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1. Yang WT, Tse GM, Lam PK, Metreweli C, Chang J: Correlation between color power Doppler sonographic measurement of breast tumor vasculature and immunohistochemical analysis of microvessel density for the quantitation of angiogenesis. J Ultrasound Med; 2002 Nov;21(11):1227-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation between color power Doppler sonographic measurement of breast tumor vasculature and immunohistochemical analysis of microvessel density for the quantitation of angiogenesis.
  • OBJECTIVE: To record the correlation between color power Doppler sonographic measurement of breast tumor vasculature and immunohistochemical analysis of microvessel density for the quantitation of angiogenesis.
  • METHODS: Women with palpable breast masses scheduled for excision biopsy were scanned with two- and three-dimensional color power Doppler sonography before and after the administration of a sonographic contrast agent.
  • Vessel counts were performed on two- and three-dimensional sonographic images before and after contrast agent administration.
  • The sonographic measure of tumor vascularity was correlated with microvessel density.
  • RESULTS: Pathologic examination showed 43 breast cancers and 14 benign breast masses.
  • Higher microvessel density was noted in malignant than benign breast masses (P < .0005).
  • Color power Doppler sonographic measurement of tumor vessel number showed a significant positive correlation with tumor size (P < .05) and progesterone receptor negativity (P < .05).
  • A significant positive correlation was observed between microvessel density and the number of intratumoral blood vessels assessed by both two- and three-dimensional color power Doppler sonography (P < .05).
  • The administration of a sonographic contrast agent did not improve correlation with microvessel density.
  • CONCLUSIONS: A significant correlation was shown between color power Doppler sonographic measurement of tumor vascularity and microvessel density by immunohistochemical analysis.
  • Further improvement in Doppler sonographic techniques to map capillary vessel flow should be explored to improve the current association with pathologic findings.
  • [MeSH-major] Breast Neoplasms / blood supply. Breast Neoplasms / ultrasonography. Neovascularization, Pathologic / ultrasonography. Ultrasonography, Doppler, Color. Ultrasonography, Mammary

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  • (PMID = 12418764.001).
  • [ISSN] 0278-4297
  • [Journal-full-title] Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine
  • [ISO-abbreviation] J Ultrasound Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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2. Vincensini D, Dedieu V, Eliat PA, Vincent C, Bailly C, de Certaines J, Joffre F: Magnetic resonance imaging measurements of vascular permeability and extracellular volume fraction of breast tumors by dynamic Gd-DTPA-enhanced relaxometry. Magn Reson Imaging; 2007 Apr;25(3):293-302
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Vascular permeability (k(ep), min(-1)) and extracellular volume fraction (v(e)) are tissue parameters of great interest to characterize malignant tumor lesions.
  • Indeed, it is well known that tumors with high blood supply better respond to therapy than poorly vascularized tumors, and tumors with large extracellular volume tend to be more malignant than tumors showing lower extracellular volume.
  • Furthermore, the transport of therapeutic agents depends on both extracellular volume fraction and vessel permeability.
  • Thus, before treatment, these tissue parameters may prove useful to evaluate tumor aggressiveness and to predict responsiveness to therapy and variations during cytotoxic therapies could allow to assess treatment efficacy and early modified therapy schedules in case of poor responsiveness.
  • In this work, blood-tissue permeability and extracellular volume fraction information were derived from magnetic resonance imaging dynamic longitudinal relaxation rate (R(1)) mapping obtained after an intravenous bolus injection of Gd-DTPA in a group of 92 female patients with breast lesions, 68 of these being histologically proven to be with carcinoma.
  • For the sake of comparison, 24 benign lesions were studied.
  • As a consequence of neoangiogenesis, results showed a higher permeability in malignant than in benign lesions, whereas the extracellular volume fraction value did not allow any discrimination between benign and malignant lesions.
  • [MeSH-major] Breast Neoplasms / blood supply. Breast Neoplasms / pathology. Capillary Permeability. Gadolinium DTPA. Image Interpretation, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Microcirculation / pathology

