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1. Ahmadi SA, Moinfar M, Gohari Moghaddam K, Bahadori M: Practical application of angiogenesis and vasculogenic mimicry in prostatic adenocarcinoma. Arch Iran Med; 2010 Nov;13(6):498-503
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  • BACKGROUND: Tumor growth depends on vascular blood supply.
  • The novel discovery of non-endothelialized vessel-like channels in malignant tumors called vasculogenic mimicry has provided new insights about tumor behavior and also serves as a potential target for drug therapy.
  • RESULTS: We found a direct positive relationship between higher microvessel density and tumor grade (P<0.001), presence of vascular invasion (P<0.001) and percent of involved tissue (P<0.001); however, no such relationship was found with vasculogenic mimicry and only a weak correlation was noted between vasculogenic mimicry and perineurial invasion (P=0.03).
  • CONCLUSION: Unlike other cancers and despite the results of in vitro studies on prostatic adenocarcinoma, we were not able to demonstrate a significant relationship between vasculogenic mimicry channels and histologic grading as one of the most important prognostic factors; however, this may be due to an inherent limitation of prostatic tissue imposed by abundant smooth muscle fibers stained by this method.
  • [MeSH-major] Adenocarcinoma / blood supply. Neovascularization, Pathologic / pathology. Prostatic Neoplasms / blood supply

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  • (PMID = 21039005.001).
  • [ISSN] 1735-3947
  • [Journal-full-title] Archives of Iranian medicine
  • [ISO-abbreviation] Arch Iran Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antigens, CD34
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2. Bullitt E, Ewend M, Vredenburgh J, Friedman A, Lin W, Wilber K, Zeng D, Aylward SR, Reardon D: Computerized assessment of vessel morphological changes during treatment of glioblastoma multiforme: report of a case imaged serially by MRA over four years. Neuroimage; 2009 Aug;47 Suppl 2:T143-51
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  • [Title] Computerized assessment of vessel morphological changes during treatment of glioblastoma multiforme: report of a case imaged serially by MRA over four years.
  • A patient with glioblastoma multiforme underwent serial computerized analysis of tumor-associated vasculature defined from magnetic resonance angiographic (MRA) scans obtained over almost a four year period.
  • The clinical course included tumor resection with subsequent radiation therapy, a long symptom-free interval, emergence of a new malignant focus, resection of that focus, a stroke, and treatment with chemotherapy and anti-angiogenic therapy.
  • Image analysis methods included segmentation of vessels from each MRA and statistical comparison of vessel morphology over 4 regions of interest (the initial tumor site, the second tumor site, a distant control region, and the entire brain) to the same 4 regions of interest in 50 healthy volunteers (26 females and 24 males; mean age 39 years).
  • Results suggested that following completion of focal radiation therapy (RT) vessel shape abnormalities, if elevated at the time of RT completion, may progressively normalize for months in focal regions, that progressively severe vessel shape abnormalities can precede the emergence of a gadolinium enhancing lesion by months, that lesion resection can produce a dramatic but highly transient drop in abnormal vessel tortuosity both focally and globally, and that treatment with anti-angiogenic agents does not necessarily normalize vessel shape.
  • Quantitative measurements of vessel morphology as defined from MRA may provide useful insights into tumor development and response to therapy.

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  • (PMID = 19103295.001).
  • [ISSN] 1095-9572
  • [Journal-full-title] NeuroImage
  • [ISO-abbreviation] Neuroimage
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / EB000219-10; United States / NCI NIH HHS / CA / R01 CA124608; United States / NCI NIH HHS / CA / CA124608-03; United States / NCI NIH HHS / CA / R01 CA124608-03; United States / NIBIB NIH HHS / EB / R01 EB000219; United States / NIBIB NIH HHS / EB / R01 EB000219-11; United States / NIBIB NIH HHS / EB / R01 EB000219-10; United States / NIBIB NIH HHS / EB / EB000219-11
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Other-IDs] NLM/ NIHMS138759; NLM/ PMC2752720
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3. Helfrich I, Scheffrahn I, Bartling S, Weis J, von Felbert V, Middleton M, Kato M, Ergün S, Augustin HG, Schadendorf D: Resistance to antiangiogenic therapy is directed by vascular phenotype, vessel stabilization, and maturation in malignant melanoma. J Exp Med; 2010 Mar 15;207(3):491-503
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  • [Title] Resistance to antiangiogenic therapy is directed by vascular phenotype, vessel stabilization, and maturation in malignant melanoma.
  • We hypothesized that the level of vessel maturation is critically involved in the response to antiangiogenic therapies.
  • To test this hypothesis, we evaluated the vascular network in spontaneously developing melanomas of MT/ret transgenic mice after using PTK787/ZK222584 for anti-VEGF therapy but also analyzed human melanoma metastases taken at clinical relapse in patients undergoing adjuvant treatment using bevacizumab.
  • Both experimental settings showed that tumor vessels, which are resistant to anti-VEGF therapy, are characterized by enhanced vessel diameter and normalization of the vascular bed by coverage of mature pericytes and immunoreactivity for desmin, NG-2, platelet-derived growth factor receptor beta, and the late-stage maturity marker alpha smooth muscle actin.
  • Our findings emphasize that the level of mural cell differentiation and stabilization of the vascular wall significantly contribute to the response toward antiangiogenic therapy in melanoma.
  • This study may be useful in paving the way toward a more rational development of second generation antiangiogenic combination therapies and in providing, for the first time, a murine model to study this.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Drug Resistance, Neoplasm. Melanoma / drug therapy. Melanoma / genetics

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  • [ErratumIn] J Exp Med. 2013 Apr 8;210(4):853. Augustin, Helmut G [added]
  • (PMID = 20194633.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 8466
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Desmin; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC2839146
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4. Eberhard A, Kahlert S, Goede V, Hemmerlein B, Plate KH, Augustin HG: Heterogeneity of angiogenesis and blood vessel maturation in human tumors: implications for antiangiogenic tumor therapies. Cancer Res; 2000 Mar 1;60(5):1388-93
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  • [Title] Heterogeneity of angiogenesis and blood vessel maturation in human tumors: implications for antiangiogenic tumor therapies.
  • MVD counts assess the presence of blood vessels but do not give an indication of the degree of angiogenesis and the functional status of the tumor neovasculature.
  • To analyze angiogenesis and the functional status of the tumor vascular bed, we have quantitated endothelial cell proliferation and the recruitment of pericytes in human tumors [glioblastomas (n = 30), renal cell carcinomas (n = 22), colon carcinomas (n = 18), mammary carcinomas (n = 24), lung carcinomas (n = 15), and prostate carcinomas (n = 19)].
  • Tissue sections were examined applying double-labeling immunohistochemical techniques to detect proliferating endothelial cells and to colocalize endothelial cells and pericytes.
  • (c) proliferating tumor versus endothelial cell index; and (d) microvessel pericyte coverage index (MPI).
  • Based on endothelial cell proliferation, angiogenesis was found to be present in all tumors with characteristic and significant differences between the tumor types (glioblastomas, PCI = 9.6 +/- 6.1%; renal cell carcinomas, PCI = 9.4 +/- 5.2%; colon carcinomas, PCI = 7.8 +/- 5.2%; mammary carcinomas, PCI = 5.0 +/- 4.8%; lung carcinomas, PCI = 2.6 +/- 2.5%; prostate carcinomas, PCI = 2.0 +/- 1.4%).
  • There was a considerable degree of heterogeneity in the intensity of angiogenesis within each tumor group, as indicated by large standard deviations.
  • Even in the most angiogenic tumors, angiogenesis was found to be 4 to 20 times less intense as compared with the physiological angiogenesis in the growing ovarian corpus rubrum (PCI = 40.6 +/- 6.2%).
  • Varying degrees of pericyte recruitment to the tumor microvasculature were determined in the different tumor types (glioblastomas, MPI = 12.7 +/- 7.9%; renal cell carcinomas, MPI = 17.9 +/- 7.8%; colon carcinomas, MPI = 65.4 +/- 10.5%; mammary carcinomas, MPI = 67.3 +/- 14.2%; lung carcinomas, MPI = 40.8 +/- 14.5%; prostate carcinomas, MPI = 29.6 +/- 9.5%).
  • The data demonstrate distinct quantitative variations in the intensity of angiogenesis in malignant human tumors.
  • Furthermore, the varying degrees of pericyte recruitment indicate differences in the functional status of the tumor vasculature in different tumors that may reflect varying degrees of maturation of the tumor vascular bed.
  • [MeSH-major] Neoplasms / blood supply. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cattle. Cell Differentiation. Cell Division. Endothelium, Vascular / pathology. Humans. Pericytes / pathology

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  • [ErratumIn] Cancer Res 2000 Jul 1;60(13):3668
  • (PMID = 10728704.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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5. Sathornsumetee S, Rich JN: Antiangiogenic therapy in malignant glioma: promise and challenge. Curr Pharm Des; 2007;13(35):3545-58
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  • [Title] Antiangiogenic therapy in malignant glioma: promise and challenge.
  • Malignant glioma represents one of the most lethal and angiogenic cancers.
  • Angiogenesis is a fundamental process of blood vessel growth that is a hallmark of cancer.
  • Although several molecular mechanisms contribute to tumor angiogenesis in gliomas, the vascular endothelial growth factor (VEGF) pathway appears particularly important and has been a prominent therapeutic target in cancer treatment.
  • Several preclinical studies have demonstrated efficacy of antiangiogenic agents in both subcutaneous and orthotopic malignant glioma xenograft models.
  • Recently, a phase II clinical trial of bevacizumab, a neutralizing monoclonal antibody to VEGF, in combination with irinotecan has demonstrated promising radiographic response and survival benefit in patients with recurrent malignant glioma.
  • Despite the encouraging results of antiangiogenic therapies in malignant glioma, there are several challenges to be overcome to achieve optimal clinical benefit.
  • Identification of biomarkers to predict response or resistance and to monitor antiangiogenic effects is important to enrich for patients who are likely to respond to therapy and to define the optimal biological dose.
  • At present, antiangiogenic therapies remain palliative suggesting that overcoming antiangiogenic resistance may require multi-targeted agents, combination of agents targeting different angiogenic pathways or multi-modality combination with radiation, chemotherapy, other targeted therapeutics or immunotherapy.
  • In this review, we will discuss the current development, promise and challenge of antiangiogenic therapy in malignant glioma.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Angiogenic Proteins / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Brain Neoplasms / drug therapy. Glioma / drug therapy. Neovascularization, Pathologic / prevention & control. Signal Transduction / drug effects
  • [MeSH-minor] Angiopoietins / antagonists & inhibitors. Angiopoietins / metabolism. Animals. Antibodies, Monoclonal / pharmacology. Biomarkers, Pharmacological / metabolism. Combined Modality Therapy. Drug Resistance, Neoplasm. Fibroblast Growth Factors / antagonists & inhibitors. Fibroblast Growth Factors / metabolism. Hepatocyte Growth Factor / antagonists & inhibitors. Hepatocyte Growth Factor / metabolism. Humans. Integrins / antagonists & inhibitors. Integrins / metabolism. Protein Kinase C / antagonists & inhibitors. Protein Kinase C / metabolism. Protein Kinase Inhibitors / pharmacology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / metabolism. Receptor, TIE-2 / antagonists & inhibitors. Receptor, TIE-2 / metabolism. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / metabolism. Stem Cell Transplantation. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18220791.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA116659; United States / NINDS NIH HHS / NS / NS047409; United States / NINDS NIH HHS / NS / NS054276
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Angiogenic Proteins; 0 / Angiopoietins; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Biomarkers, Pharmacological; 0 / Integrins; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; 62031-54-3 / Fibroblast Growth Factors; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.11.13 / Protein Kinase C
  • [Number-of-references] 192
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6. Duncan FJ, Wulff BC, Tober KL, Ferketich AK, Martin J, Thomas-Ahner JM, Allen SD, Kusewitt DF, Oberyszyn TM, Vanbuskirk AM: Clinically relevant immunosuppressants influence UVB-induced tumor size through effects on inflammation and angiogenesis. Am J Transplant; 2007 Dec;7(12):2693-703
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  • [Title] Clinically relevant immunosuppressants influence UVB-induced tumor size through effects on inflammation and angiogenesis.
  • Immunosuppressive therapies allow long-term patient and transplant survival, but are associated with increased development of UV-induced skin cancers, particularly squamous cell carcinomas.
  • The mechanisms by which CsA, MMF, tacrolimus (TAC) or sirolimus (SRL), alone or in dual combinations, influence tumor development and progression are not completely understood.
  • In the current study, chronically UV-exposed mice treated with SRL alone or in combination with CsA or TAC developed more tumors than mice treated with vehicle or other immunosuppressants, but the tumors were significantly smaller and less advanced.
  • Mice treated with CsA or TAC developed significantly larger tumors than vehicle-treated mice, and a larger percentage in the CsA group were malignant.
  • The addition of MMF to CsA, but not to TAC, significantly reduced tumor size.
  • Immunosuppressant effects on UVB-induced inflammation and tumor angiogenesis may explain these findings.
  • CsA enhanced both UVB-induced inflammation and tumor blood vessel density, while MMF reduced inflammation.
  • Addition of MMF to CsA reduced tumor size and vascularity.
  • SRL did not affect inflammation, but significantly reduced tumor vascularity.
  • Thus the choice of immunosuppressants has important implications for tumor number, size and progression, likely due to the influence of immunosuppressants on UVB-induced inflammation and angiogenesis.
  • [MeSH-minor] Animals. Blood Vessels / drug effects. Blood Vessels / pathology. Cyclosporine / adverse effects. Cyclosporine / pharmacology. Disease Models, Animal. Drug Therapy, Combination. Female. Inflammation / drug therapy. Inflammation / etiology. Inflammation / pathology. Mice. Mice, Hairless. Mycophenolic Acid / adverse effects. Mycophenolic Acid / analogs & derivatives. Mycophenolic Acid / pharmacology. Sirolimus / adverse effects. Sirolimus / pharmacology. Tacrolimus / adverse effects. Tacrolimus / pharmacology

