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1. Kawaguchi T, Yamagishi SI, Sata M: Structure-function relationships of PEDF. Curr Mol Med; 2010 Apr;10(3):302-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although PEDF does not inhibit either serine or cysteine proteinases, PEDF exerts diverse physiological activities including anti-angiogenesis, anti-vasopermeability, anti-tumor, and neurotrophic activities.
  • In this review, we summarize structural features of PEDF that could affect various target organs such as blood vessels, tumors, and the central nervous system.

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  • (PMID = 20236052.001).
  • [ISSN] 1875-5666
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Eye Proteins; 0 / Nerve Growth Factors; 0 / Protease Inhibitors; 0 / Receptors, Neuropeptide; 0 / Serpins; 0 / pigment epithelium-derived factor; 0 / pigment epithelium-derived factor receptor; IY9XDZ35W2 / Glucose
  • [Number-of-references] 142
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2. Nakasu Y, Nakasu S, Saito A, Horiguchi S, Kameya T: Pituicytoma. Two case reports. Neurol Med Chir (Tokyo); 2006 Mar;46(3):152-6
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  • Pituicytoma is a rare tumor in the sellar or suprasellar region with distinct histological characteristics of glial neoplasm.
  • They underwent transcranial partial resection of a suprasellar tumor.
  • The tumors were characterized by storiform pattern of elongated cells immunoreactive for S-100 protein and glial fibrillary acidic protein.
  • Ultrastructural study showed abundant cytoplasmic intermediate filaments and tumor/blood vessel basal lamina, but no desmosomes between tumor cells.
  • The residual tumors showed no changes in size without adjuvant therapy at 56 and 18 months after surgery.
  • Pituicytoma is a glial neoplasm of adults with low proliferative activity.
  • [MeSH-major] Glioma / pathology. Glioma / surgery. Pituitary Neoplasms / pathology. Pituitary Neoplasms / surgery

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  • (PMID = 16565586.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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3. Zhang L, Giraudo E, Hoffman JA, Hanahan D, Ruoslahti E: Lymphatic zip codes in premalignant lesions and tumors. Cancer Res; 2006 Jun 1;66(11):5696-706
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  • [Title] Lymphatic zip codes in premalignant lesions and tumors.
  • Blood vessels in tumors are morphologically and functionally distinct from normal resting blood vessels.
  • We probed lymphatic vessels in premalignant lesions and tumors by in vivo screening of phage-displayed peptide libraries, asking whether they too have distinctive signatures.
  • Thus, tumor development is associated with organ- and stage-specific changes in lymphatics.
  • Systemic treatment of mice with fusions of a lymphatic homing peptide and a proapoptotic motif reduced the number of tumor lymphatics in prostate tumor and melanoma, forecasting future lymphatic targeting agents for detection and therapeutic intervention.
  • [MeSH-major] Lymphatic System / pathology. Neoplasms / blood supply. Precancerous Conditions / blood supply
  • [MeSH-minor] Animals. Female. Humans. Male. Melanoma / blood supply. Melanoma / metabolism. Melanoma / pathology. Mice. Mice, Inbred C57BL. Neovascularization, Pathologic / pathology. Oligopeptides / metabolism. Prostatic Neoplasms / blood supply. Prostatic Neoplasms / pathology. Protein Tyrosine Phosphatase, Non-Receptor Type 22. Protein Tyrosine Phosphatases / metabolism. Rabbits. Skin Neoplasms / blood supply. Skin Neoplasms / metabolism. Skin Neoplasms / pathology. Substrate Specificity. Uterine Cervical Neoplasms / blood supply. Uterine Cervical Neoplasms / metabolism. Uterine Cervical Neoplasms / pathology

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  • [ErratumIn] Cancer Res. 2006 Jul 1;66(13):6894
  • (PMID = 16740707.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 104898; United States / NCI NIH HHS / CA / P01 CA 82713; United States / NCI NIH HHS / CA / P30 CA 30199; United States / NCI NIH HHS / CA / R01 CA115410; United States / NCI NIH HHS / CA / T32 CA77109-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; EC 3.1.3.48 / PTPN22 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 22; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Ptpn22 protein, mouse
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4. Mutsaers AJ: Metronomic chemotherapy. Top Companion Anim Med; 2009 Aug;24(3):137-43
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  • The basis for success with this currently investigational approach may be rooted in continuous drug exposure to susceptible cancer cells, inhibition of tumor blood vessel growth-a process known as tumor angiogenesis, and/or alterations in tumor immunology.
  • There is still much to be learned in this field, especially with regard to optimization of the proper drugs, dose, schedule, and tumor applications.
  • Preliminary clinical trial results have now been reported in both human and veterinary medicine, including adjuvant treatment of canine splenic hemangiosarcoma and incompletely resected soft tissue sarcoma, and, further, more powerful studies are currently ongoing.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Dog Diseases / drug therapy. Sarcoma / veterinary. Soft Tissue Neoplasms / veterinary

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  • (PMID = 19732732.001).
  • [ISSN] 1938-9736
  • [Journal-full-title] Topics in companion animal medicine
  • [ISO-abbreviation] Top Companion Anim Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents
  • [Number-of-references] 56
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5. Wacnik PW, Baker CM, Herron MJ, Kren BT, Blazar BR, Wilcox GL, Hordinsky MK, Beitz AJ, Ericson ME: Tumor-induced mechanical hyperalgesia involves CGRP receptors and altered innervation and vascularization of DsRed2 fluorescent hindpaw tumors. Pain; 2005 May;115(1-2):95-106
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  • [Title] Tumor-induced mechanical hyperalgesia involves CGRP receptors and altered innervation and vascularization of DsRed2 fluorescent hindpaw tumors.
  • Functional and anatomical relationships among primary afferent fibers, blood vessels, and cancers are poorly understood.
  • However, recent evidence suggests that physical and biochemical interactions between these peripheral components are important to both tumor biology and cancer-associated pain.
  • To determine the role of these peripheral components in a mouse model of cancer pain, we quantified the change in nerve and blood vessel density within a fibrosarcoma tumor mass using stereological analysis of serial confocal optical sections of immunostained hind paw.
  • To this end we introduced the Discoma coral-derived red fluorescent protein (DsRed2) into the NCTC 2472 fibrosarcoma line using the Sleeping Beauty transposon methodology, thus providing a unique opportunity to visualize tumor-nerve-vessel associations in context with behavioral assessment of tumor-associated hyperalgesia.
  • Tumors from hyperalgesic mice are more densely innervated with calcitonin gene related peptide (CGRP)-immunoreactive nerve fibers and less densely vascularized than tumors from non-hyperalgesic mice.
  • As hyperalgesia increased from Day 5 to 12 post-implantation, the density of protein gene product 9.5 (PGP9.5)-immunoreactive nerves and CD31-immunoreactive blood vessels in tumors decreased, whereas CGRP-immunoreactive nerve density remained unchanged.
  • Importantly, intra-tumor injection of a CGRP1 receptor antagonist (CGRP 8-37) partially blocked the tumor-associated mechanical hyperalgesia, indicating that local production of CGRP may contribute to tumor-induced nociception through a receptor-mediated process.
  • The results describe for the first time the interaction among sensory nerves, blood vessels and tumor cells in otherwise healthy tissue, and our assessment supports the hypothesis that direct tumor cell-axon communication may underlie, at least in part, the occurrence of cancer pain.
  • [MeSH-major] Fibrosarcoma / blood supply. Fibrosarcoma / metabolism. Hindlimb / blood supply. Hindlimb / innervation. Hyperalgesia / metabolism. Receptors, Calcitonin Gene-Related Peptide / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Male. Mice. Mice, Inbred C3H. Plant Proteins. Ribosome Inactivating Proteins, Type 1

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  • (PMID = 15836973.001).
  • [ISSN] 0304-3959
  • [Journal-full-title] Pain
  • [ISO-abbreviation] Pain
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / 5T 32-DEO 7288-02; United States / NCI NIH HHS / CA / R01-CA72669; United States / NCI NIH HHS / CA / R01-CA84233; United States / NHLBI NIH HHS / HL / R01-HL49997
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Plant Proteins; 0 / Receptors, Calcitonin Gene-Related Peptide; 0 / Ribosome Inactivating Proteins, Type 1
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6. Dong Z, Nör JE: Transcriptional targeting of tumor endothelial cells for gene therapy. Adv Drug Deliv Rev; 2009 Jul 2;61(7-8):542-53
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  • [Title] Transcriptional targeting of tumor endothelial cells for gene therapy.
  • It is well known that angiogenesis plays a critical role in the pathobiology of tumors.
  • Transcriptional targeting of tumor endothelial cells involves the use of specific promoters for selective expression of therapeutic genes in the endothelial cells lining the blood vessels of tumors.
  • Recently, several genes that are expressed specifically in tumor-associated endothelial cells have been identified and characterized.
  • These discoveries have enhanced the prospectus of transcriptionally targeting tumor endothelial cells for cancer gene therapy.
  • In this manuscript, we review the promoters, vectors, and therapeutic genes that have been used for transcriptional targeting of tumor endothelial cells, and discuss the prospects of such approaches for cancer gene therapy.