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  • (PMID = 17371717.001).
  • [ISSN] 0730-725X
  • [Journal-full-title] Magnetic resonance imaging
  • [ISO-abbreviation] Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; K2I13DR72L / Gadolinium DTPA
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3. Blok R, Blok K, Jeleń M, Gryboś M: [Analysis of prognostic factors for the extent of vascularity of serous ovarian cancer on the basis of CD34 antigen expression]. Ginekol Pol; 2004 Feb;75(2):91-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: Ovarian neoplasms are very important problem in medicine, because they account for 23% of all female genital neoplasms, and they are the cause of 47% deaths among women suffering from gynecological cancers.
  • Progression of neoplasmatic disease depends also on dynamism of angiogenesis, because better oxygen and nutrition substances supply increase tumor growth.
  • To increase the tumor volume of 1 mm3, the development of new vessels is needed, and that also increases the risk of distant metastases.
  • The control group for CD34 levels were 15 patients with benign serous adenomas.
  • The microscopic (200x) evaluation of blood vessel in paraffin samples were made by showing the reaction of endothelial CD34 antigen with DAKO serum (Monoclonal Mouse Anti Human CD34 class 1-N 1574 LSAB).
  • No difference in vascularity was observed at the level of total vascularisation of serous ovarian cancers (0.021 mm2) and in benign serous adenomas (0.023 mm2).
  • [MeSH-major] Antigens, CD34 / metabolism. Biomarkers, Tumor / metabolism. Cystadenocarcinoma, Serous / blood supply. Endothelium, Vascular / pathology. Neovascularization, Pathologic / immunology. Ovarian Neoplasms / blood supply
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Cystadenoma, Serous / blood supply. Disease Progression. Female. Humans. Immunohistochemistry. Middle Aged. Neoplasm Staging. Prognosis. Risk Factors. Survival Analysis. Time Factors

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  • (PMID = 15108579.001).
  • [ISSN] 0017-0011
  • [Journal-full-title] Ginekologia polska
  • [ISO-abbreviation] Ginekol. Pol.
  • [Language] pol
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor
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4. Lederle W, Stark HJ, Skobe M, Fusenig NE, Mueller MM: Platelet-derived growth factor-BB controls epithelial tumor phenotype by differential growth factor regulation in stromal cells. Am J Pathol; 2006 Nov;169(5):1767-83
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  • [Title] Platelet-derived growth factor-BB controls epithelial tumor phenotype by differential growth factor regulation in stromal cells.
  • Platelet-derived growth factor (PDGF) stimulates tumor growth and progression by affecting tumor and stromal cells.
  • In the HaCaT skin carcinogenesis model, transfection of immortal nontumorigenic and PDGF-receptor-negative HaCaT keratinocytes with PDGF-B induced formation of benign tumors.
  • In vivo, persistent PDGF-B expression induced enhanced tumor cell proliferation but only transiently stimulated stromal cell proliferation and angiogenesis.
  • Accordingly, in HaCaT/PDGF-B transplants, initially enhanced VEGF expression by stromal fibroblasts was subsequently reduced, followed by down-regulation of angiogenesis, myofibroblast accumulation, and vessel maturation.
  • The PDGF-induced, persistently increased expression of the hepatocyte growth factor by fibroblasts in vitro and in vivo was most probably responsible for enhanced epithelial cell proliferation and benign tumor formation.
  • Thus, by paracrine stimulation of the stroma, PDGF-BB induced epithelial hyperproliferation, thereby promoting tumorigenicity, whereas the time-limited activation of the stroma followed by stromal maturation provides a possible explanation for the benign tumor phenotype.
  • [MeSH-major] Epithelial Cells / drug effects. Epithelial Cells / pathology. Growth Substances / pharmacology. Neoplasms / pathology. Phenotype. Platelet-Derived Growth Factor / pharmacology. Stromal Cells / drug effects
  • [MeSH-minor] Actins / metabolism. Cell Proliferation / drug effects. Cell Transformation, Neoplastic. Cells, Cultured. Endostatins / metabolism. Fibroblasts / cytology. Fibroblasts / drug effects. Hepatocyte Growth Factor / pharmacology. Humans. Keratinocytes / cytology. Keratinocytes / pathology. Mesoderm / cytology. Neovascularization, Physiologic / drug effects. Paracrine Communication / drug effects. Proto-Oncogene Proteins c-sis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Platelet-Derived Growth Factor / metabolism. Time Factors. Transfection. Up-Regulation / drug effects. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 17071599.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Endostatins; 0 / Growth Substances; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 0 / platelet-derived growth factor BB; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Other-IDs] NLM/ PMC1780216
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5. Zhou Z, Zhang S, Hua L, Zhong W, Jin Z: Leukoplakia and angiopoiesis resistance of Herba Erigerontis. Chin J Dent Res; 2000 Nov;3(3):56-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To evaluate the effects of Herba Erigerontis on angiopoiesis and carcinogenesis; to seek an effective drug for prevention of leukoplakia progression to carcinoma and to stop the mechanism of angiopoiesis.
  • Ink perfusion, analysis of images, resin cast form of micro-vessel, a-SMA detection and histopathological examination were applied to observe their changing patterns.
  • RESULTS: The rate of leukoplakia conversion to tumor of the Herba Erigerontis group was half that of model group.
  • There was no significant difference between angeion vessel area and density (P > 0.05) in these 2 groups, which were elevated compared to the control.
  • CONCLUSIONS: Herba Erigerontis has the function of inhibiting leukoplakia progression to tumor.
  • It has no obvious effect on angio-hyperplasia and expansion in the course of leukoplakia progression to tumor.
  • However, it may preserve the angio-configuration and spatial arrangement and keep intact the angeion vessel wall.
  • Its mechanism of promoting blood circulation may be through removing blood stasis and benign angiopoiesis so as to resist carcinogenesis.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Carbon. Drugs, Chinese Herbal / therapeutic use. Leukoplakia, Oral / prevention & control. Mouth Neoplasms / prevention & control. Neovascularization, Pathologic / prevention & control
  • [MeSH-minor] Actins / analysis. Actins / genetics. Animals. Blood Circulation / drug effects. Carcinoma / blood supply. Carcinoma / pathology. Carcinoma / prevention & control. Coloring Agents. Corrosion Casting. Cricetinae. Disease Models, Animal. Disease Progression. Gene Expression Regulation, Neoplastic / genetics. Image Processing, Computer-Assisted. Mesocricetus. Microcirculation / pathology. Muscle, Smooth, Vascular / pathology. Up-Regulation