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  • (PMID = 17941958.001).
  • [ISSN] 1600-6135
  • [Journal-full-title] American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
  • [ISO-abbreviation] Am. J. Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16058; United States / NCI NIH HHS / CA / R01 CA 109204; United States / NCI NIH HHS / CA / R03 CA 110054
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
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7. Siemann DW, Chaplin DJ, Horsman MR: Vascular-targeting therapies for treatment of malignant disease. Cancer; 2004 Jun 15;100(12):2491-9
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  • [Title] Vascular-targeting therapies for treatment of malignant disease.
  • BACKGROUND: Tumor endothelium represents a valuable target for cancer therapy.
  • The vasculature plays a critical role in the survival and continued growth of solid tumor masses; in addition, the inherent differences between tumor blood vessels and blood vessels associated with normal tissue make the tumor vasculature a unique target on which to base the design of novel therapeutics, which may allow highly selective treatment of malignant disease.
  • Therapeutic strategies that target and disrupt the already formed vessel networks of growing tumors are actively being pursued.
  • The goal of these approaches is to induce a rapid and catastrophic shutdown of the vascular function of the tumor so that blood flow is arrested and tumor cell death due to the resulting oxygen and nutrient deprivation and buildup of waste products occurs.
  • METHODS: Biologic approaches and small-molecule drugs that can be used to damage tumor vasculature have been identified.
  • Physiologic, histologic/morphologic, and immunohistochemical assessments have demonstrated that profound disruption of the tumor vessel network can be observed minutes to hours after treatment.
  • RESULTS: Loss of patent blood vessels, decreased tumor blood flow, extensive necrosis, and secondary ischemia-induced tumor cell death have been well documented in a variety of preclinical tumor models treated with agents such as DMXAA, CA4DP, and ZD6126.
  • The use of such agents in conjunction with irradiation and other chemotherapeutic agents has led to improved treatment outcomes.
  • CONCLUSIONS: The targeting of tumors' supportive blood vessel networks could lead to improvements in cancer cure rates.
  • It is likely that this approach will prove to be most efficacious when used in concert with conventional treatment strategies.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Animals. Clinical Trials as Topic. Combined Modality Therapy. Endothelium, Vascular / drug effects. Organophosphorus Compounds / therapeutic use. Stilbenes / therapeutic use. Xanthones / therapeutic use

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  • [Copyright] Copyright 2004 American Cancer Society.
  • [CommentIn] Cancer. 2005 Jul 1;104(1):216-7; author reply 217 [15895372.001]
  • (PMID = 15197790.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84408; United States / NCI NIH HHS / CA / CA89655
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / N-acetylcochinol-O-phosphate; 0 / Organophosphorus Compounds; 0 / Stilbenes; 0 / Xanthones; 0829J8133H / vadimezan; I5590ES2QZ / fosbretabulin
  • [Number-of-references] 83
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8. Tanaka N, Kato H, Inose T, Kimura H, Faried A, Sohda M, Nakajima M, Fukai Y, Miyazaki T, Masuda N, Fukuchi M, Kuwano H: Expression of carbonic anhydrase 9, a potential intrinsic marker of hypoxia, is associated with poor prognosis in oesophageal squamous cell carcinoma. Br J Cancer; 2008 Nov 4;99(9):1468-75
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  • Hypoxic conditions are known to be associated with resistance to chemotherapy and radiotherapy, and with poor cancer prognosis.
  • We examined CA9 expression in surgical specimens from oesophageal squamous cell carcinoma (ESCC) patients (n=127) using immunohistochemistry and real-time RT-PCR.
  • We also examined CA9 expression and cell proliferation in ESCC cell lines (TE-2, TE-8 and TE-15) and an immortalised human oesophageal cell line (CHEK-1) using real-time RT-PCR, Western blotting, ELISA and MTT assay.
  • Immunohistochemistry, high expression of CA9 was found in 63 of the 127 primary tumour specimens and was correlated with poor outcome (P=0.0003) and more aggressive/less favourable clinicopathological parameters (tumour size (P=0.0235), tumour depth (P<0.0001), regional lymph node metastasis (P=0.0031), distant lymph node metastasis (P=0.0077), stage (P<0.0001) and blood vessel invasion (P=0.006)).
  • CA9 is correlated with poor prognosis and malignant phenotype in patients with ESCC, and was upregulated by hypoxia.
  • It is suggested that control of CA9 expression might improve the effectiveness of chemotherapy and radiotherapy in ESCC.
  • [MeSH-major] Antigens, Neoplasm / analysis. Carbonic Anhydrases / analysis. Carcinoma, Squamous Cell / enzymology. Esophageal Neoplasms / enzymology
  • [MeSH-minor] Adult. Aged. Biomarkers. Cell Hypoxia. Cell Line, Tumor. Cell Proliferation. Female. Humans. Male. Middle Aged. Prognosis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

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  • (PMID = 18841153.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers; 0 / RNA, Messenger; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2579701
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9. Umscheid TW, Rouhani G, Morlang T, Lorey T, Klein PJ, Ziegler P, Stelter WJ: Hemangiosarcoma after endovascular aortic aneurysm repair. J Endovasc Ther; 2007 Feb;14(1):101-5

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  • Systemic chemotherapy followed.
  • The tumor recurred after 12 months, with pulmonary metastases and tumor embolic occlusion of his left femoral artery.
  • Thrombectomy was performed, and a second course of chemotherapy was administered.
  • The patient died 24 months after the conversion procedure.
  • CONCLUSION: Morphological changes of the aneurysm wall seen on computed tomographic scans of EVAR patients may not be incidental or signs of infection; rather, a malignant tumor of the aorta or lymphatic disease, although rare, have to be taken into consideration as well.
  • [MeSH-major] Aortic Aneurysm, Abdominal / surgery. Blood Vessel Prosthesis Implantation / adverse effects. Hemangiosarcoma / etiology. Stents
  • [MeSH-minor] Fatal Outcome. Humans. Klinefelter Syndrome / complications. Male. Middle Aged. Polyethylene Terephthalates. Tomography, X-Ray Computed

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  • (PMID = 17291154.001).
  • [ISSN] 1526-6028
  • [Journal-full-title] Journal of endovascular therapy : an official journal of the International Society of Endovascular Specialists
  • [ISO-abbreviation] J. Endovasc. Ther.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Polyethylene Terephthalates
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10. Farhadi MR, Capelle HH, Erber R, Ullrich A, Vajkoczy P: Combined inhibition of vascular endothelial growth factor and platelet-derived growth factor signaling: effects on the angiogenesis, microcirculation, and growth of orthotopic malignant gliomas. J Neurosurg; 2005 Feb;102(2):363-70
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  • [Title] Combined inhibition of vascular endothelial growth factor and platelet-derived growth factor signaling: effects on the angiogenesis, microcirculation, and growth of orthotopic malignant gliomas.
  • OBJECT: The goal of this study was to determine the effects of SU6668, a polyvalent receptor tyrosine kinase inhibitor against vascular endothelial growth factor receptor-2, platelet-derived growth factor receptor-beta, and fibroblast growth factor-1 on tumor growth, angiogenesis, and microcirculation in an orthotopic malignant glioma model.
  • METHODS: Fluorescently labeled C6 malignant glioma cells were implanted into a long-term cranial window, which had been prepared in nude mice.
  • The animals were treated with intraperitoneal injections of SU6668 (75 mg/kg/day) immediately (five animals) or 7 days (five animals) following tumor implantation.
  • Control mice received intraperitoneal injections of vehicle (50 microl dimethylsulfoxide) immediately (five animals) or 7 days (four animals) after tumor implantation.
  • Tumor growth, angiogenesis, and microcirculation were assessed by performing intravital fluorescence videomicroscopy over a 14-day observation period.
  • To assess the effects of SU6668 on overall survival, C6 glioma cells were implanted stereotactically into the brains of 24 additional animals and treatment was initiated on Day 7.
  • In both the immediate and delayed experimental setting, SU6668 treatment resulted in a significant reduction of total and functional tumor vessel densities (both p < 0.05), reflecting a suppression of angiogenesis and impairment of tumor perfusion.
  • As a consequence, tumor growth was significantly inhibited (p < 0.05).
  • Histological analysis demonstrated reduced tumor growth and less mass effect on the adjacent brain of treated animals.
  • The survival experiments confirmed the importance of our results in that survival was significantly prolonged following SU6668 therapy (p < 0.05).
  • This also applies to malignant gliomas, despite the uniqueness of the cerebral microenvironment and the singular pathobiology of this tumor entity.
  • [MeSH-major] Brain Neoplasms / blood supply. Glioma / blood supply. Indoles / pharmacology. Neovascularization, Pathologic / physiopathology. Platelet-Derived Growth Factor / antagonists & inhibitors. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrroles / pharmacology. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Brain / drug effects. Brain / pathology. Cell Division / drug effects. Cell Division / physiology. Cell Line, Tumor. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Mice. Mice, Nude. Microcirculation / drug effects. Microcirculation / physiology. Microscopy, Fluorescence. Microscopy, Video. Neoplasm Transplantation. Rats. Receptor, Platelet-Derived Growth Factor beta / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor beta / physiology. Transplantation, Heterologous. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / physiology

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  • (PMID = 15739567.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indoles; 0 / Platelet-Derived Growth Factor; 0 / Pyrroles; 0 / Vascular Endothelial Growth Factor A; 9RL37ZZ665 / orantinib; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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11. Hicklin DJ, Ellis LM: Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis. J Clin Oncol; 2005 Feb 10;23(5):1011-27
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  • [Title] Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis.
  • New blood vessel formation (angiogenesis) is a fundamental event in the process of tumor growth and metastatic dissemination.
  • Hence, the molecular basis of tumor angiogenesis has been of keen interest in the field of cancer research.
  • The VEGF/VEGF-receptor axis is composed of multiple ligands and receptors with overlapping and distinct ligand-receptor binding specificities, cell-type expression, and function.
  • In addition, VEGF mediates vessel permeability, and has been associated with malignant effusions.
  • The well-established role of VEGF in promoting tumor angiogenesis and the pathogenesis of human cancers has led to the rational design and development of agents that selectively target this pathway.
  • Studies with various anti-VEGF/VEGF-receptor therapies have shown that these agents can potently inhibit angiogenesis and tumor growth in preclinical models.
  • Recently, an anti-VEGF antibody (bevacizumab), when used in combination with chemotherapy, was shown to significantly improve survival and response rates in patients with metastatic colorectal cancer and thus, validate VEGF pathway inhibitors as an important new treatment modality in cancer therapy.
  • [MeSH-major] Neoplasms / blood supply. Neovascularization, Pathologic / physiopathology. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Animals. Antineoplastic Agents / therapeutic use. Humans. Receptors, Vascular Endothelial Growth Factor / physiology. Signal Transduction / physiology

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  • (PMID = 15585754.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA74821; United States / NCI NIH HHS / CA / U54-CA90810
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 240
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12. Barnett FH, Scharer-Schuksz M, Wood M, Yu X, Wagner TE, Friedlander M: Intra-arterial delivery of endostatin gene to brain tumors prolongs survival and alters tumor vessel ultrastructure. Gene Ther; 2004 Aug;11(16):1283-9
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  • [Title] Intra-arterial delivery of endostatin gene to brain tumors prolongs survival and alters tumor vessel ultrastructure.
  • Glioblastoma multiforme (GBM) is an incurable malignant brain tumor, usually fatal within 1 year of diagnosis.
  • Using a syngeneic rat 9L gliosarcoma model, we have developed a novel drug delivery method in which naked plasmid DNA is selectively targeted to brain tumors via intra-arterial injection.
  • Using a plasmid encoding the antiangiogenic endostatin, transgene expression can be detected in tumor cells in vivo, and therapeutic efficacy is observed.
  • Administration of this plasmid resulted in an 80% tumor volume reduction 1 week after treatment and enhanced survival time by up to 47%.
  • Treated tumors exhibited a 40% decrease in the number of tumor vessels; ultrastructural analysis of remaining tumor vessels demonstrated a number of changes including markedly narrowed or collapsed lumens.
  • We conclude that intra-arterial injection of plasmids selectively targets therapeutic genes to CNS neoplasms.
  • This method of gene therapy holds promise for the treatment of these highly malignant brain tumors.
  • [MeSH-major] Brain Neoplasms / therapy. Endostatins / genetics. Genetic Therapy / methods. Glioblastoma / therapy
  • [MeSH-minor] Animals. Blood-Brain Barrier / physiopathology. Capillary Permeability / physiology. Gene Expression Regulation, Neoplastic / genetics. Immunohistochemistry / methods. Injections, Intra-Arterial. Male. Microscopy, Electron / methods. Neoplasm Invasiveness. Neovascularization, Pathologic. Plasmids. Rats. Rats, Inbred F344. Reverse Transcriptase Polymerase Chain Reaction / methods. Treatment Outcome