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  • (PMID = 19393703.001).
  • [ISSN] 1872-8294
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097248; United States / NCI NIH HHS / CA / CA097248-06A10006; United States / NIDCR NIH HHS / DE / R21 DE019279; United States / NIDCR NIH HHS / DE / R01-DE15948; United States / NIDCR NIH HHS / DE / R01 DE014601-01; United States / NCI NIH HHS / CA / P50-CA97248; United States / NIDCR NIH HHS / DE / R01 DE014601; United States / NIDCR NIH HHS / DE / R01 DE016586-01; United States / NIDCR NIH HHS / DE / R01-DE14601; United States / NIDCR NIH HHS / DE / R01 DE016586; United States / NIDCR NIH HHS / DE / R21 DE019279-01; United States / NIDCR NIH HHS / DE / R01 DE015948-01; United States / NIDCR NIH HHS / DE / R01-DE16586; United States / NIDCR NIH HHS / DE / R01 DE015948; United States / NIDCR NIH HHS / DE / R21-DE19279; United States / NCI NIH HHS / CA / P50 CA097248-06A10006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 167
  • [Other-IDs] NLM/ NIHMS124992; NLM/ PMC2727054
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7. Huamani J, Willey C, Thotala D, Niermann KJ, Reyzer M, Leavitt L, Jones C, Fleishcher A, Caprioli R, Hallahan DE, Kim DW: Differential efficacy of combined therapy with radiation and AEE788 in high and low EGFR-expressing androgen-independent prostate tumor models. Int J Radiat Oncol Biol Phys; 2008 May 1;71(1):237-46
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  • [Title] Differential efficacy of combined therapy with radiation and AEE788 in high and low EGFR-expressing androgen-independent prostate tumor models.
  • PURPOSE: To determine the efficacy of combining radiation (XRT) with a dual epidermal growth factor receptor (EGFR)/vascular endothelial growth factor receptor inhibitor, AEE788, in prostate cancer models with different levels of EGFR expression.
  • Tumor xenografts were established for DU145 and PC-3 on hind limbs of athymic nude mice assigned to four treatment groups:.
  • Tumor blood flow and growth measurements were performed using immunohistochemistry and imaging.
  • Concurrent AEE788 + XRT compared with either alone led to significant tumor growth delay in DU145 tumors.
  • Conversely, PC-3 tumors derived no added benefit from combined-modality therapy.
  • In DU145 tumors, a significant decrease in tumor blood flow with combination therapy was shown by using power Doppler sonography and tumor blood vessel destruction on immunohistochemistry.
  • Maldi-spectrometry (MS) imaging showed that AEE788 is bioavailable and heterogeneously distributed in DU145 tumors undergoing therapy.
  • These findings correlated with differences in EGFR expression and showed effects on both tumor cell proliferation and vascular destruction.

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  • (PMID = 18337021.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA125757; United States / NCI NIH HHS / CA / CA112385; United States / NCI NIH HHS / CA / R01 CA112385-04; United States / NCI NIH HHS / CA / R01 CA089674; United States / NCI NIH HHS / CA / R01 CA112385; United States / NCI NIH HHS / CA / R01 CA089674-08; United States / NCI NIH HHS / CA / CA112385-04; United States / NCI NIH HHS / CA / P30-CA68485; United States / NCI NIH HHS / CA / CA89674; United States / NCI NIH HHS / CA / R01 CA140220; United States / NCI NIH HHS / CA / P50 CA090949; United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / R01 CA088076; United States / NCI NIH HHS / CA / CA89888; United States / NCI NIH HHS / CA / CA70937; United States / NCI NIH HHS / CA / P50-CA90949; United States / NCI NIH HHS / CA / CA88076; United States / NCI NIH HHS / CA / CA089674-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AEE 788; 0 / Neoplasm Proteins; 0 / Purines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Other-IDs] NLM/ NIHMS46624; NLM/ PMC2441843
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8. Dijkgraaf I, Boerman OC: Radionuclide imaging of tumor angiogenesis. Cancer Biother Radiopharm; 2009 Dec;24(6):637-47
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  • [Title] Radionuclide imaging of tumor angiogenesis.
  • In order to grow and metastasize, tumors need a constant supply of oxygen and nutrients.
  • For growth beyond 1-2 mm in size, tumors are dependent on angiogenesis.
  • Therefore, there is a great interest in techniques to visualize angiogenesis in growing tumors noninvasively.
  • Several markers have been described that are preferentially expressed on newly formed blood vessels in tumors (alpha(v)beta(3) integrin, vascular endothelial growth factor, and its receptor, prostate-specific membrane antigen) and in the extracellular matrix surrounding newly formed blood vessels (extra domain B of fibronectin, Tenascin-C, matrix metalloproteinases, and Robo-4).
  • Several ligands targeting these markers have been tested as a radiotracer for imaging angiogenesis in tumors.
  • In this review, an overview on the currently used nuclear imaging probes for noninvasive visualization of tumor angiogenesis is given.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neoplasms / radionuclide imaging. Neovascularization, Pathologic / radionuclide imaging
  • [MeSH-minor] Alternative Splicing. Animals. Endothelium, Vascular / enzymology. Endothelium, Vascular / pathology. Fluorodeoxyglucose F18. Humans. Indium Radioisotopes. Integrin alphaVbeta3 / physiology. Magnetic Resonance Imaging. Matrix Metalloproteinases / metabolism. Mice. Neoplasm Metastasis. Neoplasms, Experimental / radionuclide imaging. Oligopeptides / analysis. Positron-Emission Tomography. Receptors, Immunologic / analysis. Receptors, Peptide / analysis. Receptors, Vascular Endothelial Growth Factor / analysis. Receptors, Vascular Endothelial Growth Factor / genetics

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  • (PMID = 20025543.001).
  • [ISSN] 1557-8852
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Indium Radioisotopes; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 0 / Receptors, Immunologic; 0 / Receptors, Peptide; 0 / arginyl-glycyl-aspartic acid directed cell adhesion receptor; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 99896-85-2 / arginyl-glycyl-aspartic acid; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 133
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9. 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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  • 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.
  • 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.

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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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10. Yu Y, Liu N, Sassaroli A, Fantini S: Near-infrared spectral imaging of the female breast for quantitative oximetry in optical mammography. Appl Opt; 2009 Apr 1;48(10):D225-35
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  • We then apply a previously developed spatial second-derivative algorithm to an edge-corrected intensity image (N-image) to enhance the visibility and resolution of optical inhomogeneities in breast tissue such as blood vessels and tumors.
  • Our initial measurements on two healthy human subjects have generated high-resolution optical mammograms displaying a network of blood vessels with values of hemoglobin saturation typically falling within the 60%-95% range, which is physiologically reasonable.
  • This approach to spectral imaging and oximetry of the breast has the potential to efficiently exploit the high intrinsic contrast provided by hemoglobin in breast tissue and to contribute a useful tool in the detection, diagnosis, and monitoring of breast pathologies.
  • [MeSH-major] Breast / blood supply. Optics and Photonics / methods. Oximetry / methods. Spectroscopy, Near-Infrared

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  • (PMID = 19340113.001).
  • [ISSN] 1539-4522
  • [Journal-full-title] Applied optics
  • [ISO-abbreviation] Appl Opt
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA95885
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins
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11. Rafat N, Beck GCh, Schulte J, Tuettenberg J, Vajkoczy P: Circulating endothelial progenitor cells in malignant gliomas. J Neurosurg; 2010 Jan;112(1):43-9
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  • OBJECT: Recent experimental work suggests that circulating endothelial progenitor cells (cEPCs) are recruited to the angiogenic vascular system of malignant gliomas.
  • Consequently, the level of cEPCs has been proposed as a novel biomarker for the diagnosis and monitoring of these lesions.
  • The aim of the present study was to examine the level of cEPCs and the level of EPC mobilizing mediators in the blood of patients with malignant gliomas.
  • METHODS: Peripheral blood mononuclear cells from the whole blood of 12 patients with malignant gliomas (all glioblastomas multiforme [GBMs]), 10 with metastases to the brain, and 10 healthy volunteers were isolated using Ficoll density gradient centrifugation.
  • Histological analysis of tumor blood vessel density was performed by CD34 immunohistochemical staining.
  • In addition, the patients in the GBM group with higher levels of cEPCs had significantly higher tumor blood vessel densities (1.71 +/- 1.17% of total area) compared with patients who had low levels of cEPCs (0.62 +/- 0.28% of total area; p < 0.02).
  • CONCLUSIONS: Endothelial progenitor cells are increasingly mobilized in patients with malignant gliomas, and their levels correlate with tumor angiogenic activity.
  • [MeSH-major] Brain Neoplasms / blood. Brain Neoplasms / metabolism. Endothelial Cells / metabolism. Glioblastoma / blood. Glioblastoma / metabolism. Stem Cells / metabolism
  • [MeSH-minor] Antigens, CD / metabolism. Antigens, CD34 / metabolism. Blood / metabolism. Female. Glycoproteins / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / blood. Humans. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Neovascularization, Pathologic / blood. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Peptides / metabolism. Vascular Endothelial Growth Factor A / blood. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • (PMID = 19522573.001).
  • [ISSN] 1933-0693
  • [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 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / Peptides; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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12. Ciric E, Sersa G: Radiotherapy in combination with vascular-targeted therapies. Radiol Oncol; 2010 Jun;44(2):67-78
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  • [Title] Radiotherapy in combination with vascular-targeted therapies.
  • BACKGROUND: Given the critical role of tumor vasculature in tumor development, considerable efforts have been spent on developing therapeutic strategies targeting the tumor vascular network.
  • Antiangiogenic agents (AAs) aim to interfere with the process of angiogenesis, preventing new tumor blood vessel formation.
  • Vascular-disrupting agents (VDAs) target existing tumor vessels causing tumor ischemia and necrosis.
  • CONCLUSIONS: Strong biological rationale exist for combining vascular-targeted therapies with radiation.
  • AAs and VDAs were shown to alter the tumor microenvironment in such a way as to enhance responses to radiation.
  • However, concerns about increased normal tissue toxicity, have been raised.

