroblasts and numerous small vessels.

Biopsy↗

PubMed1995

A quantitative investigation of immunocytochemically stained blood vessels in normal, benign, premalignant and malignant human oral cheek epithelium.

The present study was designed to determine whether increased vascularity occurs during malignant transformation of human oral cheek epithelium. Nine normal (N) samples were taken from the resection margins of benign lesions; the pathological lesions were classified as chronic inflammation (CI; n = 11), fibrous hyperplasia (FH; n = 12), lichen planus (LIP; n = 8), dysplasia (DYS; n = 5), squamous cell carcinoma (SCC; n = 25; well differentiated [SCCWD]; n = 10; moderately to poorly differentiated [SCCMPD]; n = 15) and epithelium adjacent to carcinomas (EAC; n = 6). Sections were stained with monoclonal antibody (mAb) against vimentin using an ABC immunoperoxidase technique. All blood vessels present within a depth of 0.9 mm of lamina propria were quantified irrespective of their morphology. The blood vessel parameters quantified were volume density (VVBV, CT), number per unit area (NABV, CT), length per unit volume (LVBV, CT) and mean transverse sectional area (ABV). VVBV, CT increased significantly between normal and all pathological groups. Amongst the pathological groups, statistical differences were detected between CI and SCC, CI and EAC, FH and SCCWD, FH and EAC, LIP and SCC, LIP and EAC, DYS and SCCWD and DYS and EAC. The EAC group had the highest VVBV, CT and the values of NABV, CT and LVBV, CT were significantly higher in all the pathological groups when compared with the normal group. No significant differences were detected between any of the pathological group. The parameter ABV increased significantly between normal and DYS, FH, SCC, EAC, FH and EAC, FH and SCC, CI and EAC, CI and SCC, LIP and EAC and LIP and SCC. Spearman rank correlations detected a positive correlation between the severity of oral lesions and all of the blood vessel parameters. We conclude that a mAb against vimentin improved the identification of smaller blood vessels and the blood vessel data suggest that angiogenesis occurs in premalignant and malignant lesions of human oral cheek epithelium. Angiogenesis seems to play an essential role in sustaining the actively growing and transforming cells.

Adolescent↗

PubMed1980

[Possibilities for ocular vessel coagulation (author's transl)].

Present-day possibilities of influencing pathological ocular vessels using an argon laser are presented. A distinction is made here between indirect methods such as area coagulation and direct methods with which specific vessels are treated. Whereas clinical tests involving vessel coagulation with pigmented epithelium absorption have already been carried out more or less successfully, selective vessel coagulation with hemoglobin absorption is still largely at the experimental stage. Our own experiments on animals have shown, however, that with the selection of a suitable coagulation technique and the use of suitable exposure parameters, vessel occlusion can be induced with the argon laser. To achieve this, shortening of the exposure times is particularly necessary.

Aged↗

PubMed1995

Controlling the vasculature: angiogenesis, anti-angiogenesis and vascular targeting of gene therapy.

Angiogenesis is the development of new blood vessels from an existing vascular bed. Normal vascular proliferation occurs only during embryonic development, the female reproductive cycle and wound repair. By contrast, many pathological conditions (for example, cancer, atherosclerosis and diabetic retinopathy), are characterized by persistent, unregulated angiogenesis. Conversely, inadequate angiogenesis can lead to failure of ulcers to heal and myocardial infarction. Control of vascular development could permit new therapeutic approaches to these disorders. For example, several anti-angiogenic drugs are currently undergoing clinical trials for the treatment of cancer, whereas enhancement of angiogenesis by exogenous growth factors can prevent or limit the damage in chronic wounds and duodenal ulcers. Here Tai-Ping Fan, Rhys Jaggar and Roy Bicknell highlight recent achievements and discuss the prospects of receptor antagonists, enzyme inhibitors, tumour suppressor genes and vascular targeted approaches, especially that of gene therapy, in the future development of angiotherapy.

Animals↗

PubMedDate not supplied

[Role of the vascular component in growth of solid tumors: a historical review].

Angiogenesis is a fundamental biological process by which new capillary blood vessels are formed. It is essential in many physiological conditions, such as embryonic development, ovulation and wound repair, and pathological ones, such as arthritis, diabetic retinopathy, and tumours. Solid tumours have angiogenesis capacity, and tumour growth and metastasis are angiogenesis-dependent. Neoplastic cell populations can grow to form a clinically evident tumour only if the host produces a vascular network sufficient to sustain tumour growth. Furthermore, the new blood vessels provide a gateway for tumour cells to enter the circulation and metastasize to distant sites. Tumour angiogenesis is essentially mediated by angiogenic molecules elaborated by tumour cells. We review here the most important literature on this topic and emphasize the crucial and paradigmatic role of this biological process and its relevance in a possible anti-angiogenic therapeutic approach to the treatment of solid tumours.

Animals↗

PubMed1978

[The tumor angiogenesis factor (TAF)].