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  • (PMID = 15164099.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R24EY14174
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endostatins
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13. Rak J, Yu JL: Oncogenes and tumor angiogenesis: the question of vascular "supply" and vascular "demand". Semin Cancer Biol; 2004 Apr;14(2):93-104
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  • [Title] Oncogenes and tumor angiogenesis: the question of vascular "supply" and vascular "demand".
  • Among novel promising approaches that have recently entered the scene of anti-cancer therapy angiogenesis inhibition and targeting cancer-causing genes (e.g. oncogenes) are of particular interest as potentially highly synergistic.
  • One reason for this is that transforming genetic lesions driving cancer progression (e.g. mutations of ras and/or p53) are thought to be causative for the onset of tumor angiogenesis and thereby responsible for build up of vascular supply which is essential for cancer cell survival, malignant growth, invasion and metastasis.
  • However, many of the same genetic alterations that emerge during disease progression and repeated rounds of mutagenic and/or apoptosis causing therapy could alter cellular hypoxia-, growth factor- and apoptotic pathways in such a manner, as to also render cancer cells (partially) refractory to the detrimental consequences of poor blood vessel accessibility (density), ischemia, hypoxia and growth factor deprivation.
  • As recent experimental evidence suggests, such cancer cells could therefore display a reduced vascular demand and remain viable even in poorly perfused regions of the tumor as well as possess an overall growth/survival advantage.
  • Therefore, we propose that analysis of oncogenic pathways and gene expression profiling of cancer cells may lead to important clues as to potential efficacy of anti-angiogenic therapies, the direct target of which is the host vasculature, but which are ultimately aimed at (indirect) destruction/control of the cancer cells population.
  • We also suggest that oncogene (tumor suppressor)-directed therapies may help reverse diminished vascular demand of highly transformed cancer cells and thereby facilitate (sensitize tumors to) therapies directed against vascular supply of cancers and their metastases.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neoplasms / drug therapy. Neovascularization, Pathologic / drug therapy. Proto-Oncogenes / genetics
  • [MeSH-minor] Blood Vessels / drug effects. Blood Vessels / growth & development. Genes, ras. Humans. Signal Transduction. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15018893.001).
  • [ISSN] 1044-579X
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 147
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14. Varras M, Tsikini A, Polyzos D, Samara Ch, Akrivis Ch: Internal hemorrhage caused by a twisted malignant ovarian dysgerminoma: ultrasonographic findings of a rare case and review of the literature. Clin Exp Obstet Gynecol; 2004;31(1):73-8
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  • [Title] Internal hemorrhage caused by a twisted malignant ovarian dysgerminoma: ultrasonographic findings of a rare case and review of the literature.
  • The purpose of the study is the description of a right ovarian malignant dysgerminoma presenting as an abdominal emergency.
  • The patient was sexually active and bimanual gynecological examination revealed the presence of a large lobulated solid tumor in the position of the right adnexa.
  • A superficial tumoral vessel actively bleeding was seen.
  • Pathologic analysis revealed a malignant dysgerminoma of the right ovary, expanding to the mesosalpinx.
  • The patient was assigned to FIGO Stage IIC and referred for platinum-based chemotherapy.
  • CONCLUSION: Ovarian malignant dysgerminoma may present as an acute abdomen because of torsion, passive blood congestion, rupture of superficial tumoral vessels and subsequent intra-abdominal hemorrhage.
  • Ovarian dysgerminoma should be part of the differential diagnosis in a young woman with acute surgical abdomen and a solid heterogeneous pelvic mass detected by ultrasonographic scan.

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  • (PMID = 14998196.001).
  • [ISSN] 0390-6663
  • [Journal-full-title] Clinical and experimental obstetrics & gynecology
  • [ISO-abbreviation] Clin Exp Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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15. Ghanem N, Riede U, Uhrmeister P, Weigang E, Altehoefer C: Epithelioid angiosarcoma of the aorta. Vasa; 2002 Nov;31(4):269-73

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  • Primary malignant tumors of the aorta are extremely rare.
  • Review of the literature indicates that there are nearly 100 recorded cases of primary malignant tumors of the aorta.
  • The purpose of this article is to present an additional case of the primary malignant tumors of the aorta which initially has been misinterpretated as atherosclerosic disease.
  • This aortic tumor was of endothelial origin and immunohistochemical studies classified the tumor as an epithelioid angiosarcoma.
  • The treatment resulted in an abdominal aortic repair.
  • MRI of the spine revealed multifocal metastatic disease of the axial skeleton and a subsequent chemotherapy was performed.
  • The patient died 17 months after the initial diagnosis.
  • [MeSH-major] Aorta, Thoracic. Aortic Diseases / diagnosis. Hemangiosarcoma / diagnosis. Vascular Neoplasms / diagnosis
  • [MeSH-minor] Arteriosclerosis / diagnosis. Arteriosclerosis / pathology. Arteriosclerosis / surgery. Blood Vessel Prosthesis Implantation. Diagnosis, Differential. Diagnostic Imaging. Humans. Male. Middle Aged

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  • (PMID = 12510553.001).
  • [ISSN] 0301-1526
  • [Journal-full-title] VASA. Zeitschrift für Gefässkrankheiten
  • [ISO-abbreviation] VASA
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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16. Baretti R, Schaumann B, Meyer R, Alfaouri D, Hetzer R: [Metastasizing malignant germ cell tumor of the testis with infiltration of the thoracic aorta--a case for metastasis surgery]. Dtsch Med Wochenschr; 2000 Sep 29;125(39):1164-6
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  • [Title] [Metastasizing malignant germ cell tumor of the testis with infiltration of the thoracic aorta--a case for metastasis surgery].
  • [Transliterated title] Metastasierender maligner Keimzelltumor des Hodens mit Infiltration der Aorta thoracica--Kasuistik zur Metastasenchirurgie.
  • Five years later the first mediastinal metastases were treated with high-dosage chemotherapy and autologous germ-cell transplantation, and remaining paraaortic--mediastinal tumour tissue was resected.
  • A curing treatment seemed impossible, because the aortic wall had been invaded.
  • TREATMENT AND COURSE: Five months after re-thoracotomy the metastasis and the invaded aortic segment were resected, the latter replaced by a vascular prosthesis.
  • Histology indicated metastasis of a malignant teratoma of intermediate type.
  • CONCLUSION: Combined orchidectomy, lymphadenectomy, high-dosage chemotherapy with cisplatin and autologous germ-cell transplantation at present constitute the standard treatment of malignant testicular germ-cell tumour.
  • In case of metastatic infiltration of vital structures, such as the aortic wall, special operative procedures can prolong the period of remission when the success of a standard treatment seems limited.
  • [MeSH-minor] Adult. Aortic Diseases / radiography. Aortic Diseases / surgery. Blood Vessel Prosthesis. Chemotherapy, Adjuvant. Humans. Lymph Node Excision. Male. Mediastinal Neoplasms / secondary. Mediastinal Neoplasms / surgery. Orchiectomy. Retroperitoneal Space. Tomography, X-Ray Computed

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  • (PMID = 11075244.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] GERMANY
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17. Hua HQ: [Contemporary study of strengthening body resistance and archaeus herbs on malignant tumor]. Zhongguo Zhong Yao Za Zhi; 2008 May;33(9):1095-7
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  • [Title] [Contemporary study of strengthening body resistance and archaeus herbs on malignant tumor].
  • [Strengthening body resistance and archaeus herbs are those medicines used on asthenia syndrome of tumor, which can harmonize yin and yang, replenish deficiency of qi and blood, and improve entrails function, enhance physical capacity, and improve immunity function.
  • Study shows that strengthening body resistance and archaeus herbs have many effects, such as improving and adjusting immunity function, protecting bone marrow, improving haematogenesis function, raising digest and absorb function, improving substance metabolism, preventing gene mutation, inhibiting tumor cell proliferation, inducing tumor cell differentiation or apoptosis, resisting tumor invasion and metastasis, inhibiting formation of tumor vessel and activity of telomerase, etc.
  • [MeSH-major] Drugs, Chinese Herbal / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Bone Marrow / drug effects. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Enzyme Activation / drug effects. Telomerase / metabolism

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  • (PMID = 18652363.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; EC 2.7.7.49 / Telomerase
  • [Number-of-references] 28
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18. Kang CH, Kim YT, Jheon SH, Sung SW, Kim JH: Surgical treatment of malignant mediastinal nonseminomatous germ cell tumor. Ann Thorac Surg; 2008 Feb;85(2):379-84
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  • [Title] Surgical treatment of malignant mediastinal nonseminomatous germ cell tumor.
  • BACKGROUND: The aim of this study was to evaluate the role of surgical treatment for mediastinal nonseminomatous germ cell tumors (MNSGCT) and identify the factors of long-term survival.
  • Three different regimens were used for preoperative chemotherapy, and 14 patients (66.7%) achieved partial response, 4 (19.0%) had stable disease, and 2 (9.5%) had progressive disease.
  • The most common cause of incomplete resection was great vessel invasion (n = 3).
  • Viable germ cell tumor was identified in pathology specimens in 12 (57.1%), total necrosis in 7 (33.3%), and remnant teratoma in 2 (9.5%).
  • Risk factors for poor overall survival by multivariate analysis were beta-human chorionic gonadotrophin (beta-HCG) elevation at initial diagnosis (p = 0.02) and incomplete resection (p = 0.002).
  • CONCLUSIONS: Surgical resection of MNSGCT after chemotherapy showed favorable long-term survival.
  • An elevated beta-HCG level at initial diagnosis was associated with a poor prognosis despite multimodality therapy.
  • [MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / blood. Mediastinal Neoplasms / mortality. Mediastinal Neoplasms / surgery. Neoplasm Recurrence, Local / mortality. Neoplasms, Germ Cell and Embryonal / mortality. Neoplasms, Germ Cell and Embryonal / surgery
  • [MeSH-minor] Adolescent. Adult. Analysis of Variance. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / blood. Biopsy, Needle. Chemotherapy, Adjuvant. Child. Combined Modality Therapy. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Preoperative Care / methods. Probability. Prognosis. Proportional Hazards Models. Registries. Retrospective Studies. Risk Assessment. Survival Analysis. Thoracotomy / methods. Treatment Outcome

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  • (PMID = 18222229.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human
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19. Beekman KW, Colevas AD, Cooney K, Dipaola R, Dunn RL, Gross M, Keller ET, Pienta KJ, Ryan CJ, Smith D, Hussain M: Phase II evaluations of cilengitide in asymptomatic patients with androgen-independent prostate cancer: scientific rationale and study design. Clin Genitourin Cancer; 2006 Mar;4(4):299-302
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  • Two randomized trials demonstrated an improvement in survival with docetaxel-based chemotherapy for patients with metastatic, androgen-independent prostate disease.
  • However, the effect of current therapy is suboptimal in that it is complicated by toxicities and has no curative potential.
  • Blocking the ligation of integrins by antagonists promotes apoptosis of proliferative angiogenic cells, thereby suspending new blood vessel formation, which is essential for the growth of malignant disease.
  • In prostate cancer specifically, integrins are known to be involved in metastases with differential expression on tumor cells.
  • Cilengitide also inhibited tumor growth in various in vivo systems.
  • Two Cancer Therapy Evaluation Program-sponsored, multicenter, phase II trials are designed to evaluate the safety and efficacy of this agent in patients with androgen-independent prostate cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Prostatic Neoplasms / drug therapy. Snake Venoms / therapeutic use

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  • (PMID = 16729916.001).
  • [ISSN] 1558-7673
  • [Journal-full-title] Clinical genitourinary cancer
  • [ISO-abbreviation] Clin Genitourin Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / P01 CA093900; United States / NCI NIH HHS / CA / P50CA69568
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Integrins; 0 / Snake Venoms; 4EDF46E4GI / Cilengitide
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20. Ma ZS, Huynh TH, Ng CP, Do PT, Nguyen TH, Huynh H: Reduction of CWR22 prostate tumor xenograft growth by combined tamoxifen-quercetin treatment is associated with inhibition of angiogenesis and cellular proliferation. Int J Oncol; 2004 May;24(5):1297-304
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  • [Title] Reduction of CWR22 prostate tumor xenograft growth by combined tamoxifen-quercetin treatment is associated with inhibition of angiogenesis and cellular proliferation.
  • Combination chemotherapy is increasingly practiced for the treatment of malignant prostate cancers.
  • The aim of this study was to evaluate the in vivo efficacy of combined tamoxifen and quercetin in prostate tumor xenografts.
  • Severe combined immune deficient (SCID) mice inoculated with CWR22 prostate tumor cells were treated with either tamoxifen (10 mg/kg/week), quercetin (200 mg/kg/day) or combined tamoxifen-quercetin for 28 days.
  • Tamoxifen decreased the Ki-67 index by 52.4%, reduced the vascular endothelial growth factor (VEGF) 121 and VEGF165 mRNA by 18.6 and 21.8%, respectively, and suppressed the blood vessel formation, while quercetin modulated the expression and phosphorylation of cdc-2 and cyclin B1, and inhibited the Ki-67 index by 66.0%.
  • Combined tamoxifen-quercetin effectively delayed the appearance of tumors, inhibited the final tumor volume by 73.3% and reduced the endpoint tumor weight by 67.1% (p<0.05).
  • The Ki-67 index, VEGF121, VEGF165 mRNA and microvessel density (MVD) were decreased by 66.9, 22.1, 40.1 and 59.0%, respectively, by the combined treatment.
  • These findings indicate that tamoxifen inhibits CWR22 prostate tumor by modulating the angiogenesis and its antineoplastic effects can be potentiated by combined use with quercetin.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Neovascularization, Pathologic / prevention & control. Prostatic Neoplasms / blood supply. Prostatic Neoplasms / therapy. Quercetin / therapeutic use. Tamoxifen / therapeutic use
  • [MeSH-minor] Animals. CDC2 Protein Kinase / metabolism. Cell Division / drug effects. Cyclin B / metabolism. Cyclin B1. Drug Therapy, Combination. Humans. Ki-67 Antigen / metabolism. Male. Mice. Mice, SCID. Microcirculation. Phosphorylation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Transplantation, Heterologous. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15067354.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / CCNB1 protein, human; 0 / Ccnb1 protein, mouse; 0 / Cyclin B; 0 / Cyclin B1; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 094ZI81Y45 / Tamoxifen; 9IKM0I5T1E / Quercetin; EC 2.7.11.22 / CDC2 Protein Kinase
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21. Patten SG, Adamcic U, Lacombe K, Minhas K, Skowronski K, Coomber BL: VEGFR2 heterogeneity and response to anti-angiogenic low dose metronomic cyclophosphamide treatment. BMC Cancer; 2010 Dec 15;10:683
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  • [Title] VEGFR2 heterogeneity and response to anti-angiogenic low dose metronomic cyclophosphamide treatment.
  • BACKGROUND: Targeting tumor vasculature is a strategy with great promise in the treatment of many cancers.
  • METHODS: Double immunofluorescent staining was performed on formalin-fixed paraffin embedded sections of treated and control SW480 (colorectal) and WM239 (melanoma) xenografts, and tissue microarrays of human colorectal carcinoma and melanoma.
  • Xenografts were developed using RAG1-/- mice by injection with WM239 or SW480 cells and mice were treated with 20 mg/kg/day of cyclophosphamide in their drinking water for up to 18 days.
  • Treated and control tissues were characterized by double immunofluorescence using the mural cell marker α-SMA and CD31, while the ratio of desmin/CD31 was also determined by western blot.
  • Hypoxia in treated and control tissues were quantified using both western blotting for HIF-1α and immunohistochemistry of CA-IX.
  • RESULTS: VEGFR2 is heterogeneously expressed in tumor vasculature in both malignant melanoma and colorectal carcinoma.
  • We observed a significant decrease in microvascular density (MVD) in response to low dose metronomic cyclophosphamide chemotherapy in both malignant melanoma (with higher proportion VEGFR2 positive blood vessels; 93%) and colorectal carcinoma (with lower proportion VEGFR2 positive blood vessels; 60%) xenografts.
  • This reduction in MVD occurred in the absence of a significant anti-tumor effect.
  • We also observed less hypoxia in treated melanoma xenografts, despite successful anti-angiogenic blockade, but no change in hypoxia of colorectal xenografts, suggesting that decreases in tumor hypoxia reflect a complex relationship with vascular density.
  • Based on α-SMA staining and the ratio of desmin to CD31 expression as markers of tumor blood vessel functionality, we found evidence for increased stabilization of colorectal microvessels, but no such change in melanoma vessels.
  • CONCLUSIONS: Overall, our study suggests that while heterogeneous expression of VEGFR2 is a feature of human tumors, it may not affect response to low dose metronomic cyclophosphamide treatment and possibly other anti-angiogenic approaches.
  • It remains to be seen whether this heterogeneity is partly responsible for the variable clinical success seen to date with targeted anti-VEGFR2 therapy.