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  • (PMID = 22933894.001).
  • [ISSN] 1318-2099
  • [Journal-full-title] Radiology and oncology
  • [ISO-abbreviation] Radiol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovenia
  • [Other-IDs] NLM/ PMC3423684
  • [Keywords] NOTNLM ; antiangiogenic agents / radiotherapy / vascular-disrupting agents
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13. Verhoeff JJ, Stalpers LJ, Claes A, Hovinga KE, Musters GD, Peter Vandertop W, Richel DJ, Leenders WP, van Furth WR: Tumour control by whole brain irradiation of anti-VEGF-treated mice bearing intracerebral glioma. Eur J Cancer; 2009 Nov;45(17):3074-80
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  • [Title] Tumour control by whole brain irradiation of anti-VEGF-treated mice bearing intracerebral glioma.
  • AIM OF THE STUDY: Tumour angiogenesis and invasion are key features of glioblastoma multiforme (GBM).
  • VEGF inhibition controls the bulk tumour growth by inhibition of angiogenesis, but does not inhibit the invasive tumour component.
  • We investigated if invasive tumour growth can be controlled by combining anti-VEGF treatment with irradiation of tumour plus surrounding brain in an orthotopic murine model for GBM.
  • Pegaptanib (a slow-releasing aptamer against VEGF) was injected in the tumour bed either or not followed by irradiation treatment with implanted I-125 seeds.
  • RESULTS: VEGF inhibition by locally deposited pegaptanib decreased tumour blood vessel density, and increased tumour hypoxia.
  • Pegaptanib treatment still allowed the formation of tumour satellites.
  • Irradiation decreased tumour size and suppressed formation of satellites.
  • Tumour size directly correlated with PFS.
  • CONCLUDING STATEMENT: The anti-tumour effects of local VEGF inhibition are partially circumvented by the formation of invasive tumour satellites.
  • Additional irradiation is effective in slowing down proliferation of these invasive tumour components.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Aptamers, Nucleotide / therapeutic use. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Animals. Combined Modality Therapy. Disease Models, Animal. Disease-Free Survival. Female. Humans. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Transplantation. Neovascularization, Pathologic / prevention & control. Treatment Outcome. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 19734041.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Aptamers, Nucleotide; 0 / Vascular Endothelial Growth Factor A; 0 / pegaptanib
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14. Sandler A: Bevacizumab in non small cell lung cancer. Clin Cancer Res; 2007 Aug 1;13(15 Pt 2):s4613-6
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  • Angiogenesis, the growth of new vessels from preexisting vessels, is a fundamental step in tumor growth and progression.
  • Vascular endothelial growth factor (VEGF) is a key angiogenic factor implicated in tumor blood vessel formation and permeability.
  • Based on the favorable results of a prior randomized, phase II trial, the Eastern Cooperative Oncology Group conducted a trial (E4599) to evaluate the efficacy of bevacizumab in combination with paclitaxel and carboplatin in patients with recurrent or advanced stage IIIB or IV nonsquamous cell NSCLC.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bevacizumab. Clinical Trials as Topic. Erlotinib Hydrochloride. Humans. Quinazolines / therapeutic use. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 17671151.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Quinazolines; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab; DA87705X9K / Erlotinib Hydrochloride
  • [Number-of-references] 28
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15. Zhang YF, Wang JC, Bian DY, Zhang X, Zhang Q: Targeted delivery of RGD-modified liposomes encapsulating both combretastatin A-4 and doxorubicin for tumor therapy: in vitro and in vivo studies. Eur J Pharm Biopharm; 2010 Mar;74(3):467-73
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  • [Title] Targeted delivery of RGD-modified liposomes encapsulating both combretastatin A-4 and doxorubicin for tumor therapy: in vitro and in vivo studies.
  • Arg-Gly-Asp (RGD) modified doxorubicin-loaded liposomes could improve anticancer effect, and vascular disrupting agents (VDAs) could induce a rapid and selective shutdown of the blood vessels of tumors.
  • We propose that RGD-modified liposomes for co-encapsulation and sequential release of vascular disrupting agent combretastatin A-4 (CA-4) and cytotoxic agent doxorubicin (Dox) could enhance tumor inhibition responses.
  • Flow cytometry and laser confocal scanning microscopy clearly showed that RGD-modification promoted intracellular uptake of liposomal drugs by B16/B16F10 melanoma tumor cells and human umbilical vein endothelial cells (HUVECs).
  • Therapeutic benefits were examined on B16F10 melanoma tumors subcutaneously growing in C57BL/6 mice.
  • In vivo study demonstrated that RGD-modified liposomes exhibited the most pronounced tumor regression effect when both CA-4 and Dox were co-encapsulated.
  • These results suggest that the targeted drug delivery system for co-encapsulation of vascular disrupting agents and anticancer agents may be a promising strategy for cancer treatment.
  • [MeSH-minor] Animals. Cell Culture Techniques. Cell Line, Tumor. Cell Survival / drug effects. Drug Combinations. Drug Compounding. Drug Delivery Systems. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Flow Cytometry. Humans. Liposomes. Male. Mice. Mice, Inbred C57BL. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20064608.001).
  • [ISSN] 1873-3441
  • [Journal-full-title] European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft für Pharmazeutische Verfahrenstechnik e.V
  • [ISO-abbreviation] Eur J Pharm Biopharm
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; 0 / Drug Combinations; 0 / Liposomes; 0 / Oligopeptides; 0 / Stilbenes; 80168379AG / Doxorubicin; 99896-85-2 / arginyl-glycyl-aspartic acid; I5590ES2QZ / fosbretabulin
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16. Okada Y: Relationships of cervical lymph node metastasis to histopathological malignancy grade, tumor angiogenesis, and lymphatic invasion in tongue cancer. Odontology; 2010 Jul;98(2):153-9
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  • [Title] Relationships of cervical lymph node metastasis to histopathological malignancy grade, tumor angiogenesis, and lymphatic invasion in tongue cancer.
  • Further, the growth and progress of the tumor are known to be profoundly related to histological malignancy, tumor angiogenesis, and lymphangiogenesis.
  • In addition, blood vessel density, lymph vessel density, and lymphatic invasion in the tumor were evaluated immunohistochemically using CD31, CD34, D2-40, and AE1/AE3, and then the relationships of CLN metastasis to these parameters were investigated.
  • Histological malignancy grade, blood vessel density, and lymphatic invasion were significantly related to CLN metastasis (P < 0.05), but there was no relationship between lymph vessel density and CLN metastasis.
  • However, double immunostaining showed that lymphatic invasion by tumor cells was significantly related to CLN metastasis.
  • The results indicate that Anneroth's histological malignancy grade of 16 or more, tumor blood vessel density of more than 37, and the presence of lymphatic invasion by tumor cells can be predictive factors for CLN metastases in tongue SCC.
  • [MeSH-major] Carcinoma, Squamous Cell / secondary. Lymphatic Metastasis / pathology. Neovascularization, Pathologic / pathology. Tongue Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / analysis. Antibodies, Monoclonal, Murine-Derived. Antigens, CD31 / analysis. Antigens, CD34 / analysis. Biomarkers, Tumor / analysis. Blood Vessels / pathology. Cell Nucleus / pathology. Female. Humans. Keratins / analysis. Lymphangiogenesis / physiology. Lymphatic Vessels / pathology. Male. Middle Aged. Mitosis. Neck. Neoplasm Invasiveness. Neoplasm Staging

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  • (PMID = 20652794.001).
  • [ISSN] 1618-1255
  • [Journal-full-title] Odontology
  • [ISO-abbreviation] Odontology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / monoclonal antibody D2-40; 68238-35-7 / Keratins
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17. Derleth C, Mayer IA: Antiangiogenic therapies in early-stage breast cancer. Clin Breast Cancer; 2010;10 Suppl 1:E23-31
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  • Angiogenesis, which is crucial for the growth and spread of cancer cells, has become an important target for antineoplastic therapies in a variety of malignant tumors.
  • Vascular endothelial growth factor and its receptor promote formation of new blood vessels in tumors.
  • Most of these side effects are grade 1 or 2 and are easily manageable; however, there remain a small percentage of patients who sustain life-threatening vascular events, bleeding, or wound-healing complications.

