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)

Brunner's gland hamartoma is a rare duodenal tumor, which grew larger than 2 cm in diameter in a very limited number of cases. Since the first description in a patient with fatal duodenal intussusception by Cruveilhier in 1835, approximately 143 cases have been reported in the English literature, and only 25 cases had tumor growth to more than 2 cm in diameter. To the best of our knowledge, only 4 cases have been reported in Taiwan. We present three of Brunner's gland hamartomas. In one patient the tumor was located on the secondary portion of the duodenum, which presented with massive tumor bleeding and measured 3.0 cm in diameter. The other two were both located on the duodenal bulb, which presented with abdominal pain and measured 2.0 and 1.3 cm in diameter, respectively. One of the patients received endoscopic ultrasonography which showed specific findings. Two patients received laparotomy and tumor excision; the other one received endoscopic polypectomy. All 3 patients recovered well without any complications.
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PMID:Brunner's gland hamartomas: report of three cases. 1049 34

Growth of new blood vessels (angiogenesis) is essential for embryo development as well as for wound healing and progression of a number of diseases such as cancer, inflammatory conditions, eye diseases, psoriasis, and rheumatoid arthritis in the adult. Current paradigms explain blood vessel growth entirely by sprouting angiogenesis or by vessel splitting through so called intussusceptive angiogenesis. However, these mechanisms are mainly derived from experiments on the developing embryo while less is known about angiogenesis in the adult during, e.g., wound healing, tumor growth, and inflammation. Recently we showed that blood vessel growth in the adult can be induced and directed by mechanical forces that naturally develop during healing or remodeling of tissues. In contrast to sprouting and intussusception, the new biomechanical hypothesis assumes that functional blood vessels are passively translocated which, if found generic, may drastically change the approach for developing anti- and pro-angiogenic therapies in the treatment of a variety of diseases.
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PMID:A new mechanism of blood vessel growth - hope for new treatment strategies. 1977 38

Intussusception is an alternative to the sprouting mode of angiogenesis. The advantage of this mechanism of vascular growth is that blood vessels are generated more rapidly and the capillaries thereby formed are less leaky. This review article summarizes our current knowledge concerning the role played by intussusceptive microvascular growth in tumor growth. Interestingly, an angiogenic switch from sprouting to intussusceptive angiogenesis occurs after treatment with angiogenesis inhibitors and may be considered as a tumor-protective adaptative response.
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PMID:Intussusceptive microvascular growth in tumors. 2219 20

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

Newly formed microcapillary networks arising in adult organisms by angiogenic and inflammatory stimuli contribute to pathologies such as corneal and retinal blindness, tumor growth, and metastasis. Therapeutic inhibition of pathologic angiogenesis has focused on targeting the VEGF pathway, while comparatively little attention has been given to remodeling of the new microcapillaries into a stabilized, functional, and persistent vascular network. Here, we used a novel reversible model of inflammatory angiogenesis in the rat cornea to investigate endogenous factors rapidly invoked to remodel, normalize and regress microcapillaries as part of the natural response to regain corneal avascularity. Rapid reversal of an inflammatory angiogenic stimulus suppressed granulocytic activity, enhanced recruitment of remodelling macrophages, induced capillary intussusception, and enriched pathways and processes involving immune cells, chemokines, morphogenesis, axonal guidance, and cell motility, adhesion, and cytoskeletal functions. Whole transcriptome gene expression analysis revealed suppression of numerous inflammatory and angiogenic factors and enhancement of endogenous inhibitors. Many of the identified genes function independently of VEGF and represent potentially new targets for molecular control of the critical process of microvascular remodeling and regression in the cornea.
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PMID:Factors regulating capillary remodeling in a reversible model of inflammatory corneal angiogenesis. 2756 55