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  • (PMID = 21159176.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / #MOP-81213
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Antigens, Neoplasm; 0 / Desmin; 0 / HIF1A protein, human; 0 / Homeodomain Proteins; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 128559-51-3 / RAG-1 protein; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC3009683
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22. Kirches E, Warich-Kirches M: 2-methoxyestradiol as a potential cytostatic drug in gliomas? Anticancer Agents Med Chem; 2009 Jan;9(1):55-65
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  • [Title] 2-methoxyestradiol as a potential cytostatic drug in gliomas?
  • Gliomas of astrocytic origin show only a limited chemotherapy response.
  • Chemoresistance is most pronounced in glioblastoma multiforme, the most common and most malignant glioma, with median survival times not much longer than one year.
  • Failure of chemotherapy partly relies on protective mechanisms against the commonly used DNA alkylating agents, but also on the constitutive activation of the pro-survival PI3K-Akt pathway in glioma cells, which inhibits apoptosis.
  • Therefore, new drugs with an alternative mechanism, independent of DNA alkylation, are required.
  • The microtubule targeting drug 2-methoxyestradiol (2-ME) efficiently induces mitotic arrest, apoptosis, but also autophagic cell death in glioma cells in vitro.
  • Moreover, it may be able to inhibit vascularization of the highly vascular gliobastomas, because the drug influences blood vessel sprouting via a HIF-1-dependent mechanism.
  • Compounds, sulphamoylated at positions 3 and 17, combine sufficient toxicity against tumor cells with resistance against metabolic degradation and sufficient plasma levels in experimental animals.
  • They were found to be superior in some animal models of tumor growth and vascularization, following oral application.
  • [MeSH-major] Estradiol / analogs & derivatives. Glioma / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Autophagy / drug effects. Humans. Treatment Outcome. Tubulin Modulators / therapeutic use

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  • (PMID = 19149482.001).
  • [ISSN] 1875-5992
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tubulin Modulators; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
  • [Number-of-references] 79
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23. Drappatz J, Wen PY: Non-cytotoxic drugs as potential treatments for gliomas. Curr Opin Neurol; 2004 Dec;17(6):663-73
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  • [Title] Non-cytotoxic drugs as potential treatments for gliomas.
  • PURPOSE OF REVIEW: Despite advances in surgery, radiation therapy, and chemotherapy, malignant gliomas continue to be associated with a poor prognosis.
  • Even the most intensive combinations of radiotherapy and chemotherapy are not curative.
  • In recent years our understanding of how tumor cells overcome cell cycle control, evade programmed cell death, induce blood vessel formation, and escape immune regulation has increased substantially.
  • Significant efforts are directed towards the development of novel experimental therapies to target these molecular and biological mechanisms that lead to the development and growth of brain tumors.
  • This review summarizes the most recent developments in non-cytotoxic therapy for malignant gliomas, such as targeted molecular drugs, inhibitors of angiogenesis and intratumoral therapy.
  • RECENT FINDINGS: The first generation of studies using these novel therapies is nearing completion.
  • In general, most of these treatments are well tolerated, but single-agent activity is modest.
  • There is significant interest in combining these therapies with each other and with conventional cytotoxic therapies such as radiation therapy and chemotherapy.
  • SUMMARY: These new therapeutic approaches for malignant gliomas are showing modest activity.
  • As we learn to use these agents more effectively, and as an increasing number of new and potentially promising agents are developed, it is likely that therapies for malignant gliomas will improve over the next few years.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brain Neoplasms / drug therapy. Glioma / drug therapy
  • [MeSH-minor] Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / immunology. Drug Therapy, Combination. Enzyme Inhibitors / pharmacology. Enzyme Inhibitors / therapeutic use. Growth Inhibitors / pharmacology. Growth Inhibitors / therapeutic use. Humans. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / physiopathology. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 15542974.001).
  • [ISSN] 1350-7540
  • [Journal-full-title] Current opinion in neurology
  • [ISO-abbreviation] Curr. Opin. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Growth Inhibitors; 0 / Recombinant Fusion Proteins
  • [Number-of-references] 99
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24. Takano S, Kamiyama H, Tsuboi K, Matsumura A: Angiogenesis and antiangiogenic therapy for malignant gliomas. Brain Tumor Pathol; 2004;21(2):69-73
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  • [Title] Angiogenesis and antiangiogenic therapy for malignant gliomas.
  • Angiogenesis is crucial to the growth of malignant gliomas.
  • Therefore, antiangiogenic therapy represents a new, promising therapeutic modality for malignant gliomas.
  • This study was designed to define the malignant glioma cases most suitable for antiangiogenic therapy in humans and to demonstrate the efficacy of antiangiogenic therapy in animals.
  • Protein expression of the most potent angiogenic factor, vascular endothelial growth factor (VEGF), and its specific natural inhibitor, soluble Flt-1, as well as vessel architecture, including vessel density, area, and diameter, was evaluated in human malignant glioma samples (24 glioblastomas, 13 anaplastic astrocytomas).
  • Among these, VEGF >1000ng/ml, VEGF/soluble Fltl ratio >1, vessel density >30, and vessel area >7% were prognostic factors for malignant gliomas.
  • Based on these results, we performed three different antiangiogenic experiments targeted to inhibit VEGF expression in a human malignant glioma (U87) mouse model: anti-VEGF neutralized antibody intraperitoneal injection; interferon-beta intramusclar injection; and transfection of an endogenous nonspecific angiogenesis inhibitor, thrombospondin-1, into glioma cells caused inhibition of VEGF secretion and/or mRNA expression and resulted in glioma growth inhibition of 70%, 84%, and 50%, respectively, compared with control.
  • We conclude that malignant gliomas with high degrees of VEGF expression and vessel areas are good candidates for antiangiogenic therapy, especially that designed to inhibit VEGF expression.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Brain Neoplasms / blood supply. Brain Neoplasms / drug therapy. Glioma / blood supply. Glioma / drug therapy
  • [MeSH-minor] Animals. Biomarkers, Tumor / analysis. Blotting, Western. Extracellular Matrix Proteins / biosynthesis. Humans. In Vitro Techniques. Interferon-beta / therapeutic use. Mice. Myosin Heavy Chains. Neovascularization, Pathologic / drug therapy. Nonmuscle Myosin Type IIB. Prognosis. Thrombospondin 1 / genetics. Thrombospondin 1 / metabolism. Transfection. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / immunology. Vascular Endothelial Growth Factor Receptor-1

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  • [CommentIn] Brain Tumor Pathol. 2005;22(1):51 [18095105.001]
  • (PMID = 15700836.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins; 0 / Thrombospondin 1; 0 / Vascular Endothelial Growth Factor A; 77238-31-4 / Interferon-beta; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Flt1 protein, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 3.6.1.- / Nonmuscle Myosin Type IIB; EC 3.6.1.- / nonmuscle myosin type IIB heavy chain; EC 3.6.4.1 / Myosin Heavy Chains
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25. de Bont ES, Guikema JE, Scherpen F, Meeuwsen T, Kamps WA, Vellenga E, Bos NA: Mobilized human CD34+ hematopoietic stem cells enhance tumor growth in a nonobese diabetic/severe combined immunodeficient mouse model of human non-Hodgkin's lymphoma. Cancer Res; 2001 Oct 15;61(20):7654-9
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  • [Title] Mobilized human CD34+ hematopoietic stem cells enhance tumor growth in a nonobese diabetic/severe combined immunodeficient mouse model of human non-Hodgkin's lymphoma.
  • Autologous peripheral blood stem cell mobilization is increasingly applied in the treatment of hematological malignancies.
  • Despite the frequent clinical use in a setting of residual disease, it is not known whether mobilization of hematopoietic stem cells might facilitate tumor outgrowth in vivo.
  • This hemangioblast, characterized by the expression of CD34 and vascular endothelial growth factor receptor (VEGFR)-2, is released from the bone marrow by mobilization and might be able to result in not only the generation of peripheral blood cells but vasculogenesis due to differentiation of the hemangioblast along the endothelial lineage [in addition to VEGFR-2 expression, angiopoietin-2 (ANG-2) expression can also be found in this stage].
  • New vessel formation in the tumor is critical for tumor growth.
  • A xenotransplant model was established with 10 x 10(6) Daudi cells (non-Hodgkin's lymphoma) s.c. injected in the neck region of nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice, who were sublethally irradiated with 2 Gy.
  • At day 10 after tumor inoculation, half of the mice were given 0.5 x 10(6) human CD34+ cells i.v., whereas the other half were given PBS i.v.
  • The human CD34+ cells were obtained from leukapheresis samples of myeloma patients undergoing autologous peripheral blood stem cell mobilization.
  • We compared tumor growth and human-specific VEGFR-2 and ANG-2 expression in the two groups.
  • Tumor growth is enhanced 2-fold when mobilized hematopoietic human CD34+ cells are given compared with PBS controls (P = 0.004).
  • Malignant tumors are capable of incorporating human CD34+ hematopoietic cells.
  • This study questions the safety of leukapheresis in patients with (residual) tumor and has important implications for further development of intensive chemotherapy protocols with autologous stem cell rescue.

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  • (PMID = 11606408.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiopoietin-2; 0 / Antigens, CD34; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Receptors, Growth Factor; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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26. Boozari B, Kubicka S: [Differentiated therapy of liver tumors]. Internist (Berl); 2010 Jan;51(1):53-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Differentiated therapy of liver tumors].
  • Focal nodular hyperplasia is a polyclonal hyperplasia of liver cells as a result of locally enhanced blood flow because of vessel malformations.
  • Solitary HNFalpha-inactivated and inflammatory adenomas larger than 5 cm should be removed because of risk of tumor rupture or bleeding, while beta-catenin mutated adenomas should be surgically removed at any stage because of risk of malignant transformation.
  • The prognosis of patients with HCC is dependent on the tumor stage, but also on the liver function.
  • Resection is the treatment of choice for HCC in patients without liver cirrhosis.
  • Transarterial chemoembolization is an effective treatment for more advanced HCC in patients with good liver function.
  • Patients with unresectable cholangiocarcinomas should be treated with a chemotherapy consisting of Gemcitabine-Cisplatin-combination.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Hepatocellular / therapy. Chemoembolization, Therapeutic / methods. Liver Neoplasms / therapy. Liver Transplantation

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  • [Cites] Hepatology. 2009 Feb;49(2):453-9 [19065676.001]
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  • (PMID = 20062959.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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27. Norris AJ, Sartippour MR, Lu M, Park T, Rao JY, Jackson MI, Fukuto JM, Brooks MN: Nitroxyl inhibits breast tumor growth and angiogenesis. Int J Cancer; 2008 Apr 15;122(8):1905-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nitroxyl inhibits breast tumor growth and angiogenesis.
  • Because of the importance of glycolysis in many malignant cells, we thus propose that HNO can adversely affect tumor growth.
  • We report here for the first time that HNO suppresses the proliferation of both estrogen receptor (ER)-positive and ER-negative human breast cancer cell lines, in a dose dependent manner.
  • Mice treated with HNO either injected into the tumor itself or via the intraperitoneal approach had smaller xenograft tumor size.
  • In addition to significantly decreased blood vessel density in the HNO-treated tumors, we observed lower levels of circulating serum vascular endothelial growth factor (VEGF).
  • Accordingly, there was a decrease in total HIF-1alpha (hypoxia-inducible factor) protein in HNO-treated tumor cells.
  • Further studies showed inhibition of GAPDH activity in HNO-treated human breast cancer cell lines and in HNO-treated tumor tissue derived from xenografts.
  • One explanation for the multiplicity of actions observed after HNO treatment could be the effect from the initial inhibition of GAPDH, providing a potential therapeutic avenue based upon blocking glycolysis resulting in decreased HIF-1alpha, thus leading to angiogenesis inhibition.
  • Therefore, HNO appears to act via mechanism(s) different from those of existing breast cancer drugs, making it a potential candidate to overcome known and emerging drug resistance pathways.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Enzyme Inhibitors / pharmacology. Glyceraldehyde-3-Phosphate Dehydrogenases / antagonists & inhibitors. Glycolysis / drug effects. Nitrogen Oxides / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / drug effects. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, SCID. Nitrites / pharmacology. Transplantation, Heterologous. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18076071.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nitrites; 0 / Nitrogen Oxides; 0 / Vascular Endothelial Growth Factor A; 14332-28-6 / nitroxyl; 18550-55-5 / oxyhyponitrite; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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28. Horn LC, Vogel M: [Gestational trophoblastic disease. Non-villous forms of gestational trophoblastic disease]. Pathologe; 2004 Jul;25(4):281-91
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  • The non-villous forms of gestational trophoblastic disease (GTD) include a wide range of morphologic different lesions and cover a wide range of differential diagnosis.
  • Choriocarcinomas (CCA) represent the most malignant form displaying a dimorphic pattern with proliferation of syncytio- and zytotrophoblast.
  • An early start of chemotherapy is of great prognostic impact.
  • Placental site nodule (PSN) and exaggerated placental site (EPS) are non-neoplastic lesions of the intermediate trophoblast without tumorous appearance, whereas placental site trophoblastic tumor (PSTT) and epitheloid trophoblastic tumor (ETT) represent tumorous neoplasms with a potential for local invasion and metastases.
  • In PSTT the monomorphic, occasional multinucleated giant cells separating individual muscle fibers and charactersitically blood vessel walls are extensively replaced by trophoblastic cells and fibrinoid material.
  • Typically small blood vessels with preserved walls are located within the center of glycogen-rich monomorphous proliferation of trophoblastic cells.

