Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021933 (intussusception)
 3,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumours establish their blood supply via a number of processes in addition to angiogenesis. These include vasculogenesis, vascular remodelling, intussusception and possibly vascular mimicry in certain tumours. The mainstay of the assessment of tumour vascularity has been counting the number of immunohistochemically identified microvessels in vascular hot spots. Nevertheless, several other techniques are available, including Chalkley counting, vascular grade and the use of image analysis systems. Angiogenic activity can furthermore be assessed in histological samples by measuring the molecules involved in the establishment of the tumour vasculature, including angiogenic growth factors and their receptors, cell adhesion molecules, proteases and markers of activated, proliferating, cytokine stimulated or angiogenic vessels, such as CD105. Measuring the maturity of vessels may give an indication of the proportion of the tumour vasculature that is functional. Other reagents that can identify hypoxia-activated pathways are also being developed. The histological assessment of tumour vascularity is mainly used in the research setting but may also have applications in the clinic if appropriate methodology and trained observers perform the studies. Gene arrays may be able to provide an angiogenesis profile. Continued study into the processes involved in generating a tumour blood supply is likely to identify new markers that may be more accurate measures.
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PMID:Histological quantitation of tumour angiogenesis. 1556 6

Over the last few years, great advances in our understanding in tumor neovascularization have emerged, with several new mechanisms of neovascularization being proposed. Solid tumors establish a vasculature through angiogenesis, vasculogenesis, vascular remodeling, co-option, and possibly also intussusception and vascular mimicry. Quantitative measurements of the tumor vasculature have generally measured the number of microvessels, highlighted using immunohistochemistry and antibodies to factor VIII-related antigen at high power over a defined field area. The generation of more sensitive and specific markers--in particular antibodies to CD34--together with the use of a Chalkley eyepiece graticule have improved the objectivity of the assessment of tumor vascularity. The protocol for this is discussed, with several variations such as vascular grade, microvessel density, and the alterations required for the assessment of vascularity in in situ breast disease. Also outlined are potential other measures of the angiogenic activity of breast tumors including the use of angiogenic factors and their receptors, endothelial cell proliferation, vessel maturation index, cell adhesion molecules, proteolytic enzymes, and the recently identified hypoxic markers.
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PMID:Quantitative angiogenesis in breast cancer. 1649 1

Tumor neovascularization acquires vessels through a number of processes, including angiogenesis, vasculogenesis, vascular remodelling, intussusception, and possibly vascular mimicry in certain tumors. The end result of the tumor vasculature has been quantified by counting the number of immunohistochemically identified microvessels in areas of maximal vascularity so-called hot spots. Other techniques have been developed, such as Chalkley counting and the use of image analysis systems that are robust and reproducible as well as more objective. Many of the molecular pathways that govern tumor neovascularization have been identified, and many reagents are now available to study these tissue sections. These include angiogenic growth factors and their receptors, cell adhesion molecules, proteases, and markers of activated, proliferating, cytokine-stimulated, or angiogenic vessels, such as CD105. It is also possible to differentiate quiescent from active vessels. Other reagents that can identify proteins involved in microenvironmental influences such as hypoxia have also been generated. Although the histological assessment of tumor vascularity is used mostly in the research context, it may also have clinical applications if appropriate methodology and trained observers perform the studies.
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PMID:Assessing tumor angiogenesis in histological samples. 1930 64

Solid tumour growth is dependent on the development of an adequate blood supply. For years, sprouting angiogenesis has been considered an exclusive mechanism of tumour vascularization. However, over the last years, several other mechanisms have been identified, including vessel-co-option, intussusception, recruitment of endothelial precursor cells (EPCs) and even mechanisms that do not involve endothelial cells, a process called vasculogenic mimicry (VM). The latter describes a mechanism by which highly aggressive tumour cells can form vessel-like structures themselves, by virtue of their high plasticity. VM has been observed in several tumour types and its occurrence is strongly associated with a poor prognosis. This review will focus on signalling molecules and cascades involved in VM. In addition, we will discuss the presence of VM in relation to ongoing cancer research. Finally, we describe the clinical significance of VM regarding anti-angiogenesis treatment modalities.
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PMID:Signalling pathways in vasculogenic mimicry. 2007 7