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  • (PMID = 20587404.001).
  • [ISSN] 1938-0666
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA098131; United States / NCI NIH HHS / CA / 2P50 CA098131-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Other-IDs] NLM/ NIHMS406908; NLM/ PMC3471531
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18. Mulder WJ, Strijkers GJ, Habets JW, Bleeker EJ, van der Schaft DW, Storm G, Koning GA, Griffioen AW, Nicolay K: MR molecular imaging and fluorescence microscopy for identification of activated tumor endothelium using a bimodal lipidic nanoparticle. FASEB J; 2005 Dec;19(14):2008-10
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  • [Title] MR molecular imaging and fluorescence microscopy for identification of activated tumor endothelium using a bimodal lipidic nanoparticle.
  • In oncological research, there is a great need for imaging techniques that specifically identify angiogenic blood vessels in tumors on the basis of differences in the expression level of biomolecular markers.
  • In the present study, we aimed to image angiogenesis by detecting the expression of alphavbeta3 in tumor bearing mice with a combination of magnetic resonance imaging (MRI) and fluorescence microscopy.
  • It was established by the use of ex vivo fluorescence microscopy that RGD liposomes and RAD liposomes accumulated in the tumor by different mechanisms.
  • RGD liposomes were specifically associated with activated tumor endothelium, while RAD liposomes were located in the extravascular compartment.
  • This study demonstrates that MR molecular imaging of angiogenesis is feasible by using a targeted contrast agent specific for the alphavbeta3-integrin, and that the multimodality imaging approach gave insight into the exact mechanism of accumulation in the tumor.
  • [MeSH-major] Lipids / chemistry. Magnetic Resonance Imaging / methods. Microscopy, Fluorescence / methods. Nanostructures. Neoplasms / metabolism
  • [MeSH-minor] Animals. Antigens, CD31 / biosynthesis. Binding, Competitive. Cell Proliferation. Cells, Cultured. Disease Models, Animal. Endothelium, Vascular / cytology. Integrin alphaVbeta3 / metabolism. Liposomes / chemistry. Mice. Microscopy, Confocal. Models, Biological. Neovascularization, Pathologic. Oligopeptides / chemistry. Umbilical Veins / cytology

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  • (PMID = 16204353.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Integrin alphaVbeta3; 0 / Lipids; 0 / Liposomes; 0 / Oligopeptides; 99896-85-2 / arginyl-glycyl-aspartic acid
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19. Nagy JA, Chang SH, Shih SC, Dvorak AM, Dvorak HF: Heterogeneity of the tumor vasculature. Semin Thromb Hemost; 2010 Apr;36(3):321-31
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  • [Title] Heterogeneity of the tumor vasculature.
  • The blood vessels supplying tumors are strikingly heterogeneous and differ from their normal counterparts with respect to organization, structure, and function.
  • Six distinctly different tumor vessel types have been identified, and much has been learned about the steps and mechanisms by which they form.
  • Four of the six vessel types (mother vessels, capillaries, glomeruloid microvascular proliferations, and vascular malformations) develop from preexisting normal venules and capillaries by angiogenesis.
  • The two remaining vessel types (feeder arteries and draining veins) develop from arterio-venogenesis, a parallel, poorly understood process that involves the remodeling of preexisting arteries and veins.
  • All six of these tumor vessel types can be induced to form sequentially in normal mouse tissues by an adenoviral vector expressing vascular endothelial growth factor (VEGF)-A164.
  • Current antiangiogenic cancer therapies directed at VEGF-A or its receptors have been of only limited benefit to cancer patients, perhaps because they target only the endothelial cells of the tumor blood vessel subset that requires exogenous VEGF-A for maintenance.
  • A goal of future work is to identify therapeutic targets on tumor blood vessel endothelial cells that have lost this requirement.

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  • [Copyright] Thieme Medical Publishers.
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  • (PMID = 20490982.001).
  • [ISSN] 1098-9064
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL064402; United States / NCI NIH HHS / CA / P01 CA92644; United States / NHLBI NIH HHS / HL / HL-64402; United States / NCI NIH HHS / CA / P01 CA092644; United States / NCI NIH HHS / CA / P01 CA092644-08; United States / NHLBI NIH HHS / HL / R01 HL064402-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 60
  • [Other-IDs] NLM/ NIHMS354169; NLM/ PMC3278036
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20. Littlepage LE, Sternlicht MD, Rougier N, Phillips J, Gallo E, Yu Y, Williams K, Brenot A, Gordon JI, Werb Z: Matrix metalloproteinases contribute distinct roles in neuroendocrine prostate carcinogenesis, metastasis, and angiogenesis progression. Cancer Res; 2010 Mar 15;70(6):2224-34
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  • Prostate tumors often contain neuroendocrine differentiation, which correlates with androgen-independent progression and poor prognosis.
  • CR2-TAg mice treated with AG3340/Prinomastat, an MMP inhibitor that blocks activity of MMP-2, MMP-9, MMP-13, and MMP-14, had reduced tumor burden.
  • At 24 weeks CR2-TAg; MMP-2(-/-) mice showed reduced tumor burden, prolonged survival, decreased lung metastasis, and decreased blood vessel density, whereas deficiencies in MMP-7 or MMP-9 did not influence tumor growth or survival.
  • Mice deficient for MMP-7 had reduced endothelial area coverage and decreased vessel size, and mice lacking MMP-9 had increased numbers of invasive foci and increased perivascular invasion, as well as decreased tumor blood vessel size.
  • Together, these results suggest distinct contributions by MMPs to the progression of aggressive prostate tumor and to helping tumors cleverly find alternative routes to malignant progression.

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  • (PMID = 20215503.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS063456; United States / NCI NIH HHS / CA / CA072006-09; United States / NCI NIH HHS / CA / CA58207; United States / NCI NIH HHS / CA / P01 CA072006-09; United States / NCI NIH HHS / CA / CA058207-10; United States / NCI NIH HHS / CA / CA089520-05; United States / NCI NIH HHS / CA / CA103534; United States / NCI NIH HHS / CA / F32 CA103534; United States / NCI NIH HHS / CA / CA089520; United States / NCI NIH HHS / CA / CA072006-08; United States / NCI NIH HHS / CA / P01 CA072006-08; United States / NCI NIH HHS / CA / P50 CA089520-05; United States / NCI NIH HHS / CA / CA072006; United States / NCI NIH HHS / CA / P50 CA058207; United States / NCI NIH HHS / CA / P01 CA072006-10; United States / NCI NIH HHS / CA / CA072006-10; United States / NCI NIH HHS / CA / P50 CA058207-10; United States / NCI NIH HHS / CA / T32 CA108462; United States / NCI NIH HHS / CA / R01 CA057621; United States / NCI NIH HHS / CA / P50 CA089520; United States / NCI NIH HHS / CA / P01 CA072006
  • [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 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Matrix Metalloproteinase Inhibitors; 0 / Organic Chemicals; 10T6626FRK / prinomastat; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.23 / Matrix Metalloproteinase 7; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS171775; NLM/ PMC2840052
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21. Zhang X, Galardi E, Duquette M, Lawler J, Parangi S: Antiangiogenic treatment with three thrombospondin-1 type 1 repeats versus gemcitabine in an orthotopic human pancreatic cancer model. Clin Cancer Res; 2005 Aug 1;11(15):5622-30
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  • Subsequently, the effects of 3TSR and/or gemcitabine on tumor growth, tumor necrosis, microvessel density, cancer cell proliferation, apoptosis, and endothelial cell apoptosis were analyzed.
  • RESULTS: After 3 weeks of treatment, 3TSR reduced tumor volume by 65%, and gemcitabine by 84%.
  • Tumor volume was not statistically different between gemcitabine group and combinatorial treatment group.
  • Extensive necrotic areas were observed in tumors from 3TSR-treated mice, whereas tumors from gemcitabine and combinatorially treated mice were less necrotic than control tumors.
  • 3TSR reduced tumor microvessel density and increased tumor blood vessel endothelial cell apoptosis.
  • A delicate balance between normalization and excessive regression of tumor vasculature is important when initiating alternative combinatorial regimens for treatment of patients with pancreatic cancer.