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  • (PMID = 15184992.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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29. Hagihara N, Walbridge S, Olson AW, Oldfield EH, Youle RJ: Vascular protection by chloroquine during brain tumor therapy with Tf-CRM107. Cancer Res; 2000 Jan 15;60(2):230-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular protection by chloroquine during brain tumor therapy with Tf-CRM107.
  • Tf-CRM107 has been infused intratumorally into patients with malignant brain tumors.
  • Although approximately half of the patients exhibit tumor responses, patients receiving higher doses of Tf-CRM107 may develop magnetic resonance image (MRI) evidence of toxicity indicative of small vessel thrombosis or petechial hemorrhage.
  • To widen the therapeutic window of Tf-CRM107, we explored ways to prevent this damage to the vasculature.
  • We reasoned that the vasculature may be protected to a greater extent than tumor from Tf-CRM107 infused into brain parenchyma by i.v. injection of reagents with low blood-brain barrier permeability that block the toxicity of Tf-CRM107.
  • Chloroquine, a well-characterized antimalarial drug, blocks the toxicity of diphtheria toxin and Tf-CRM107.
  • Moreover, chloroquine treatment completely blocked the brain damage detected by MRI caused by intracerebral infusion of 0.05 microg of Tf-CRM107.
  • U251 gliomas, chloroquine treatment had little effect on the antitumor efficacy of Tf-CRM107.
  • Thus, chloroquine treatment may be useful to reduce the toxicity of Tf-CRM107 for normal brain without inhibiting antitumor efficacy and increase the therapeutic window of Tf-CRM107 for brain tumor therapy.
  • [MeSH-major] Bacterial Toxins / therapeutic use. Bacterial Toxins / toxicity. Brain Neoplasms / drug therapy. Cerebrovascular Circulation / drug effects. Chloroquine / pharmacology. Immunotoxins / therapeutic use. Immunotoxins / toxicity. Transferrin / therapeutic use. Transferrin / toxicity
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Dose-Response Relationship, Drug. Glioblastoma / drug therapy. Glioblastoma / pathology. Gliosarcoma / drug therapy. Gliosarcoma / pathology. Humans. Magnetic Resonance Imaging. Mice. Mice, Nude. Rats. Rats, Inbred F344. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 10667564.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Bacterial Toxins; 0 / Immunotoxins; 0 / Tf-CRM107; 0 / Transferrin; 886U3H6UFF / Chloroquine
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30. Qu B, Guo L, Ma J, Lv Y: Antiangiogenesis therapy might have the unintended effect of promoting tumor metastasis by increasing an alternative circulatory system. Med Hypotheses; 2010 Feb;74(2):360-1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiangiogenesis therapy might have the unintended effect of promoting tumor metastasis by increasing an alternative circulatory system.
  • Antiangiogenesis therapy is one of the most promising approaches to cancer treatment.
  • Vascularization of tumor is a complex and heterogenous process.
  • So far, it has been demonstrated that several additional mechanisms can provide the tumor with oxygen and nutrients.
  • Moreover, it is now clear that vascularization of tumor does not necessarily depend on endothelial cells proliferation and sprouting of new capillaries.
  • Vasculogenic mimicry (VM) as an alternative circulatory system, has been described in multiple malignant tumor types, and considered to be associated with a poor prognosis for the patient.
  • VM serves as an adjunct to the existing vasculature system, thereby aiding tumor growth as well as contributing to the metastatic process.
  • Moreover, hypoxia has been confirmed to promote some tumor cells to form vessel-like tubes in vitro and express genes associated with VM.
  • Yet, the current antiangiogenesis strategies, which are directed mainly against the tumor endothelium and then cause hypoxia of tumor cells, have no effect on VM.
  • Our central hypothesis is that when the endothelium-dependent vessels are inhibited by the effective angiogenesis inhibitors, the hypoxia of tumor cells caused by antiangiogenesis may increase VM compensatively which can replace the job of endothelium-dependent vessels to maintain the tumor blood supply and provide a convenient route of tumor metastasis.
  • As a result, antiangiogenesis therapy might have the unintended effect of promoting tumor metastasis by increasing VM.
  • Thus, treatment strategies that target the tumor microcirculation should not only target endothelium-dependent vessels, but also take VM into account in tumors presenting VM.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Angiogenesis Inhibitors / adverse effects. Neoplasm Metastasis / physiopathology. Neoplasms / chemically induced. Neoplasms / drug therapy. Neoplastic Cells, Circulating / metabolism. Neovascularization, Pathologic / chemically induced
  • [MeSH-minor] Humans. Microcirculation / drug effects. Models, Biological

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  • (PMID = 19744799.001).
  • [ISSN] 1532-2777
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
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31. Johansson G, Mahller YY, Collins MH, Kim MO, Nobukuni T, Perentesis J, Cripe TP, Lane HA, Kozma SC, Thomas G, Ratner N: Effective in vivo targeting of the mammalian target of rapamycin pathway in malignant peripheral nerve sheath tumors. Mol Cancer Ther; 2008 May;7(5):1237-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective in vivo targeting of the mammalian target of rapamycin pathway in malignant peripheral nerve sheath tumors.
  • Malignant peripheral nerve sheath tumors (MPNST) are chemoresistant sarcomas with poor 5-year survival that arise in patients with neurofibromatosis type 1 (NF1) or sporadically.
  • We tested three drugs for single and combinatorial effects on collected MPNST cell lines and in MPNST xenografts.
  • The mammalian target of rapamycin complex 1 inhibitor RAD001 (Everolimus) decreased growth 19% to 60% after 4 days of treatment in NF1 and sporadic-derived MPNST cell lines.
  • Treatment of subcutaneous sporadic MPNST cell xenografts with RAD001 significantly, but transiently, delayed tumor growth, and decreased vessel permeability within xenografts.
  • The results support the consideration of RAD001 therapy in NF1 patient and sporadic MPNST.
  • The preclinical tests described allow rapid screening strata for drugs that block MPNST growth, prior to tests in more complex models, and should be useful to identify drugs that synergize with RAD001.

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  • (PMID = 18483311.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS028840-09; United States / NINDS NIH HHS / NS / R01 NS028840; United States / NINDS NIH HHS / NS / R01 NS028840-09; United States / NINDS NIH HHS / NS / R01 NS28840-17
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 0 / Quinazolines; 9HW64Q8G6G / Everolimus; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.1 / ribosomal protein S6 kinase, 70kD, polypeptide 2; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS187346; NLM/ PMC2855168
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32. Kamiyama H, Takano S, Ishikawa E, Tsuboi K, Matsumura A: Anti-angiogenic and immunomodulatory effect of the herbal medicine "Juzen-taiho-to" on malignant glioma. Biol Pharm Bull; 2005 Nov;28(11):2111-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-angiogenic and immunomodulatory effect of the herbal medicine "Juzen-taiho-to" on malignant glioma.
  • Anti-neoplastic effects on malignant gliomas have been reported by means of the enhancement of the immune function in both animals and humans.
  • We evaluated whether JTT has anti-angiogenic effects on malignant glioma growth in vitro and in vivo.
  • In vitro, the anti-proliferative effect of JTT on malignant glioma cells and endothelial cells was assessed by cell proliferation assay.
  • In vivo, a subcutaneous model of malignant glioma with different-aged mice (old, 43 weeks; young, 8 weeks) was used.
  • After oral administration of JTT to mice, their immunological function and angiogenic status of tumor tissues were assessed by flow cytometry and immunohistochemistry, respectively.
  • In vivo, the NK (natural killer) cell ratio within PBMC (peripheral blood mononuclear cells) and NK activity of fresh splenocytes obtained from JTT-treated old mice were significantly increased compared to the ratio and activity in control mice.
  • In old mice, the vessel area of tumor tissues in JTT treatment groups was significantly decreased.
  • JTT not only increased host immunological function but also exerted anti-angiogenic effects on malignant glioma growth.
  • JTT would be useful as an adjuvant medicine for malignant gliomas through its enhancement of systemic immunological function and its anti-angiogenic action.
  • [MeSH-major] Angiogenesis Inhibitors. Drugs, Chinese Herbal / pharmacology. Glioma / drug therapy. Glioma / pathology. Immunologic Factors
  • [MeSH-minor] Animals. Antigens, CD31 / metabolism. Body Weight / drug effects. Body Weight / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Flow Cytometry. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16272699.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Drugs, Chinese Herbal; 0 / Immunologic Factors; 0 / Ki-67 Antigen; 0 / Vascular Endothelial Growth Factor A; 0 / juzentaihoto
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33. Okazaki T, Ebihara S, Takahashi H, Asada M, Kanda A, Sasaki H: Macrophage colony-stimulating factor induces vascular endothelial growth factor production in skeletal muscle and promotes tumor angiogenesis. J Immunol; 2005 Jun 15;174(12):7531-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Macrophage colony-stimulating factor induces vascular endothelial growth factor production in skeletal muscle and promotes tumor angiogenesis.
  • Although M-CSF has been used for myelosuppression due to chemotherapy in patients with solid tumors, the effect of exogenous M-CSF on tumor angiogenesis has not been studied.
  • In this study we showed that M-CSF has the ability to accelerate solid tumor growth by enhancing angiogenesis with a novel mechanism.
  • M-CSF accelerated intratumoral vessel density in tumors inoculated into mice, although it did not accelerate the proliferation of malignant cells and cultured endothelial cells in vitro.
  • Moreover, M-CSF treatment induced the systemic elevation of vascular endothelial growth factor (VEGF).
  • VEGFR-2 kinase inhibitor significantly impaired the effect of M-CSF on tumor growth.
  • Even after treatment with carageenan and anti-CD11b mAb in mice, M-CSF increased VEGF production in skeletal muscles, suggesting that systemic VEGF elevation was attributed to skeletal muscle VEGF production.
  • These results suggest that M-CSF promotes tumor growth by increasing endothelial progenitor cells and activating angiogenesis, and the effects of M-CSF are largely based on the induction of systemic VEGF from skeletal muscles.
  • [MeSH-major] Carcinoma, Lewis Lung / blood supply. Carcinoma, Lewis Lung / immunology. Macrophage Colony-Stimulating Factor / physiology. Muscle, Skeletal / metabolism. Neovascularization, Pathologic / immunology. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] Animals. Cell Line. Cell Proliferation. Endothelium, Vascular / immunology. Endothelium, Vascular / pathology. Humans. Male. Mice. Mice, Inbred C57BL. Microcirculation / immunology. Microcirculation / pathology. NIH 3T3 Cells. Neoplastic Cells, Circulating / immunology. Neoplastic Cells, Circulating / pathology. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Signal Transduction / immunology. Stem Cells / immunology. Stem Cells / pathology. Tumor Cells, Cultured

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  • (PMID = 15944252.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Vascular Endothelial Growth Factor A; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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34. Brassens S, Chevalier JM, Leblainvaux M: [A strange case of phlebitis]. Ann Cardiol Angeiol (Paris); 2003 Dec;52(6):375-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This sarcoma developed from the smooth muscle of a leg vessel, probably a vein.
  • Leiomyosarcoma is a malignant mesenchymal tumor of specialized connective tissue, with a strong potential for local proliferation and metastatic spread.
  • The diagnosis suggested by imaging techniques (in particular MRI) is first and foremost immunohistochemical.
  • The treatment is surgical when possible, associated with radiotherapy and chemotherapy as appropriate.
  • The prognosis is especially poor when the diagnosis is made at the metastatic stage.
  • [MeSH-major] Leiomyosarcoma / diagnosis. Popliteal Vein / pathology. Thrombophlebitis / diagnosis
  • [MeSH-minor] Aged. Aged, 80 and over. Fatal Outcome. Humans. Knee / blood supply. Lung Neoplasms / secondary. Male