The cellular and molecular mechanisms of tumor angiogenesis and its prospects for anti-angiogenic cancer therapy are major issues in almost all current concepts of both cancer biology and targeted cancer therapy. Currently, (1) sprouting angiogenesis, (2) vascular co-option, (3) vascular intussusception, (4) vasculogenic mimicry, (5) bone marrow-derived vasculogenesis, (6) cancer stem-like cell-derived vasculogenesis and (7) myeloid cell-driven angiogenesis are all considered to contribute to tumor angiogenesis. Many of these processes have been described in developmental angiogenesis; however, the relative contribution and relevance of these in human brain cancer remain unclear. Preclinical tumor models support a role for sprouting angiogenesis, vascular co-option and myeloid cell-derived angiogenesis in glioma vascularization, whereas a role for the other four mechanisms remains controversial and rather enigmatic. The anti-angiogenesis drug Avastin (Bevacizumab), which targets VEGF, has become one of the most popular cancer drugs in the world. Anti-angiogenic therapy may lead to vascular normalization and as such facilitate conventional cytotoxic chemotherapy. However, preclinical and clinical studies suggest that anti-VEGF therapy using bevacizumab may also lead to a pro-migratory phenotype in therapy resistant glioblastomas and thus actively promote tumor invasion and recurrent tumor growth. This review focusses on (1) mechanisms of tumor angiogenesis in human malignant glioma that are of particular relevance for targeted therapy and (2) controversial issues in tumor angiogenesis such as cancer stem-like cell-derived vasculogenesis and bone-marrow-derived vasculogenesis.
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PMID:Tumor angiogenesis and anti-angiogenic therapy in malignant gliomas revisited. 2314 92

Angiogenesis is essential for tumor growth and metastasis. Over the last decades, a substantial progress has been achieved in defining different patterns of tumor microcirculation. Sprouting angiogenesis, the oldest model of microcirculation, is the de novo vessel formation from preexisting blood vessels. Vessel splitting and hijacking, also known, respectively, as intussusception and cooption, are alternative models that account for tumor resistance to antiangiogenic therapy. In addition to remodeling the microenvironment, the tumor cell can undergo intrinsic changes and survive hypoxic conditions by acquiring stem cell properties. In line with the concept of pluripotency, tumor cells can form vascular mimicry structures creating their own microcirculation despite a latent vessel growth. The recent identification of the polyploid giant cancer cells and tumor-derived erythrocytes is the most innovative survival mechanism in hypoxia and provides a potential target for more effective therapies.
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PMID:From sprouting angiogenesis to erythrocytes generation by cancer stem cells: evolving concepts in tumor microcirculation. 2516 40

Tumor neovascularization acquires their vessels through a number of processes including angiogenesis, vasculogenesis, vascular remodeling, intussusception, and possibly vascular mimicry in certain tumors. The end result of the tumor vasculature has been quantified by counting the number of immunohistochemically identified microvessels in areas of maximal vascularity, so-called hot spot. Other techniques have been developed such as Chalkley counting and the use of image analysis systems that are robust and reproducible as well as being more objective. Many of the molecular pathways that govern tumor neovascularization have been identified and many reagents are now available to study these tissue sections. These include angiogenic growth factors and their receptors and cell adhesion molecules, proteases, and markers of activated, proliferating, cytokine-stimulated, or angiogenic vessels, such as CD105. It is also possible to differentiate quiescent from active vessels. Other reagents that can identify proteins involved in microenvironmental influences such as hypoxia have also been generated. Although the histological assessment of tumor vascularity is used mostly in the research context, it may also have clinical applications if appropriate methodology and trained observers perform the studies.
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PMID:Assessing Tumor Angiogenesis in Histological Samples. 2717 43

Activation of the tumor and stromal cell-driven angiogenic program is one of the first requirements in the tumor ecosystem for growth and dissemination. The understanding of the dynamic angiogenic tumor ecosystem has rapidly evolved over the last decades. Beginning with the canonical sprouting angiogenesis, followed by vasculogenesis and intussusception, and finishing with vasculogenic mimicry, the need for different neovascularization mechanisms is further explored. In addition, an overview of the orchestration of angiogenesis within the tumor ecosystem cellular and molecular components is provided. Clinical evidence has demonstrated the effectiveness of traditional vessel-directed antiangiogenics, stressing on the important role of angiogenesis in tumor establishment, dissemination, and growth. Particular focus is placed on the interaction between tumor cells and their surrounding ecosystem, which is now regarded as a promising target for the development of new antiangiogenics.
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PMID:Unraveling the Role of Angiogenesis in Cancer Ecosystems. 3001 50