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  • (PMID = 16061881.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA88965-01A1; United States / NHLBI NIH HHS / HL / HL 68003; United States / NCI NIH HHS / CA / CA 92644; United States / NHLBI NIH HHS / HL / R01 HL068003; United States / NCI NIH HHS / CA / K08 CA088965
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Antimetabolites, Antineoplastic; 0 / Recombinant Proteins; 0 / Thrombospondin 1; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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22. Geng L, Cuneo KC, Cooper MK, Wang H, Sekhar K, Fu A, Hallahan DE: Hedgehog signaling in the murine melanoma microenvironment. Angiogenesis; 2007;10(4):259-67
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  • This pathway has been implicated to play a role in the pathogenesis of cancer and in embryonic blood vessel development.
  • In the current study, Hedgehog signaling in tumor related vasculature and microenvironment was examined using human umbilical vein endothelial cells and B16F0 (murine melanoma) tumors models.
  • To study Hedgehog signaling in vivo a hind limb tumor model with the B16F0 cell line was used.
  • Treatment with 25 mg/kg cyclopamine significantly attenuated BrdU incorporation in tumor cells threefold (P < 0.001), in tumor related endothelial cells threefold (P = 0.004), and delayed tumor growth by 4 days.
  • Immunohistochemistry revealed that the Hedgehog receptor Patched was localized to the tumor stroma and that B16F0 cells expressed Shh peptide.
  • To study tumor related angiogenesis a vascular window model was used to monitor tumor vascularity.
  • Treatment with cyclopamine significantly attenuated vascular formation by a factor of 2.5 (P < 0.001) and altered vascular morphology.
  • Furthermore, cyclopamine reduced tumor blood vessel permeability to FITC labeled dextran while having no effect on normal blood vessels.
  • These studies suggest that Hedgehog signaling regulates melanoma related vascular formation and function.
  • [MeSH-minor] Animals. Cells, Cultured. Endothelium, Vascular / cytology. Endothelium, Vascular / metabolism. Humans. Mice. Neovascularization, Pathologic. Veratrum Alkaloids / pharmacology

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  • (PMID = 17762973.001).
  • [ISSN] 0969-6970
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA6848; United States / NCI NIH HHS / CA / P50-CA90949; United States / NCI NIH HHS / CA / R01-CA112385; United States / NCI NIH HHS / CA / R01-CA70937; United States / NCI NIH HHS / CA / R01-CA88076; United States / NCI NIH HHS / CA / R01-CA89888
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Veratrum Alkaloids; ZH658AJ192 / cyclopamine
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23. Rudin M, McSheehy PM, Allegrini PR, Rausch M, Baumann D, Becquet M, Brecht K, Brueggen J, Ferretti S, Schaeffer F, Schnell C, Wood J: PTK787/ZK222584, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor, reduces uptake of the contrast agent GdDOTA by murine orthotopic B16/BL6 melanoma tumours and inhibits their growth in vivo. NMR Biomed; 2005 Aug;18(5):308-21
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  • [Title] PTK787/ZK222584, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor, reduces uptake of the contrast agent GdDOTA by murine orthotopic B16/BL6 melanoma tumours and inhibits their growth in vivo.
  • Assessment of tumour vascularity may characterize malignancy as well as predict responsiveness to anti-angiogenic therapy.
  • Non-invasive measurement of tumour perfusion and blood vessel permeability assessed as the transfer constant, K(trans), can be provided by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI).
  • Using the orthotopic murine tumour model B16/BL6 melanoma, the small contrast agent GdDOTA (DOTAREM(R); Guerbet, Paris) was applied to assess the vascular transfer constant, K(trans), and interstitial leakage space, whereas intravascular iron oxide nanoparticles (Endorem(R); Guerbet, Paris) were used to detect relative tumour blood volume (rTBV), and in one experiment blood flow index (BFI).
  • The B16/BL6 primary tumour and lymph-node cervical (neck) metastases produced high levels of the permeability/growth factor, VEGF.
  • To probe the model, the novel VEGF receptor (VEGF-R) tyrosine kinase inhibitor, PTK787/ZK222584 (PTK/ZK) was tested for anti-tumour efficacy and its effects on DCE-MRI measured parameters of tumour vascularity.
  • Data from the non-invasive measure of tumour vascularity were compared with a histological measurement of vasculature using the DNA-staining dye H33342.
  • PTK/ZK inhibited growth of the primary and, particularly, cervical tumour metastases following chronic treatment for 2 weeks (50 or 100 mg/kg daily) of 1-week-old tumours, or with 1 week of treatment against more established (2-week-old) tumours.
  • After chronic treatment with PTK/ZK, DCE-MRI detected significant decreases in K(trans) and interstitial leakage space, but not rTBV of both primary tumours and cervical metastases.
  • Histological data at this time-point showed a significant decrease in blood vessel density of the cervical metastases but not the primary tumours.
  • However, in the cervical metastases, the mean blood vessel width was increased by 38%, suggesting overall no marked change in blood volume.
  • Thus, significant changes could be detected in the DCE-MRI measurement of tumour uptake of a small contrast agent prior to changes in tumour size, which suggests that DCE-MRI could be applied in the clinic as a rapid and sensitive biomarker for the effects of VEGF-R inhibition on tumour blood vessel permeability and thus may provide an early marker for eventual tumour response.
  • [MeSH-major] Heterocyclic Compounds / pharmacokinetics. Magnetic Resonance Imaging / methods. Melanoma / metabolism. Melanoma / pathology. Neovascularization, Pathologic / metabolism. Organometallic Compounds / pharmacokinetics. Phthalazines / administration & dosage. Pyridines / administration & dosage. Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Contrast Media. Female. Metabolic Clearance Rate. Mice. Mice, Inbred C57BL. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism

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  • [Copyright] Copyright (c) 2005 John Wiley & Sons, Ltd.
  • (PMID = 15918178.001).
  • [ISSN] 0952-3480
  • [Journal-full-title] NMR in biomedicine
  • [ISO-abbreviation] NMR Biomed
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Heterocyclic Compounds; 0 / Organometallic Compounds; 0 / Phthalazines; 0 / Pyridines; 0 / Vascular Endothelial Growth Factor A; 5DX9U76296 / vatalanib; 92923-44-9 / gadolinium 1,4,7,10-tetraazacyclododecane-N,N',N'',N'''-tetraacetate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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24. Parsons-Wingerter P, Kasman IM, Norberg S, Magnussen A, Zanivan S, Rissone A, Baluk P, Favre CJ, Jeffry U, Murray R, McDonald DM: Uniform overexpression and rapid accessibility of alpha5beta1 integrin on blood vessels in tumors. Am J Pathol; 2005 Jul;167(1):193-211
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  • [Title] Uniform overexpression and rapid accessibility of alpha5beta1 integrin on blood vessels in tumors.
  • Integrin alpha5beta1 is among the proteins overexpressed on tumor vessels and is a potential target for diagnostics and therapeutics.
  • Here, we mapped the distribution of alpha5beta1 integrin in three murine tumor models and identified sites of expression that are rapidly accessible to intravascular antibodies.
  • When examined by conventional immunohistochemistry, alpha5beta1 integrin expression was strong on most blood vessels in RIP-Tag2 transgenic mouse tumors, adenomatous polyposis coli (apc) mouse adenomas, and implanted MCa-IV mammary carcinomas.
  • The injected antibody strongly labeled tumor vessels at all time points but did not label most normal blood vessels or gain access to pancreatic ducts or intestinal smooth muscle.
  • Intense vascular labeling by anti-alpha5beta1 integrin antibody co-localized with the uniform CD31 immunoreactivity of tumor vessels and contrasted sharply with the patchy accumulation of nonspecific IgG at sites of leakage.
  • This strategy of injecting antibodies revealed the uniform overexpression and rapid accessibility of alpha5beta1 integrin on tumor vessels and may prove useful in assessing other potential therapeutic targets in cancer.

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  • (PMID = 15972964.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL-24136; United States / NHLBI NIH HHS / HL / P01 HL024136; United States / NCI NIH HHS / CA / P50-CA90270; United States / NCI NIH HHS / CA / P50 CA090270; United States / NHLBI NIH HHS / HL / R01 HL059157; United States / NHLBI NIH HHS / HL / HL-59157
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Integrin alpha5beta1
  • [Other-IDs] NLM/ PMC1603436
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25. Ji J, Hemminki K: Familial blood vessel tumors and subsequent cancers. Ann Oncol; 2007 Jul;18(7):1260-7
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  • [Title] Familial blood vessel tumors and subsequent cancers.
  • BACKGROUND: Population-based data on the familial risk for vascular tumors are largely lacking.
  • METHODS: We used the Swedish Family-Cancer Database to calculate standardized incidence ratios for specific subtypes of vascular tumors in offspring using parents as probands.
  • Kidney and endocrine gland tumors and nervous system hemangioblastomas and hemangiomas were in excess following primary nervous system hemangioblastoma and hemangioma.

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  • (PMID = 17426058.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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26. Tsuda K, Nishi M, Yamada K, Yamamoto K: [Spontaneous hemothorax in a patient with lung metastases of osteosarcoma]. Masui; 2005 Sep;54(9):1027-9
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  • A 6-year-old girl with right lung metastases of osteosarcoma was scheduled for insertion of a central venous catheter and a femoral arterial catheter under general anesthesia for arterial injection chemotherapy.
  • Chest computed tomography examination revealed a right hemothorax and rupture of the growing lung metastatic tumor.
  • Spontaneous rupture of lung metastases occurs regardless of tumor size, and occurs easily during chemotherapy because of necrosis of the tumor or disability of its repair function.
  • In our case, rupture of the lung metastatic tumor involving tumor blood vessel was thought to have caused the hemothorax.
  • [MeSH-major] Hemothorax / etiology. Lung Neoplasms / complications. Lung Neoplasms / secondary. Osteosarcoma / secondary

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  • (PMID = 16167798.001).
  • [ISSN] 0021-4892
  • [Journal-full-title] Masui. The Japanese journal of anesthesiology
  • [ISO-abbreviation] Masui
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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27. Müller R, Kömhoff M, Peters JM, Müller-Brüsselbach S: A Role for PPARbeta/delta in Tumor Stroma and Tumorigenesis. PPAR Res; 2008;2008:534294
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  • [Title] A Role for PPARbeta/delta in Tumor Stroma and Tumorigenesis.
  • However, the majority of these studies have not examined the role of PPARbeta/delta in the tumor stroma.
  • Recent evidence suggests that stromal PPARbeta/delta regulates tumor endothelial cell proliferation and promotes differentiation leading to the properly orchestrated events required for tumor blood vessel formation.