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  • (PMID = 14752921.001).
  • [ISSN] 0003-3928
  • [Journal-full-title] Annales de cardiologie et d'angéiologie
  • [ISO-abbreviation] Ann Cardiol Angeiol (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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35. Boedeker CC, Ridder GJ, Weerda N, Maier W, Klenzner T, Schipper J: [Etiology and therapy of the internal jugular vein thrombosis]. Laryngorhinootologie; 2004 Nov;83(11):743-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Etiology and therapy of the internal jugular vein thrombosis].
  • Complications include pulmonary embolism, sepsis with septic emboli to different organs and tissues as well as intracranial propagation of the thrombus with cerebral edema.
  • As any thrombosis, IJVT is precipitated by Virchow's triad: endothelial damage, alteration of blood flow and hypercoagulability.
  • Imaging procedures frequently used to diagnose an IJVT include sonography with color-coded duplex sonography, computed tomography, magnetic resonance imaging as well as magnetic resonance venography.
  • Up to date, there is no standardized treatment regimen for patients with an IJVT.
  • RESULTS: In five cases, the thrombosis was associated with a malignant tumor.
  • In four patients, it was caused by a deep neck space infection and in one case the IJVT was due to cervical, intravenous drug abuse.
  • Two patients were found to be pregnant (one tumor patient and one patient with a deep neck space infection).
  • In all cases, a ten day treatment regimen with intravenous antibiotics and anticoagulant therapy was initiated.
  • In three patients a revascularization of the affected vessel could be demonstrated with color-coded duplex sonography six months after the initial presentation.
  • Since the clinical presentation may be vague or misleading, a high degree of suspicion is required to make the diagnosis.
  • Whenever the thrombosis is not caused by an inflammatory process, a malignant tumor should be excluded.
  • We recommend a therapy with intravenous antibiotics as well as a systemic anticoagulation.
  • Ligation or resection of the internal jugular vein is reserved for patients who develop complications despite adequate medical therapy.
  • [MeSH-minor] Administration, Oral. Adult. Aged. Anti-Bacterial Agents / administration & dosage. Cefuroxime / administration & dosage. Cellulitis / complications. Cellulitis / diagnosis. Cellulitis / therapy. Diagnosis, Differential. Enoxaparin / administration & dosage. Female. Heparin / administration & dosage. Heroin Dependence / complications. Humans. Infusions, Intravenous. Long-Term Care. Male. Middle Aged. Pregnancy. Pregnancy Complications / diagnosis. Pregnancy Complications / etiology. Pregnancy Complications / therapy. Prognosis. Retrospective Studies. Substance Abuse, Intravenous / complications

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  • (PMID = 15538664.001).
  • [ISSN] 0935-8943
  • [Journal-full-title] Laryngo- rhino- otologie
  • [ISO-abbreviation] Laryngorhinootologie
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Enoxaparin; 9005-49-6 / Heparin; O1R9FJ93ED / Cefuroxime
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36. Davidoff AM, Kandel JJ: Antiangiogenic therapy for the treatment of pediatric solid malignancies. Semin Pediatr Surg; 2004 Feb;13(1):53-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiangiogenic therapy for the treatment of pediatric solid malignancies.
  • Although the past 30 years have seen remarkable progress in the treatment of childhood malignancies, not all types of cancer have enjoyed this improvement in prognosis.
  • Because of this, clinical trials are ongoing in which novel treatment approaches are being evaluated, including immunotherapy, radionuclide therapy, and the use of agents that induce tumor apoptosis or differentiation.
  • Additional treatment strategies are needed, however.
  • Angiogenesis is the biologic process of new blood vessel formation.
  • Compelling data suggest that inhibition of angiogenesis can not only prevent tumor-associated neovascularization but also affect tumor growth and spread.
  • An anticancer approach in which the tumor-induced new blood vessels are targeted is particularly appealing for several reasons.
  • First, despite the extreme molecular and phenotypic heterogeneity of human cancer, it is likely that most, if not all, tumor types require neovascularization to achieve their full malignant phenotype.
  • Therefore, antiangiogenic therapy may have broad applicability for the treatment of human cancer, as well as the many other pathologic processes that depend on angiogenesis.
  • This is in distinction to the rapidly proliferating tumor cells that do undergo a high rate of spontaneous mutation and therefore can readily generate drug-resistant clones.
  • This review discusses progress in the development of antiangiogenic therapy for the treatment of pediatric solid tumors.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neoplasms / blood supply. Neoplasms / drug therapy. Neovascularization, Pathologic / prevention & control
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Child. Drug Therapy, Combination. Genetic Therapy / methods. Humans. Models, Biological. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 14765371.001).
  • [ISSN] 1055-8586
  • [Journal-full-title] Seminars in pediatric surgery
  • [ISO-abbreviation] Semin. Pediatr. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 61
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37. Sorensen DR, Read TA, Porwol T, Olsen BR, Timpl R, Sasaki T, Iversen PO, Benestad HB, Sim BK, Bjerkvig R: Endostatin reduces vascularization, blood flow, and growth in a rat gliosarcoma. Neuro Oncol; 2002 01;4(1):1-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endostatin reduces vascularization, blood flow, and growth in a rat gliosarcoma.
  • In rats in which s.c. gliomas were grown for a total of 29 days, systemic treatment with recombinant murine endostatin induced about 50% reduction of intratumoral blood flow and tumor size after only 10 days of therapy.
  • In contrast, the blood flow to irrelevant organs was unaffected by endostatin, indicating its specificity of action.
  • Tumors were not observed to increase in size or regrow after cessation of therapy.
  • Furthermore, endostatin-treated rats with i.c. tumors had significantly longer survival time than did untreated controls.
  • In the treated rats, endostatin therapy resulted in a reduced tumor blood vessel volume and an increased tumor cell density with an increased apoptotic index within a given tumor volume, as verified by flow cytometry and by staining with deoxynucleotidyltransferase-mediated dUTP nick-end labeling.
  • This work verifies the general anti-angiogenic and antitumor effects of endostatin and indicates that the protein may also be considered as a treatment strategy for malignant brain tumors.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Brain Neoplasms / blood supply. Brain Neoplasms / physiopathology. Collagen / pharmacology. Gliosarcoma / blood supply. Gliosarcoma / physiopathology. Neovascularization, Pathologic / pathology. Peptide Fragments / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Collagen Type XVIII. Endostatins. Fluorescent Antibody Technique. Humans. Mice. Microscopy, Confocal. Microscopy, Fluorescence. Neoplasm Transplantation. Rats. Rats, Inbred Strains. Regional Blood Flow / drug effects. Skin Neoplasms. Tumor Cells, Cultured

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  • (PMID = 11772427.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR 36819; United States / NIAMS NIH HHS / AR / AR 36820
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Collagen Type XVIII; 0 / Endostatins; 0 / Peptide Fragments; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ PMC1920634
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38. Deville JL, Salas S, Figarella-Branger D, Ouafik L, Daniel L: Adrenomedullin as a therapeutic target in angiogenesis. Expert Opin Ther Targets; 2010 Oct;14(10):1059-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenomedullin as a therapeutic target in angiogenesis.
  • IMPORTANCE OF THE FIELD: Hypoxia, a frequent characteristic in the microenvironment of solid tumors, leads to adrenomedullin (AM) upregulation through the hypoxia inducible factor-1 pathway, explaining its high expression in a variety of malignant tissues.
  • AM is believed to play an important role in tumor progression and angiogenesis in many cancers.
  • Therefore, it could become a new therapeutic target.
  • AREAS COVERED IN THIS REVIEW: We performed a review of the literature based on published data to highlight AM's critical roles in tumor cell growth and cancer invasiveness, and its involvement in tumor angiogenesis through promotion of recruitment of hematopoietic progenitors, vascular morphogenesis, and blood vessel stabilization and maturation.
  • WHAT THE READER WILL GAIN: The goal of this review is to inform readers about the role of AM in tumor angiogenesis and cancer progression and, therefore, about its possible place as a new therapeutic target.
  • TAKE HOME MESSAGE: Taken together, these data support targeting the AM pathway as a new potential therapy in cancer, complementary to other existing treatments.
  • [MeSH-major] Adrenomedullin / antagonists & inhibitors. Molecular Targeted Therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Animals. Anoxia / metabolism. Cell Differentiation. Cell Proliferation. Disease Progression. Humans. Hypoxia-Inducible Factor 1 / metabolism. Mice. Neoplasms / blood supply. Neoplasms / drug therapy. Neoplasms / metabolism. Treatment Outcome. Vascular Endothelial Growth Factor A / metabolism

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  • [CommentIn] Expert Opin Ther Targets. 2010 Nov;14(11):1135-8 [20942743.001]
  • (PMID = 20846006.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Hypoxia-Inducible Factor 1; 0 / Vascular Endothelial Growth Factor A; 148498-78-6 / Adrenomedullin
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39. Cheng YY, Huang L, Lee KM, Li K, Kumta SM: Alendronate regulates cell invasion and MMP-2 secretion in human osteosarcoma cell lines. Pediatr Blood Cancer; 2004 May;42(5):410-5
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  • BACKGROUND: Osteosarcoma is the most common malignant bone tumor of childhood.
  • Significant proportions of these patients eventually develop pulmonary metastases and succumb to their disease even after conventional multi-agent chemotherapy and surgical excision.
  • Matrix metalloproteinase (MMP)-2 induced degradation of blood vessel basement membranes is an important pre-requisite for tumor invasion and metastasis.
  • Bisphosphonates (BPs) have been known to inhibit tumor growth and metastasis in some tumors such as breast cancer, renal cell carcinoma, and prostate cancer, and may do so through inhibition of MMP secretion.
  • We, therefore, tested the effect of BPs on tumor cell invasion, MMP-2 secretion, and apoptosis of osteosarcoma cell lines.
  • PROCEDURE: Two osteosarcoma cell lines (SaOS-2, U(2)OS) were treated with alendronate (50, 100, and 150 microM) for 24 and 48 hr.
  • Matrigel invasion assay was used to investigate the invasive potential of osteosarcoma cell lines before and after alendronate treatment.
  • Real-time quantitative RT-PCR was used to determine the mRNA level of MMP-2 with and without alendronate treatment.
  • Alendronate reduced the mRNA level and cellular level of MMP-2 in both cell lines in a time and dose-dependent manner.
  • Our finding suggests that alendronate downregulates MMP-2 secretion and induces apoptosis in osteosarcoma cells, which may both contribute to the reduction of invasive potential of the tumor cells.
  • [MeSH-major] Alendronate / pharmacology. Matrix Metalloproteinase 2 / secretion. Neoplasm Invasiveness / prevention & control. Osteosarcoma / pathology
  • [MeSH-minor] Apoptosis / drug effects. Cell Culture Techniques / methods. Cell Line, Tumor. Dose-Response Relationship, Drug. Extracellular Matrix Proteins. Humans. RNA / analysis

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15049011.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 63231-63-0 / RNA; EC 3.4.24.24 / Matrix Metalloproteinase 2; X1J18R4W8P / Alendronate
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40. Bechet D, Tirand L, Faivre B, Plénat F, Bonnet C, Bastogne T, Frochot C, Guillemin F, Barberi-Heyob M: Neuropilin-1 targeting photosensitization-induced early stages of thrombosis via tissue factor release. Pharm Res; 2010 Mar;27(3):468-79
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuropilin-1 targeting photosensitization-induced early stages of thrombosis via tissue factor release.
  • PURPOSE: This article characterizes the vascular effects following vascular-targeted photodynamic therapy with a photosensitizer which actively targets endothelial cells.
  • METHODS: This strategy was considered by coupling a chlorin to a heptapeptide targeting neuropilin-1 in human malignant glioma-bearing nude mice.
  • A laser Doppler microvascular perfusion monitor was used to monitor microvascular blood perfusion in tumor tissue.
  • The consequences of photosensitization on tumor vessels, tissue factor expression, fibrinogen consumption, and thrombogenic effects were studied by immunohistochemical staining.
  • RESULTS: Treatment of glioma-bearing mice with the conjugate showed a statistically significant tumor growth delay.
  • Vascular effect was characterized by a decrease in tumor tissue blood flow at about 50% baseline during treatment not related to variations in temperature.
  • This vascular shutdown was mediated by tumor blood vessels' congestion.
  • A pro-thrombotic behavior of targeted endothelial cells in the absence of ultra structural changes led to the induction of tissue factor expression from the earliest times post-treatment.
  • Expression of tissue factor-initiated thrombi formation was also related to an increase in fibrinogen consumption.
  • CONCLUSION: Using a peptide-conjugated photosensitizer targeting neuropilin-1, induction of tissue factor expression immediately post-treatment, led to the establishment of thrombogenic effects within the vessel lumen.
  • [MeSH-major] Glioma / drug therapy. Neuropilin-1 / metabolism. Photosensitizing Agents / therapeutic use. Thromboplastin / metabolism. Thrombosis / chemically induced
  • [MeSH-minor] Animals. Blood Vessels / drug effects. Blood Vessels / pathology. Endothelial Cells / drug effects. Endothelial Cells / pathology. Female. Humans. Mice. Mice, Nude. Oligopeptides / chemistry. Oligopeptides / pharmacology. Oligopeptides / therapeutic use. Photochemotherapy. Porphyrins / chemistry. Porphyrins / pharmacology. Porphyrins / therapeutic use

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  • (PMID = 20087632.001).
  • [ISSN] 1573-904X
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Photosensitizing Agents; 0 / Porphyrins; 144713-63-3 / Neuropilin-1; 2683-84-3 / chlorin; 9035-58-9 / Thromboplastin
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41. Reardon DA, Egorin MJ, Desjardins A, Vredenburgh JJ, Beumer JH, Lagattuta TF, Gururangan S, Herndon JE 2nd, Salvado AJ, Friedman HS: Phase I pharmacokinetic study of the vascular endothelial growth factor receptor tyrosine kinase inhibitor vatalanib (PTK787) plus imatinib and hydroxyurea for malignant glioma. Cancer; 2009 May 15;115(10):2188-98
Hazardous Substances Data Bank. IMATINIB MESYLATE .