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  • (PMID = 11314537.001).
  • [ISSN] 1462-6446
  • [Journal-full-title] The Chinese journal of dental research : the official journal of the Scientific Section of the Chinese Stomatological Association (CSA)
  • [ISO-abbreviation] Chin J Dent Res
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Anticarcinogenic Agents; 0 / Coloring Agents; 0 / Drugs, Chinese Herbal; 0 / chinese ink; 7440-44-0 / Carbon
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6. Kim S, Kim JH, Moon WK, Min BG: Lesion characterization using vessel permeability map to new blood pool contrast agent calculated from dynamic magnetic resonance images. J Digit Imaging; 2000 May;13(2 Suppl 1):193-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lesion characterization using vessel permeability map to new blood pool contrast agent calculated from dynamic magnetic resonance images.
  • In this study, quantitative analysis of microvascular characteristics based on dynamic MR imaging were performed both for malignant and benign lesions using two types of contrast agents (CAs).
  • A new MR macromolecular contrast medium (MMCM), 24 gadolinium-tetraazacyclododecanetetraacetic acid (DOTA)-dendrimer, was found to have a greater ability to distinguish benign from malignant lesions.
  • When a blood pool agent was used, permeability differences in the two types of lesions were the most significant findings among all parameters considered.
  • [MeSH-minor] Abscess / physiopathology. Animals. Gadolinium DTPA. Heterocyclic Compounds. Humans. Male. Neoplasms, Experimental / blood supply. Organometallic Compounds. Rabbits. Sensitivity and Specificity. Testicular Neoplasms / blood supply. Tumor Cells, Cultured

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  • (PMID = 10847398.001).
  • [ISSN] 0897-1889
  • [Journal-full-title] Journal of digital imaging
  • [ISO-abbreviation] J Digit Imaging
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Heterocyclic Compounds; 0 / Organometallic Compounds; 92923-44-9 / gadolinium 1,4,7,10-tetraazacyclododecane-N,N',N'',N'''-tetraacetate; K2I13DR72L / Gadolinium DTPA
  • [Other-IDs] NLM/ PMC3453234
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7. Frei-Jones M, McKinstry RC, Perry A, Leonard JR, Park TS, Rubin JB: Use of thalidomide to diminish growth velocity in a life-threatening congenital intracranial hemangioma. J Neurosurg Pediatr; 2008 Aug;2(2):125-9
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  • Infantile or capillary hemangioma is the most common vascular tumor of childhood.
  • Although the lesions are considered benign, 10% of affected children develop life-threatening complications (mortality rate 20-80% in this subgroup).
  • Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) have been implicated in the pathogenesis of hemangiomas, and antiangiogenesis agents are being evaluated in the treatment of these tumors.
  • Thalidomide may be an ideal therapy for life-threatening hemangiomas because it inhibits new blood vessel formation by antagonizing both the bFGF and VEGF pathways and has a more acceptable toxicity profile than other agents.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Brain Neoplasms / congenital. Brain Neoplasms / drug therapy. Hemangioma, Capillary / congenital. Hemangioma, Capillary / drug therapy. Thalidomide / therapeutic use

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  • (PMID = 18671617.001).
  • [ISSN] 1933-0707
  • [Journal-full-title] Journal of neurosurgery. Pediatrics
  • [ISO-abbreviation] J Neurosurg Pediatr
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / K30 RR022251; United States / NCRR NIH HHS / RR / TL1 RR024995; United States / NCRR NIH HHS / RR / UL1 RR024992; United States / NCRR NIH HHS / RR / UL1 RR024992; United States / NCRR NIH HHS / RR / UL1 RR024992-01; United States / NCATS NIH HHS / TR / UL1 TR000448
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 4Z8R6ORS6L / Thalidomide
  • [Other-IDs] NLM/ NIHMS101679; NLM/ PMC2737696
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