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  • (PMID = 18497874.001).
  • [ISSN] 1687-4757
  • [Journal-full-title] PPAR research
  • [ISO-abbreviation] PPAR Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2390718
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28. Kanthou C, Tozer GM: Tumour targeting by microtubule-depolymerizing vascular disrupting agents. Expert Opin Ther Targets; 2007 Nov;11(11):1443-57
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  • [Title] Tumour targeting by microtubule-depolymerizing vascular disrupting agents.
  • Low molecular weight vascular disrupting agents of the microtubule depolymerizing family cause marked and selective disruption of the established tumour blood vessel network, resulting in tumour cell necrosis.
  • Potentially, vascular disrupting agents can also interfere with angiogenesis and constitute a very promising group of novel cancer drugs.
  • In vitro analysis of their signalling activities points to the endothelial cytoskeleton as being their major target and a key player in the events that culminate in vascular collapse.
  • As more of these agents progress into the clinical setting, more research in this area is warranted in order to decipher exact mechanisms responsible for vascular disruption and to understand the reasons for drug selectivity for the tumour vasculature.
  • This information is essential in order to identify new targets within the tumour vasculature and to improve present therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Neoplasms / drug therapy

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  • (PMID = 18028009.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Stilbenes; I5590ES2QZ / fosbretabulin
  • [Number-of-references] 133
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29. Koch M, Nielsen GP, Yoon SS: Malignant tumors of blood vessels: angiosarcomas, hemangioendotheliomas, and hemangioperictyomas. J Surg Oncol; 2008 Mar 15;97(4):321-9
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  • [Title] Malignant tumors of blood vessels: angiosarcomas, hemangioendotheliomas, and hemangioperictyomas.
  • Sarcomas that arise from or resemble the components of blood vessels are uncommon and include angiosarcomas, hemangioendotheliomas, and hemangiopericytomas.
  • Diagnosis can sometimes be difficult, with the diagnosis of hemangiopericytoma versus solitary fibrous tumor currently in debate.
  • [MeSH-major] Hemangioendothelioma / diagnosis. Hemangioendothelioma / therapy. Hemangiopericytoma / diagnosis. Hemangiopericytoma / therapy. Hemangiosarcoma / diagnosis. Hemangiosarcoma / therapy
  • [MeSH-minor] Chemotherapy, Adjuvant. Combined Modality Therapy. Humans. Neoplasms, Radiation-Induced. Prognosis. Radiotherapy / adverse effects. Skin Neoplasms / diagnosis. Skin Neoplasms / etiology. Skin Neoplasms / therapy

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18286475.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 89
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30. Dreher MR, Liu W, Michelich CR, Dewhirst MW, Chilkoti A: Thermal cycling enhances the accumulation of a temperature-sensitive biopolymer in solid tumors. Cancer Res; 2007 May 1;67(9):4418-24
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  • [Title] Thermal cycling enhances the accumulation of a temperature-sensitive biopolymer in solid tumors.
  • The delivery of anticancer therapeutics to solid tumors remains a critical problem in the treatment of cancer.
  • This study reports a new methodology to target a temperature-responsive macromolecular drug carrier, an elastin-like polypeptide (ELP) to solid tumors.
  • Using a dorsal skin fold window chamber model and intravital laser scanning confocal microscopy, we show that the ELP forms micron-sized aggregates that adhere to the tumor vasculature only when tumors are heated to 41.5 degrees C.
  • Upon return to normothermia, the vascular particles dissolve into the plasma, increasing the vascular concentration, which drives more ELPs across the tumor blood vessel and significantly increases its extravascular accumulation.
  • These observations suggested that thermal cycling of tumors would increase the exposure of tumor cells to ELP drug carriers.
  • We investigated this hypothesis in this study by thermally cycling an implanted tumor in nude mice from body temperature to 41.5 degrees C thrice within 1.5 h, and showed the repeated formation of adherent microparticles of ELP in the heated tumor vasculature in each thermal cycle.
  • These results suggest that thermal cycling of tumors can be repeated multiple times to further increase the accumulation of a thermally responsive polymeric drug carrier in solid tumors over a single heat-cool cycle.
  • More broadly, this study shows a new approach--tumor thermal cycling--to exploit stimuli-responsive polymers in vivo to target the tumor vasculature or extravascular compartment with high specificity.

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  • (PMID = 17483356.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA47245; United States / NIBIB NIH HHS / EB / R01 EB00188-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alexa 488 hydrazide; 0 / Alexa fluor 546; 0 / Hydrazines; 0 / Peptides; 0 / Quinolinium Compounds; 81857-53-6 / elastin polypentapeptide; 9007-58-3 / Elastin
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31. Izukuri K, Suzuki K, Yajima N, Ozawa S, Ito S, Kubota E, Hata R: Chemokine CXCL14/BRAK transgenic mice suppress growth of carcinoma cell transplants. [corrected]. Transgenic Res; 2010 Dec;19(6):1109-17
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  • We reported previously that the forced expression of the chemokine BRAK, also called CXCL14 in head and neck squamous cell carcinoma (HNSCC) cells decreased the rate of tumor formation and size of tumor xenografts compared with mock-vector treated cells in athymic nude mice or in severe combined immunodeficiency mice.
  • This suppression occurred even though the growth rates of these cells were the same under in vitro culture conditions, suggesting that a high expression level of the gene in tumor cells is important for the suppression of tumor establishment in vivo.
  • The aim of this study was to determine whether CXCL14/BRAK transgenic mice show resistance to tumor cell xenografts or not.
  • Two lines of mice expressed over 10 times higher CXCL14/BRAK protein levels (14 and 11 ng/ml plasma, respectively) than normal blood level (0.9 ng/ml plasma), without apparent abnormality.
  • The sizes of Lewis lung carcinoma and B16 melanoma cell xenografts in Tg mice were significantly smaller than those in control wild-type mice, indicating that CXCL14/BRAK, first found as a suppressor of tumor progression of HNSCC, also suppresses the progression of a carcinoma of other tissue origin.
  • Immunohistochemical studies showed that invasion of blood vessels into tumors was suppressed in tumor xenografts of CXCL14/BRAK Tg mice.
  • These results indicate that CXCL14/BRAK suppressed tumor cell xenografts by functioning paracrine or endocrine fashion and that CXCL14/BRAK is a very promising molecular target for tumor suppression without side effects.
  • [MeSH-major] Chemokines, CXC / genetics. Chemokines, CXC / immunology. Neoplasms, Experimental / immunology. Neoplasms, Experimental / therapy
  • [MeSH-minor] Animals. Base Sequence. Carcinoma, Lewis Lung / blood supply. Carcinoma, Lewis Lung / genetics. Carcinoma, Lewis Lung / immunology. Carcinoma, Lewis Lung / therapy. Cell Line, Tumor. DNA Primers / genetics. Female. Gene Expression. Humans. Kidney / immunology. Male. Melanoma, Experimental / blood supply. Melanoma, Experimental / genetics. Melanoma, Experimental / immunology. Melanoma, Experimental / therapy. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Transplantation. RNA, Messenger / genetics. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Transplantation, Heterologous

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  • [ErratumIn] Transgenic Res. 2010 Dec;19(6):1119
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  • (PMID = 20333465.001).
  • [ISSN] 1573-9368
  • [Journal-full-title] Transgenic research
  • [ISO-abbreviation] Transgenic Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CXCL14 protein, human; 0 / Chemokines, CXC; 0 / DNA Primers; 0 / RNA, Messenger; 0 / Recombinant Proteins
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32. Paschoalin T, Carmona AK, Rodrigues EG, Oliveira V, Monteiro HP, Juliano MA, Juliano L, Travassos LR: Characterization of thimet oligopeptidase and neurolysin activities in B16F10-Nex2 tumor cells and their involvement in angiogenesis and tumor growth. Mol Cancer; 2007;6:44
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  • [Title] Characterization of thimet oligopeptidase and neurolysin activities in B16F10-Nex2 tumor cells and their involvement in angiogenesis and tumor growth.
  • BACKGROUND: Angiogenesis is a fundamental process that allows tumor growth by providing nutrients and oxygen to the tumor cells.
  • Beyond the oxygen diffusion limit from a capillary blood vessel, tumor cells become apoptotic.
  • Tumor cells may express pro-angiogenic factors and hydrolytic enzymes but also kinin-degrading oligopeptidases which have been investigated.
  • Thimet oligopeptidase (TOP) and neurolysin activities were then investigated in B16F10-Nex2 melanoma cells aiming at gene sequencing, enzyme distribution and activity, influence on tumor development, substrate specificity, hydrolytic products and susceptibility to inhibitors.
  • Active rTOP but not the inactive protein inhibited melanoma cell development in vivo increasing significantly the survival of mice challenged with the tumor cells.
  • A possible regulation of the homologous tumor enzyme in the perivascular microenvironment is suggested based on the observed rTOP inhibition by an S-nitrosothiol NO donor.
  • CONCLUSION: Data show that melanoma cells secrete endo-oligopeptidases which have an important role in tumor proliferation in vitro and in vivo. rTOP inhibited growth of subcutaneously injected B16F10-Nex2 cells in mice.
  • TOP from tumor cells and bradykinin in endothelial cells are two antagonist factors that may control angiogenesis essential for melanoma growth.
  • [MeSH-minor] Animals. Bradykinin / metabolism. Cell Extracts. Cell Line, Tumor. Cell Membrane / enzymology. Cloning, Molecular. Coculture Techniques. Collagen. Culture Media, Conditioned / metabolism. Dipeptides / pharmacology. Dose-Response Relationship, Drug. Drug Combinations. Female. Hydrolysis. Laminin. Leucine / analogs & derivatives. Leucine / pharmacology. Mice. Mice, Inbred C57BL. Neurotensin / metabolism. Nitric Oxide / metabolism. Nitric Oxide Donors / pharmacology. Oligopeptides / pharmacology. Peptides / metabolism. Phenanthrolines / pharmacology. Protease Inhibitors / pharmacology. Proteoglycans. S-Nitroso-N-Acetylpenicillamine / pharmacology. Substrate Specificity