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  • [Title] Phase I pharmacokinetic study of the vascular endothelial growth factor receptor tyrosine kinase inhibitor vatalanib (PTK787) plus imatinib and hydroxyurea for malignant glioma.
  • BACKGROUND: This study determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, vatalanib, when administered with imatinib and hydroxyurea on a continuous daily schedule among recurrent malignant glioma patients.
  • Imatinib was dosed at 400 mg per day for patients not taking enzyme-inducing antiepileptic drugs (EIAEDs; stratum A) and at 500 mg twice-a-day for patients taking EIAEDs (stratum B).
  • Pharmacokinetics of each drug were assessed.
  • RESULTS: A total of 37 recurrent patients, 34 (92%) with glioblastoma and 3 (8%) with grade 3 malignant glioma, were enrolled.
  • No patients developed intracranial hemorrhage.
  • Strategies to target tumor blood vessel endothelial cells and pericytes by inhibiting VEGFR and platelet-derived growth factor, respectively, were safe among recurrent malignant glioma patients and may enhance antiangiogenesis activity.

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  • (PMID = 19248046.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108786; United States / NINDS NIH HHS / NS / 5P50-NS20023; United States / NCRR NIH HHS / RR / M01 RR 30; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NCI NIH HHS / CA / 2P30 CA47904; United States / NCI NIH HHS / CA / P30 CA047904; United States / NINDS NIH HHS / NS / NS020023-250020; United States / NCI NIH HHS / CA / 5 R37 CA11898; United States / NCI NIH HHS / CA / 5 P50 CA 108786-4; United States / NINDS NIH HHS / NS / P50 NS020023-250020; United States / NCI NIH HHS / CA / R37 CA011898
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Phthalazines; 0 / Piperazines; 0 / Pyridines; 0 / Pyrimidines; 5DX9U76296 / vatalanib; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
  • [Other-IDs] NLM/ NIHMS113633; NLM/ PMC2691174
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42. Thors L, Bergh A, Persson E, Hammarsten P, Stattin P, Egevad L, Granfors T, Fowler CJ: Fatty acid amide hydrolase in prostate cancer: association with disease severity and outcome, CB1 receptor expression and regulation by IL-4. PLoS One; 2010 Aug 19;5(8):e12275
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  • Here we have investigated the expression of the endocannabinoid metabolising enzyme fatty acid amide hydrolase (FAAH) in a well characterised tissue microarray from patients diagnosed with prostate cancer at transurethral resection for voiding problems.
  • METHODOLOGY/PRINCIPAL FINDINGS: FAAH immunoreactivity (FAAH-IR) was assessed in formalin-fixed paraffin-embedded non-malignant and tumour cores from 412 patients with prostate cancer.
  • FAAH-IR was seen in epithelial cells and blood vessel walls but not in the stroma.
  • Tumour epithelial FAAH-IR was positively correlated with the disease severity at diagnosis (Gleason score, tumour stage, % of the specimen that contained tumour) for cases with mid-range CB(1)IR scores, but not for those with high CB(1)IR scores.
  • For the 281 cases who only received palliative therapy at the end stages of the disease, a high tumour epithelial FAAH-IR was associated with a poor disease-specific survival.
  • The correlation with CB(1)IR in the tumour tissue may be related to a common local dysregulation by a component of the tumour microenvironment.

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  • (PMID = 20808855.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA011322; United States / NIDA NIH HHS / DA / DA11322
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, Cannabinoid, CB1; 207137-56-2 / Interleukin-4; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.5.- / Amidohydrolases; EC 3.5.1.- / fatty-acid amide hydrolase
  • [Other-IDs] NLM/ PMC2924377
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43. Uhl M, Aulwurm S, Wischhusen J, Weiler M, Ma JY, Almirez R, Mangadu R, Liu YW, Platten M, Herrlinger U, Murphy A, Wong DH, Wick W, Higgins LS, Weller M: SD-208, a novel transforming growth factor beta receptor I kinase inhibitor, inhibits growth and invasiveness and enhances immunogenicity of murine and human glioma cells in vitro and in vivo. Cancer Res; 2004 Nov 1;64(21):7954-61
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  • The cytokine transforming growth factor (TGF)-beta, by virtue of its immunosuppressive and promigratory properties, has become a major target for the experimental treatment of human malignant gliomas.
  • Peripheral blood lymphocytes or purified T cells, cocultured with TGF-beta-releasing LN-308 glioma cells in the presence of SD-208, exhibit enhanced lytic activity against LN-308 targets.
  • The release of interferon gamma and tumor necrosis factor alpha by these immune effector cells is enhanced by SD-208, whereas the release of interleukin 10 is reduced.
  • Systemic SD-208 treatment initiated 3 days after the implantation of SMA-560 cells into the brains of syngeneic VM/Dk mice prolongs their median survival from 18.6 to 25.1 days.
  • Histologic analysis revealed no difference in blood vessel formation, proliferation, or apoptosis.
  • However, animals responding to SD-208 showed an increased tumor infiltration by natural killer cells, CD8 T cells, and macrophages.
  • These data define TGF-beta receptor I kinase inhibitors such as SD-208 as promising novel agents for the treatment of human malignant glioma and other conditions associated with pathological TGF-beta activity.
  • [MeSH-major] Activin Receptors, Type I / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Glioma / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Receptors, Transforming Growth Factor beta / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Humans. Male. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Signal Transduction. Transforming Growth Factor beta / antagonists & inhibitors. Transforming Growth Factor beta1. Transforming Growth Factor beta2

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  • (PMID = 15520202.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Transforming Growth Factor beta; 0 / TGFB1 protein, human; 0 / TGFB2 protein, human; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Transforming Growth Factor beta2; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / Activin Receptors, Type I
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44. Lee S: What tumor vessels can tell us. Pigment Cell Melanoma Res; 2010 Jun;23(3):309-11
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  • [Title] What tumor vessels can tell us.
  • Resistance to antiangiogenic therapy is directed by vascular phenotype, vessel stabilization,and maturation in malignant melanoma. J. Exp. Med. 207, 491-503.
  • [MeSH-major] Neoplasms / blood supply. Neovascularization, Pathologic / pathology
  • [MeSH-minor] Animals. Endothelial Cells / drug effects. Endothelial Cells / pathology. Humans. Mice. Neoplasm Metastasis. Pericytes / drug effects. Pericytes / pathology. Phenotype. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor A / pharmacology. Vascular Endothelial Growth Factor A / therapeutic use

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  • (PMID = 20403121.001).
  • [ISSN] 1755-148X
  • [Journal-full-title] Pigment cell & melanoma research
  • [ISO-abbreviation] Pigment Cell Melanoma Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A
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45. Matsumoto S, Kawaguchi N, Manabe J, Tanizawa T, Koyama S, Ae K, Shimoji T: [Surgical treatment for bone and soft tissue sarcoma]. Gan To Kagaku Ryoho; 2004 Sep;31(9):1314-8
MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.

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  • [Title] [Surgical treatment for bone and soft tissue sarcoma].
  • There are many kinds of wide excision or wide resection, which are methods to remove the tumor with surrounding tissues.
  • The curability of wide resection depends on the range and characteristics of the normal surrounding tissues.
  • Causes of the local recurrence are 1) insufficient surgical margin, 2) skip metastasis, 3) tumor thrombus, and 4) lymph node metastasis.
  • The so-called "Safety surgical margin" is the margin that prevents local recurrence due to insufficient surgical treatment.
  • Local recurrence due to other causes can not be treated by surgery alone as chemotherapy is also required.
  • For example, the infiltrative type of malignant fibrous histiocytoma requires a curative procedure.
  • On the other hand, non-infiltrative types of sarcoma or high-grade sarcoma, which are good responders to preoperative treatment, are locally controlled by an adequate wide margin procedure.
  • When the tumor is close to the bone, main vessels and/or nerves, it is sometimes very difficult to preoperatively decide whether or not to sacrifice these important organs.
  • Once postoperative complications occur, patients must remain in the hospital for a long time.
  • To prevent this, the preservation of normal tissue, meaning reduction of surgical margin, is important.
  • [MeSH-major] Bone Neoplasms / surgery. Sarcoma / surgery. Soft Tissue Neoplasms / surgery
  • [MeSH-minor] Blood Vessel Prosthesis Implantation. Humans. Lymphatic Metastasis. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control. Quality of Life. Surgical Procedures, Operative / methods. Survival Rate

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  • (PMID = 15446549.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 6
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46. Casanova ML, Blázquez C, Martínez-Palacio J, Villanueva C, Fernández-Aceñero MJ, Huffman JW, Jorcano JL, Guzmán M: Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest; 2003 Jan;111(1):43-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors.
  • Different therapeutic strategies for the treatment of these tumors are currently being investigated.
  • Given the growth-inhibiting effects of cannabinoids on gliomas and the wide tissue distribution of the two subtypes of cannabinoid receptors (CB(1) and CB(2)), we studied the potential utility of these compounds in anti-skin tumor therapy.
  • In cell culture experiments pharmacological activation of cannabinoid receptors induced the apoptotic death of tumorigenic epidermal cells, whereas the viability of nontransformed epidermal cells remained unaffected.
  • Local administration of the mixed CB(1)/CB(2) agonist WIN-55,212-2 or the selective CB(2) agonist JWH-133 induced a considerable growth inhibition of malignant tumors generated by inoculation of epidermal tumor cells into nude mice.
  • This was accompanied by impairment of tumor vascularization, as determined by altered blood vessel morphology and decreased expression of proangiogenic factors (VEGF, placental growth factor, and angiopoietin 2).
  • These results support a new therapeutic approach for the treatment of skin tumors.

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  • (PMID = 12511587.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA003590; United States / NIDA NIH HHS / DA / DA03590
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1,1-dimethylbutyl-1-deoxy-Delta(9)-THC; 0 / Angiogenesis Inducing Agents; 0 / Angiopoietin-2; 0 / Antineoplastic Agents; 0 / Benzoxazines; 0 / Cannabinoids; 0 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / Morpholines; 0 / Naphthalenes; 0 / Receptors, Cannabinoid; 0 / Receptors, Drug; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 134959-51-6 / Win 55212-2; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ PMC151833
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47. Goldbrunner RH, Bendszus M, Wood J, Kiderlen M, Sasaki M, Tonn JC: PTK787/ZK222584, an inhibitor of vascular endothelial growth factor receptor tyrosine kinases, decreases glioma growth and vascularization. Neurosurgery; 2004 Aug;55(2):426-32; discussion 432
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Flk-1 expression was positive within tumor vessels in V(+) gliomas, whereas all C6 clones were negative for fetal liver kinase-1 in vitro.
  • Early (POD 1-12) and delayed (POD 7-12) application of PTK787/ZK222584 in V(+) glioma-bearing animals resulted in a significant reduction of tumor size (71% and 36%, P < 0.05) as measured by magnetic resonance imaging volumetry.
  • Vessel density was significantly reduced (42.3% and 25.7%, P < 0.05), and areas of intratumoral necrosis were enlarged (by 1.7-fold after early treatment).
  • CONCLUSION: PTK787/ZK222584 significantly halted VEGF-mediated glioma growth by inhibition of neovascularization and proliferation, providing a promising new tool in malignant glioma therapy.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Brain Neoplasms / blood supply. Brain Neoplasms / pathology. Cell Division / drug effects. Cell Survival / drug effects. Glioma / blood supply. Glioma / pathology. Neovascularization, Pathologic / pathology. Phthalazines / pharmacology. Pyridines / pharmacology. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / transplantation
  • [MeSH-minor] Animals. Brain / pathology. Male. Neoplasm Transplantation. Rats. Rats, Sprague-Dawley. Transfection. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 15271251.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Phthalazines; 0 / Pyridines; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, rat; 5DX9U76296 / vatalanib; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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48. Philipp J, Dienst A, Unruh M, Wagener A, Grunow A, Engert A, Fries JW, Gottstein C: Soluble tissue factor induces coagulation on tumor endothelial cells in vivo if coadministered with low-dose lipopolysaccharides. Arterioscler Thromb Vasc Biol; 2003 May 1;23(5):905-10
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  • [Title] Soluble tissue factor induces coagulation on tumor endothelial cells in vivo if coadministered with low-dose lipopolysaccharides.
  • OBJECTIVE: This study was performed to evaluate the mechanisms leading to tumor vessel occlusion by tissue factor-based drugs, which are used in vascular targeting approaches for the treatment of malignant tumors.
  • METHODS AND RESULTS: The effects of nontargeted soluble tissue factor were evaluated in vitro and in vivo.
  • Tumor-bearing mice were treated with (1) the extracellular portion of tissue factor (soluble tissue factor), (2) low nontoxic doses of lipopolysaccharides, or (3) a combination thereof.
  • The combination treatment showed the best effects and resulted in selective thrombosis of tumor vessels.
  • On the basis of our data from subsequent in vitro analyses, including surface plasmon resonance measurements and endothelial cell based coagulation assays, we propose a model on how soluble tissue factor, although lacking its membrane anchor, can promote selective tumor vessel occlusion.
  • CONCLUSIONS: To our knowledge, this is the first report to describe the molecular mechanisms of coagulation induction by untargeted soluble tissue factor in vivo.
  • Combination treatments including soluble tissue factor might represent an alternative vascular targeting approach for the treatment of malignant tumors.
  • [MeSH-major] Blood Coagulation / drug effects. Embolization, Therapeutic / methods. Lipopolysaccharides / therapeutic use. Lymphoma, Non-Hodgkin / therapy. Teratocarcinoma / therapy. Thromboplastin / therapeutic use
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Drug Synergism. Drug Therapy, Combination. Enzyme Activation / drug effects. Factor Xa / biosynthesis. Humans. Mice. Mice, Inbred BALB C. Mice, SCID. Peptide Fragments / administration & dosage. Peptide Fragments / pharmacology. Peptide Fragments / therapeutic use. Recombinant Proteins / administration & dosage. Recombinant Proteins / pharmacology. Recombinant Proteins / therapeutic use. Solubility. Surface Plasmon Resonance. Tumor Necrosis Factor-alpha / analysis. Xenograft Model Antitumor Assays