The tumor Angiogenesis Factor (T.A.F.) isolated from several human and animal neoplasms by J. Folkman and S. Kumar is a factor that induces the appearance of neovessels in the tumors. After describing the methods of vasculor, physiological, experimental and in some cases pathological proliferation, the author has compared the Angiogenesis in both the natural and neoplastic tissues, then, he's studies the tumoral growth the rate of which regularized by the T.A.F. The proving, the extraction and chemical nature of this factor have been reviewed. Afterwards, the author has called to mind the notion of tumoral ecology and the various possibilities of inhibition of the tumoral growth, that is founded on the inhibition of the Angiogenesis and the therapeutical possibilities of the T.A.F. in the fight against cancer. To end up with his study, the author is now considering the possibility of using the T.A.F., extract of the sarcoma of sticker as a complement to the electontherapy in the treatment of this neoplasm.

Angiogenesis Inducing Agents↗

PubMed1995

Potentially resectable pancreatic adenocarcinoma: spiral CT assessment with surgical and pathologic correlation.

PURPOSE: To evaluate the accuracy of spiral computed tomography (CT) in assessing the resectability of small pancreatic ductal adenocarcinoma and to correlate the CT findings with histopathologic and surgical findings. MATERIALS AND METHODS: Spiral CT scans obtained in 64 patients who underwent surgery for potentially resectable pancreatic adenocarcinoma were prospectively assessed for tumor resectability. CT findings were correlated with surgically assessed extent of tumor and pathologic findings. RESULTS: Fifty-seven (89%) of 64 carcinomas were detected with spiral CT. Twenty-four carcinomas were resectable at surgery and 40 were not. The average size of resectable tumors was 3.1 cm (range, 1.0-7.5 cm). The overall accuracy of spiral CT for assessing resectability was 70%. Of resected tumors, 14 were hypoattenuating compared with the remaining pancreas and 10 were isoattenuating. Eleven tumors showed neointimal proliferation in arterioles at histologic examination. CONCLUSION: Further progress in preoperative staging of pancreatic ductal adenocarcinoma with spiral CT should be directed toward improving detection of small pancreatic tumors and assessment of early metastatic disease.

Adenocarcinoma↗

PubMed1984

[The Sparks-Mandril arterial prosthesis. An ingenious concept, a total failure. What can we learn from it?].

In spite of its ingenuity, the Sparks-mandril concept has failed to generate a satisfactory arterial substitute. Pathological analysis of prostheses retrieved from humans and explanted from dogs as part of a controlled laboratory study has demonstrated that the tissue laid down during the autogenous generation stage contains neither elastin fibers nor smooth muscle cells capable of providing the required dimensional stability of a blood vessel. The supporting polyester mesh tube has been found to stretch in vivo, resulting in dilation and lengthening of the prosthesis and the formation of aneurysm and thrombosis. It is recommended that the use of devices relying on the Sparks-mandril concept not to be reintroduced until such time as the mechanism of growth promoting factors for angiogenesis are fully understood.

Adult↗

PubMed1992

[Histopathological characteristics of rheumatoid arthritis--as a clue to elucidate its pathogenesis].

A correct histopathological diagnosis of Rheumatoid Arthritis (RA) is quite important for the decision of early phase treatment to cure it fundamentally. But, generally speaking, usual hospital pathologist is not so much experienced about RA. The purpose of this article is originally to let such pathologist familiar in RA pathology, but for the RA specialist to offer any clue to elucidate the still-unknown etio-pathogenesis of RA or to cure RA fundamentally. The "Tetralogy of RA Arthritis for pathologist" must be as follows: (1) Enormous proliferation of well-permeable granulation-tissue-type neo-vascularization, some of which became high column-endothelial and the center of primary as well as secondary follicle-like lymphoid cell cluster. (2) Lymphoid cluster in RA synovium is also pathological in function. It consisted of preferentially CD4T and B cells to produce IgG rheumatoid factor endlessly. (3) Synovial lining A and B cells proliferate as far as five layers of each, but later, the sublining D (M) and D (F) cells proliferate more and more and finally replace the lining cells. D (M) cells express macrophage marker and full of lysosome, on the contrary, D (F) cells express mesenchymal marker and contains much metalloproteinase. Both express strong Class II antigens but neither has complement activation inhibitor DAF. (4) Proliferation of these D cells with full of mesenchymal tissue destroying and inflammation accelerating activity must be playing a major role in the joint destruction of RA, some in shape of pannus and more in shape of granulation tissue in and around the bone.

Arthritis, Rheumatoid↗

PubMed1993

[Does oncogene c-ets 1 participate in the regulation of tumor angiogenesis?].

The formation of new blood vessels is an essential process in embryonic development and wound healing, for tumor growth and metastasis. In situ hybridization studies have revealed that the protooncogene c-est1 is expressed in endothelial cells at the beginning of blood vessel formation, in normal and pathological conditions. c-ets1 encodes a transcription factor, a protein which binds specifically to DNA and which regulates the transcription of genes containing these specific binding sequences in their promotors. Thus, in vitro experiments suggest that c-ets1 may activate the transcription of genes encoding collagenase 1, stromelysine 1 and urokinase plasminogen activator, proteases involved in extracellular matrix degradation. A working hypothesis is that c-ets1 takes part in regulating angiogenesis by controlling the transcription of these genes whose activity is necessary for the migration of endothelial cells from pre-existing capillaries. This hypothesis is discussed with respect to current experimental evidence and to the complexity of the regulatory network controlling gene transcription and extracellular matrix degradation.

Animals↗