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  • (PMID = 17620116.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Antineoplastic Agents; 0 / Cell Extracts; 0 / Culture Media, Conditioned; 0 / Dipeptides; 0 / Drug Combinations; 0 / JA 2 compound; 0 / Laminin; 0 / Nitric Oxide Donors; 0 / Oligopeptides; 0 / Peptides; 0 / Phenanthrolines; 0 / Protease Inhibitors; 0 / Proteoglycans; 119978-18-6 / matrigel; 31C4KY9ESH / Nitric Oxide; 39379-15-2 / Neurotensin; 51926-51-3 / prolylisoleucine; 79032-48-7 / S-Nitroso-N-Acetylpenicillamine; 9007-34-5 / Collagen; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.15 / thimet oligopeptidase; EC 3.4.24.16 / neurolysin; GMW67QNF9C / Leucine; I0J33N5627 / ubenimex; S8TIM42R2W / Bradykinin; W4X6ZO7939 / 1,10-phenanthroline
  • [Other-IDs] NLM/ PMC1965469
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33. Leung M, Kievit FM, Florczyk SJ, Veiseh O, Wu J, Park JO, Zhang M: Chitosan-alginate scaffold culture system for hepatocellular carcinoma increases malignancy and drug resistance. Pharm Res; 2010 Sep;27(9):1939-48
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  • Critically needed discovery of new therapeutics has been hindered by lack of an in vitro cell culture system that can effectively represent the in vivo tumor microenvironment.
  • METHODS: The correlation between the cell function, such as secretion of growth factors and production of ECM in vitro, and the tumor growth and blood vessel recruitment in vivo was investigated.
  • Implantation of CA scaffolds cultured with human HCC cells in mice showed accelerated tumor growth.
  • Histology revealed marked differences in morphology and organization of newly formed blood vessels between tumors produced by different pre-cultured conditions.
  • CONCLUSIONS: This 3D model of HCC, with its ability to more closely mimic the in vivo tumor behavior, may serve as an invaluable model for study and application of novel anticancer therapeutics against HCC.

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  • (PMID = 20585843.001).
  • [ISSN] 1573-904X
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB006043-03S1; United States / NCI NIH HHS / CA / CA134213-03; United States / NCI NIH HHS / CA / T32CA138312; United States / NIBIB NIH HHS / EB / EB006043-03; United States / NIBIB NIH HHS / EB / EB006043-03S1; United States / NCI NIH HHS / CA / T32 CA138312-01; United States / NIBIB NIH HHS / EB / R01EB006043; United States / NIBIB NIH HHS / EB / R01 EB006043-03; United States / NCI NIH HHS / CA / R01CA134213; United States / NCI NIH HHS / CA / T32 CA138312; United States / NCI NIH HHS / CA / R01 CA134213-03; United States / NIBIB NIH HHS / EB / R01 EB006043; United States / NCI NIH HHS / CA / R01 CA134213
  • [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 / Alginates; 0 / Antineoplastic Agents; 0 / Biocompatible Materials; 0 / Hexuronic Acids; 80168379AG / Doxorubicin; 8A5D83Q4RW / Glucuronic Acid; 8C3Z4148WZ / alginic acid; 9012-76-4 / Chitosan
  • [Other-IDs] NLM/ NIHMS222164; NLM/ PMC2917619
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34. Hasebe T, Konishi M, Iwasaki M, Endoh Y, Nakagohri T, Takahashi S, Kinoshita T, Ochiai A: Histological characteristics of tumor cells and stromal cells in vessels and lymph nodes are important prognostic parameters of extrahepatic bile duct carcinoma: a prospective study. Hum Pathol; 2005 Jun;36(6):655-64
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  • [Title] Histological characteristics of tumor cells and stromal cells in vessels and lymph nodes are important prognostic parameters of extrahepatic bile duct carcinoma: a prospective study.
  • Extrahepatic bile duct carcinomas (EHBDCs) consist of primary tumors, tumors in vessels, and tumors in lymph nodes.
  • The purpose of this study was to prospectively investigate whether the histological characteristics of tumor cells and tumor stromal cells in vessels and lymph nodes were significantly associated with the outcomes of 60 EHBDC patients as compared with the histological characteristics of tumor cells and tumor stromal cells in primary tumors.
  • Multivariate analyses, using the Cox proportional hazard regression model, showed that in EHBDCs without nodal metastasis, blood vessel tumor emboli with an angiomatous stroma significantly increased the hazard ratios (HRs) of tumor recurrence and death ( P < .05).
  • In EHBDCs with nodal metastasis, the presence of tumor necrosis in the nodal tumors significantly increased the HRs of tumor recurrence and initial distant organ metastasis ( P < .05).
  • In EHBDCs located in the distal to middle portion of the extrahepatic bile duct, blood vessel tumor emboli with an angiomatous stroma significantly increased the HRs of tumor recurrence, initial distant organ metastasis, and death ( P < .05).
  • Severe nuclear atypia of the tumor cells in lymph vessels significantly increased the HRs of tumor recurrence and initial distant organ metastasis ( P < .05).
  • In EHBDCs located in the hilar portion of the extrahepatic bile duct, the presence of nodal tumors with more than 4 mitotic figures significantly increased the HRs of tumor recurrence and initial distant organ metastasis ( P < .05).
  • Several histological characteristics of tumor cells and tumor stromal cells in vessels and lymph nodes have significant effects on tumor progression of EHBDCs.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Bile Ducts, Extrahepatic / blood supply. Bile Ducts, Extrahepatic / pathology. Lymph Nodes / pathology. Stromal Cells / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blood Vessels / pathology. Female. Humans. Lymphatic Metastasis / pathology. Male. Middle Aged. Neoplastic Cells, Circulating / pathology. Prognosis. Prospective Studies

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  • (PMID = 16021572.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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35. Siemann DW, Horsman MR: Vascular targeted therapies in oncology. Cell Tissue Res; 2009 Jan;335(1):241-8
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  • [Title] Vascular targeted therapies in oncology.
  • Neovascularization is intimately involved in tumor survival, progression, and spread, factors known to contribute significantly to treatment failures.
  • Thus, strategies targeting the tumor blood vessel support network may offer not only unique therapeutic opportunities in their own right, but also novel means of enhancing the efficacies of conventional anticancer treatments.
  • This article reviews one such therapeutic approach directed at the tumor blood vessel support network.
  • Vascular disrupting therapies seek the destruction of the established neovasculature of actively growing tumors.
  • The goal of these therapies is to cause a rapid and catastrophic shutdown in the vascular function of the tumor in order to arrest the blood flow and produce tumor cell death as a result of oxygen and nutrient deprivation and the build up of waste products.