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  • (PMID = 12649087.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / Peptide Fragments; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / lipopolysaccharide, E coli O55-B5; 9035-58-9 / Thromboplastin; EC 3.4.21.6 / Factor Xa
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49. Lamszus K, Kunkel P, Westphal M: Invasion as limitation to anti-angiogenic glioma therapy. Acta Neurochir Suppl; 2003;88:169-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Invasion as limitation to anti-angiogenic glioma therapy.
  • The inhibition of tumor angiogenesis could be an efficient therapeutic strategy for the treatment of malignant gliomas.
  • Experimentally, it was shown that especially during early stages of growth in rodent brain, glioma cells can coopt the preexistent host vasculature to recruit their blood supply in the absence of neovascularization.
  • This phenomenon was only observed in orthotopic models in which the tumor cells were implanted into the brain which is a densely vascularized environment, but not in subcutaneous models in which tumor cells are implanted into a virtual space.
  • Using an orthotopic mouse model, we analyzed whether systemic anti-angiogenic therapy with an antibody against the vascular endothelial growth factor receptor-2 (VEGFR-2) could inhibit intracerebral growth of xenografted human glioblastoma cells and what effect this treatment had on tumor morphology and invasiveness.
  • We found that anti-angiogenic therapy inhibited tumor growth by 80% compared to buffer-treated controls.
  • These satellites usually contained central vessel cores, and tumor cells often had migrated along blood vessels over long distances to eventually reach the surface and spread in the subarachnoid space.
  • Systemic anti-angiogenic therapy can thus apparently increase the invasiveness of gliomas in the orthotopic model.
  • Tumor cell invasion was tightly associated with preexistent blood vessels, suggesting that increased cooption of the host vasculature could represent a compensatory mechanism that is selected for by inhibiting adequate tumor vascularization.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / blood supply. Glioma / blood supply. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors
  • [MeSH-minor] Animals. Brain / drug effects. Brain / pathology. Humans. Mice. Microcirculation / drug effects. Microcirculation / pathology. Neoplasm Invasiveness / pathology. Neoplasm Transplantation. Rats

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  • (PMID = 14531575.001).
  • [ISSN] 0065-1419
  • [Journal-full-title] Acta neurochirurgica. Supplement
  • [ISO-abbreviation] Acta Neurochir. Suppl.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Number-of-references] 36
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50. Nabha SM, Mohammad RM, Wall NR, Dutcher JA, Salkini BM, Pettit GR, Al-Katib AM: Evaluation of combretastatin A-4 prodrug in a non-Hodgkin's lymphoma xenograft model: preclinical efficacy. Anticancer Drugs; 2001 Jan;12(1):57-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have previously reported on the in vitro activity of CA4P against a panel of malignant human B-lymphoid cell lines.
  • Tumor-bearing mice were treated at the CA4P maximum tolerated dose (MTD) of 800 mg/kg in different dose/schedules.
  • Immunohistochemical staining using anti-CD31 antibody after 6, 24, 48 and 120 h treatment revealed a significant decrease in the number of tumor blood vessels after 24 h (about 80%).
  • Only the periphery of treated tumors revealed the presence of blood vessels.
  • New blood vessel formation was noted to emerge in tumor tissues as early as 48 h following a single dose of CA4P.
  • We conclude that CA4P has antiangiogenic activity in this lymphoma model and the use of this agent should be explored clinically in the treatment of non-Hodgkin's lymphoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Lymphoma, Non-Hodgkin / drug therapy. Prodrugs / pharmacology. Stilbenes / pharmacology. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Female. Humans. Maximum Tolerated Dose. Mice. Mice, Inbred ICR. Mice, SCID. Neovascularization, Pathologic / drug therapy. Survival Rate

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  • (PMID = 11272287.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA44344-10-12; United States / NCI NIH HHS / CA / CA79837; United States / NCI NIH HHS / CA / P30 CA22453-20
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Prodrugs; 0 / Stilbenes; I5590ES2QZ / fosbretabulin
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51. Nishinari K, Wolosker N, Yazbek G, Zerati AE, Nishimoto IN: Venous reconstructions in lower limbs associated with resection of malignancies. J Vasc Surg; 2006 Nov;44(5):1046-50
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  • BACKGROUND: Patients with tumors in the limbs who undergo surgical treatment may have involvement of major vessels.
  • The objective of this study was to analyze the results from surgical treatment of a sample of patients who underwent lower limb venous reconstructions associated with the resection of malignant tumors.
  • METHODS: Follow-up was performed of 17 patients with malignant tumors involving major vessels in the lower limbs.
  • One patient experienced regional disease recurrence and is undergoing chemotherapy.
  • CONCLUSIONS: Lower limb venous reconstructions associated with tumor resection in this study gave good functional results, although the prognosis for these patients had been unfavorable.
  • [MeSH-major] Blood Vessel Prosthesis Implantation / methods. Bone Neoplasms / surgery. Muscle Neoplasms / surgery. Peripheral Vascular Diseases / surgery. Saphenous Vein / surgery. Sarcoma, Synovial / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Constriction, Pathologic. Female. Follow-Up Studies. Humans. Leg. Male. Middle Aged. Retrospective Studies. Time Factors. Treatment Outcome

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  • (PMID = 17098540.001).
  • [ISSN] 0741-5214
  • [Journal-full-title] Journal of vascular surgery
  • [ISO-abbreviation] J. Vasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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52. Turowski B, Zanella FE: Interventional neuroradiology of the head and neck. Neuroimaging Clin N Am; 2003 Aug;13(3):619-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Vascular interventions are important and helpful for treatment of various pathologies of the head and neck.
  • Interventional neuroradiology of the head and neck includes image-guided biopsies, vessel occlusion, and local chemotherapy.
  • Knowledge of anatomy, functional relationships between intra- and extracranial vessels, and pathology are the basis for therapeutic success.
  • Neuroradiologic imaging, especially CT and MR imaging, and appropriate analysis of angiographic findings help ensure indication for treatment and plan an intervention.
  • Indications for vessel occlusion are emergency situations to stop bleeding in vascular lesions (traumatic, malformation, or tumors) by reduction of pressure, preoperative reduction of blood flow to minimize the surgical risk, palliative occlusion of feeding vessels to produce tumor necrosis, or potential curative (or presurgical) occlusion of vascular malformations.
  • Pressure reduction to support normal coagulation, such as epistaxis, in hereditary hemorrhagic telangiectasia can be achieved by proximal vessel occlusion with large particles or platinum coils.
  • Examples of these interventions are: a hemangioma of the hard palate, a juvenile angiofibroma, a hemangiopericytoma, a malignant meningioma, a malignant fibrous histiocytoma, and a glomus tumor.
  • Effective treatment of vascular malformations, such as AV fistulas or angiomas, needs exact occlusion of the fistula or the angiomatous nidus, which is demonstrated in the case of an AV angioma of the base of the tongue.
  • Chemotherapy with local intra-arterial cisplatin combined with intravenous administration of sodium thiosulfate as antidote is indicated as an adjuvant modality in a multimodal regimen of oropharyngeal squamous cell carcinoma or as palliative treatment of recurrent and otherwise untreatable malignant tumors of the head and neck.
  • Palliative treatment of a bleeding oropharyngeal cancer is another example of interventional treatment.
  • Selective treatment, either occluding or pharmacologic, may be preoperative, palliative, or curative.
  • The objective is reduction of surgical risk, improvement of quality of life, or curative therapy of a lesion.
  • Thus, the interventional treatment should not be associated with morbidity or mortality.
  • The benefits, risks, and expected damages of neuroradiologic interventions must be balanced during the informed consent procedure with the patient.
  • [MeSH-major] Head and Neck Neoplasms / radiography. Head and Neck Neoplasms / therapy. Neuroradiography. Radiology, Interventional

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  • (PMID = 14631695.001).
  • [ISSN] 1052-5149
  • [Journal-full-title] Neuroimaging clinics of North America
  • [ISO-abbreviation] Neuroimaging Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 40
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53. Wakabayashi I, Groschner K: Vascular actions of anthracycline antibiotics. Curr Med Chem; 2003 Mar;10(5):427-36
Hazardous Substances Data Bank. NITRIC OXIDE .

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  • Anthracycline antibiotics are of particular value in the therapy of malignant diseases and exert profound effects not only on tumor cells but also on cells in the cardiovascular system.
  • These quinone drugs affect vascular tone by a multitude of mechanisms, including acute modulation of Ca(2+) homeostasis, altered expression of membrane proteins and enzymes that are involved in the control of smooth muscle contraction, and generation of autoregulatory mediators, such as nitric oxide and endothelin.
  • Anthracyclines interfere with blood coagulation-fibrinolysis balance due to its effects on the production of prostacyclin, plasminogen activator and plasminogen activator inhibitor in the endothelium.
  • The intensity and quality of anthracycline actions on blood vessel function are highly variable and may depend not only on the chemical structure of anthracycline but also on the type of blood vessel as well as the metabolic and redox status of the vascular tissue.
  • Vascular actions of anthracyclines are possibly involved in both beneficial as well as toxic and undesirable side-effects such as tumor progress.
  • Further investigations are required to clarify the relation between specific modifications of vascular cell function and clinical events observed during antineoplastic therapy with anthracyclines.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Blood Vessels / drug effects
  • [MeSH-minor] Animals. Humans. Muscle Contraction / drug effects. Muscle, Smooth, Vascular / drug effects. Muscle, Smooth, Vascular / physiopathology. Nitric Oxide / metabolism. Structure-Activity Relationship

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  • (PMID = 12570699.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 198
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54. van Eekelen M, Sasportas LS, Kasmieh R, Yip S, Figueiredo JL, Louis DN, Weissleder R, Shah K: Human stem cells expressing novel TSP-1 variant have anti-angiogenic effect on brain tumors. Oncogene; 2010 Jun 3;29(22):3185-95
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  • Novel therapeutic agents combined with innovative modes of delivery and non-invasive imaging of drug delivery, pharmacokinetics and efficacy are crucial in developing effective clinical anticancer therapies.
  • In this study, we have created and characterized multiple novel variants of anti-angiogenic protein thrombospondin (aaTSP-1) that comprises unique regions of three type-I-repeats of TSP-1 and used engineered human neural stem cells (hNSC) to provide sustained on-site delivery of secretable aaTSP-1 to tumor-vasculature.
  • Using human glioma cells and hNSC engineered with different combinations of fluorescent and bioluminescent marker proteins and employing multi-modality imaging techniques, we show that aaTSP-1 targets the vascular-component of gliomas and a single administration of hNSC-aaTSP-1 markedly reduces tumor vessel-density that results in inhibition of tumor-progression and increased survival in mice bearing highly malignant human gliomas.
  • We also show that therapeutic hNSC do not proliferate and remain in an un-differentiated state in the brains of glioma-bearing mice.
  • This study provides a platform for accelerated development of future cell-based therapies for cancer.

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  • (PMID = 20305695.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA131980; United States / NCI NIH HHS / CA / P50 CA086355; United States / NINDS NIH HHS / NS / R01 NS071197; United States / NCI NIH HHS / CA / R21CA131980; United States / NCI NIH HHS / CA / P50 CA86355
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Thrombospondin 1
  • [Other-IDs] NLM/ NIHMS387544; NLM/ PMC3390229
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55. Di Benedetto M, Starzec A, Vassy R, Perret GY, Crépin M, Kraemer M: Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative. Br J Cancer; 2003 Jun 16;88(12):1987-94
Genetic Alliance. consumer health - Epidermoid Carcinoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative.
  • In vivo, we explored the effects of NaPaC (15 mg kg(-1)) on A431 xenograft growth starting the drug administration at the time of tumour cell inoculation (early treatment) and 1 week later, when tumours were well established (late treatment).
  • Early treatment was more efficient on tumour inhibition (70% vs control) than late treatment (50% vs control).
  • Early and late NaPaC-treatment increased the aponecrosis in tumour by 70 and 30%, respectively.
  • Whatever treatment, NaPaC inhibited the intratumour endothelial cell density in the same manner.
  • In contrast, vessel area was decreased only when NaPaC was injected early (35%).
  • These results show that NaPaC has a potent inhibitory effect, dependent on treatment outset, on epidermoid carcinoma growth associated with an intratumour microvascular network diminution and an aponecrosis increase.
  • As this drug is nontoxic at efficient dose, it offers interesting perspectives for the therapy of malignant lesions.
  • [MeSH-major] Carcinoma, Squamous Cell / blood supply. Dextrans / pharmacology
  • [MeSH-minor] Animals. Cell Division / drug effects. Endothelial Growth Factors. Endothelium, Vascular / metabolism. Humans. Intercellular Signaling Peptides and Proteins. Lymphokines. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic. Time Factors. Transplantation, Heterologous. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 12799647.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0 / phenylacetate carboxymethyl benzylamide dextran; K3R6ZDH4DU / Dextrans
  • [Other-IDs] NLM/ PMC2741107
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56. Zätterström UK, Fukai N, Olsen BR: [A fragment of collagen XVIII inhibits angiogenesis]. Tidsskr Nor Laegeforen; 2000 Nov 30;120(29):3547-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Malignant tumours may produce substances with both stimulatory and inhibitory effect on angiogenesis.
  • RESULTS: The angiogenesis inhibitor, endostatin, is a 20 kDa C-terminal fragment of collagen XVIII, a proteoglycan/collagen found in vessel walls and basement membranes.
  • The outcome of ongoing clinical trials will determine the role of endostatin as a possible angiogenesis-inhibiting drug in the future.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Collagen / chemistry. Neoplasms / blood supply. Neovascularization, Pathologic / drug therapy. Peptide Fragments / administration & dosage
  • [MeSH-minor] Animals. Endothelial Growth Factors / administration & dosage. Endothelial Growth Factors / chemistry. Humans. Mice. Tumor Cells, Cultured

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  • (PMID = 11188382.001).
  • [ISSN] 0029-2001
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Endothelial Growth Factors; 0 / Peptide Fragments; 9007-34-5 / Collagen
  • [Number-of-references] 21
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