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  • (PMID = 18752004.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA089655-07; United States / NCI NIH HHS / CA / CA084408; United States / NCI NIH HHS / CA / CA084408-09A1; United States / NCI NIH HHS / CA / CA089655; United States / NCI NIH HHS / CA / R01 CA089655-07; United States / NCI NIH HHS / CA / R01 CA089655; United States / NCI NIH HHS / CA / R01 CA084408; United States / NCI NIH HHS / CA / R01 CA084408-09A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; S88TT14065 / Oxygen
  • [Number-of-references] 47
  • [Other-IDs] NLM/ NIHMS159149; NLM/ PMC2788502
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36. Magnon C, Opolon P, Connault E, Mir LM, Perricaudet M, Martel-Renoir D: Canstatin gene electrotransfer combined with radiotherapy: preclinical trials for cancer treatment. Gene Ther; 2008 Nov;15(21):1436-45
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  • The long lasting circulating blood level of CanHSA (20 ng ml(-1)) resulted in a profound disorganization of the tumor blood vessel network.
  • However, when used as a curative treatment, on well-established tumors, CanHSA electrogenetherapy was ineffective in reducing tumor growth.
  • We demonstrated a better efficacy (P=0.01) of the bitherapy over irradiation alone, as a result of strong vessel disorganization and dramatic increase of tumor cells apoptosis.
  • [MeSH-major] Breast Neoplasms / therapy. Collagen Type IV / genetics. Genetic Therapy / methods. Peptide Fragments / genetics. Prostatic Neoplasms / therapy. Recombinant Fusion Proteins / therapeutic use
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Combined Modality Therapy. Electroporation. Female. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Nude. Muscle, Skeletal / metabolism. Radiotherapy Dosage. Serum Albumin / genetics. Xenograft Model Antitumor Assays

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  • (PMID = 18548116.001).
  • [ISSN] 1476-5462
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / COL4A2 protein, human; 0 / Collagen Type IV; 0 / Peptide Fragments; 0 / Recombinant Fusion Proteins; 0 / Serum Albumin
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37. Lankester KJ, Maxwell RJ, Pedley RB, Dearling JL, Qureshi UA, El-Emir E, Hill SA, Tozer GM: Combretastatin A-4-phosphate effectively increases tumor retention of the therapeutic antibody, 131I-A5B7, even at doses that are sub-optimal for vascular shut-down. Int J Oncol; 2007 Feb;30(2):453-60
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  • [Title] Combretastatin A-4-phosphate effectively increases tumor retention of the therapeutic antibody, 131I-A5B7, even at doses that are sub-optimal for vascular shut-down.
  • Radioimmunotherapy using 131I-A5B7, an anti-CEA antibody, in combination with the vascular disrupting agent, combretastatin A4-phosphate (CA-4-P, 200 mg/kg), has produced tumor cures in SW1222 colorectal xenografts.
  • CA-4-P causes acute tumor blood vessel shutdown, which can be monitored in clinical trials using dynamic contrast enhanced magnetic resonance imaging (DCE-MRI).
  • The purpose of this study was to determine the magnitude of the anti-vascular effect of CA-4-P in the SW1222 tumor, at 200 mg/kg and at lower, more clinically relevant doses, using conventional assays; relate effects to changes in DCE-MRI parameters and determine the corresponding effects on tumor retention of 131I-A5B7.
  • The tumor vascular effects of 30, 100 and 200 mg/kg CA-4-P were determined, at 4- and 24-h post-treatment, using DCE-MRI, uptake of Hoechst 33342 for tumor vascular volume and conventional histology for necrosis.
  • The effect of CA-4-P on tumor and normal tissue 131I-A5B7 retention was also determined.
  • A significant reduction in tumor DCE-MRI kinetic parameters, the initial area under the contrast agent concentration time curve (IAUGC) and the transfer constant (Ktrans), was demonstrated at 4 h after CA-4-P, for all dose levels.
  • A similar pattern was seen for vascular volume and necrosis.
  • Despite this dose response, all three dose levels increased tumor retention of radio labeled antibody to a similar degree.
  • These results demonstrate that moderate tumor blood flow reduction following antibody administration is sufficient to improve tumor antibody retention.
  • [MeSH-minor] Animals. Cell Line, Tumor. Clinical Trials as Topic. Colorectal Neoplasms / metabolism. Combined Modality Therapy. Drug Synergism. Humans. Iodine Radioisotopes / therapeutic use. Kinetics. Magnetic Resonance Imaging. Mice. Necrosis. Neoplasm Transplantation. Time Factors

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  • (PMID = 17203228.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / A5B7 monoclonal antibody; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents, Phytogenic; 0 / Iodine Radioisotopes; 0 / Stilbenes; I5590ES2QZ / fosbretabulin
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38. Lemmens L, Claes V, Uzzell M: Managing patients with metastatic colorectal cancer on bevacizumab. Br J Nurs; 2008 Aug 14-Sep 10;17(15):944-9
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  • Bevacizumab (Avastin) is a humanized monoclonal antibody that inhibits the activity of vascular endothelial growth factor (VEGF), a key molecule controlling tumour blood vessel formation (angiogenesis).
  • By inhibiting VEGF and thus tumour angiogenesis, bevacizumab inhibits tumour growth and survival.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / nursing. Colorectal Neoplasms / pathology
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bevacizumab. Clinical Trials as Topic. Humans. Neoplasm Metastasis

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  • (PMID = 18983014.001).
  • [ISSN] 0966-0461
  • [Journal-full-title] British journal of nursing (Mark Allen Publishing)
  • [ISO-abbreviation] Br J Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
  • [Number-of-references] 47
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39. Zheng J, Zhu YM: Expression of c-erbB-2 proto-oncogene in extrahepatic cholangiocarcinoma and its clinical significance. Hepatobiliary Pancreat Dis Int; 2007 Aug;6(4):412-5
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  • [Title] Expression of c-erbB-2 proto-oncogene in extrahepatic cholangiocarcinoma and its clinical significance.
  • BACKGROUND: Many investigators have indicated that overexpression and amplification of the human proto-oncogene c-erbB-2 is an independent prognostic factor for primary tumors.
  • We studied expression of c-erbB-2 protein in tissues from extrahepatic cholangiocarcinoma, tissues peripheral to the carcinoma and normal bile ducts, and discussed the occurrence and development of extrahepatic cholangiocarcinoma.
  • Another aim was to explore possible application of the c-erbB-2 gene for clinical diagnosis, pathological differentiation and treatment of extrahepatic cholangiocarcinomas.
  • RESULTS: The rates of c-erbB-2 expression in extrahepatic cholangiocarcinomas, tissues peripheral to the carcinomas, and normal bile ducts were 80% (60/75), 56% (27/48), and 0% (0/9), respectively.
  • In the extrahepatic cholangiocarcinomas, the expression of c-erbB-2 was directly proportional to the malignant grade and tumor metastasis.
  • The expression rate of c-erbB-2 in tumors with nerve infiltration was significantly higher than in those without nerve infiltration.
  • The expression rates of c-erbB-2 in tumors with histological grade III/IV were significantly higher than in those with histological grade I.
  • The expression of c-erbB-2 was not correlated with the size or position of tumors, blood vessel infiltration or patients' sex or age.
  • The fact that the expression level of c-erbB-2 was highly correlated with differentiation grade and metastasis of the tumor suggests potential clinical importance of c-erbB-2 as a tumor biomarker in the diagnosis, treatment and prognosis of extrahepatic cholangiocarcinoma.
  • [MeSH-minor] Aged. Bile Duct Neoplasms / metabolism. Bile Ducts / metabolism. Biotin / chemistry. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged. Prognosis. Streptavidin / chemistry

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  • (PMID = 17690040.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 6SO6U10H04 / Biotin; 9013-20-1 / Streptavidin; EC 2.7.10.1 / Receptor, ErbB-2
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40. Matsushita Y, Okayama Y, Matsuo S: [The role of intraoperative ultrasonography]. Rinsho Byori; 2008 Jun;56(6):498-507
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  • US has recently been widely used for neurosurgery or abdominal surgery, 1) to check the position and size of the tumor, which can not be directly visualized, and to evaluate the relationship between the tumor and blood vessel or tissue, 2) to search for lesions not detected before surgery, 3) to search for residual tumor, 4) to carry out ultrasound-guided biopsy or puncture.

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  • (PMID = 18646635.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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41. Kim JH, Park SS, Park SH, Kim SJ, Mok YJ, Kim CS, Lee JH, Kim YS: Clinical significance of immunohistochemically-identified lymphatic and/or blood vessel tumor invasion in gastric cancer. J Surg Res; 2010 Aug;162(2):177-83
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  • [Title] Clinical significance of immunohistochemically-identified lymphatic and/or blood vessel tumor invasion in gastric cancer.
  • BACKGROUND: Tumor invasion and lymph node metastasis are significant prognostic factors for gastric cancer, and lymphatic and vascular tumor invasion are also significant risk factors for gastric cancer recurrence.
  • Recently, the immunohistochemical detection of lymphatic and blood vessel tumor invasion (LBVI) has been shown to have a higher sensitivity and specificity than hematoxylin-eosin staining methods.
  • Lymphatic vessel invasion was evaluated by immunostaining with the new selective marker, D2-40, and blood vessel invasion was assessed with anti-CD31 antibody.
  • LBVI was significantly correlated with depth of tumor invasion (P < 0.001), lymph node stage (P < 0.001), and lymph node micrometastasis (P = 0.013).
  • Univariate analysis showed tumor size, depth of tumor invasion, lymph node stage, and LBVI to have a significant impact on survival.
  • Based on multivariate analysis, however, depth of tumor invasion and lymph node stage were correlated with survival.
  • [MeSH-major] Gastrectomy / methods. Lymph Node Excision / methods. Neoplasm Invasiveness / pathology. Stomach Neoplasms / pathology. Stomach Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal. Antibodies, Monoclonal, Murine-Derived. Blood Vessels / pathology. Disease-Free Survival. Female. Humans. Immunohistochemistry / methods. Lymphatic System / pathology. Lymphatic Vessels / pathology. Male. Middle Aged. Neoplasm Recurrence, Local / epidemiology. Neoplasm Staging. Retrospective Studies. Survival Rate

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20031164.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / monoclonal antibody D2-40
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42. You WK, McDonald DM: The hepatocyte growth factor/c-Met signaling pathway as a therapeutic target to inhibit angiogenesis. BMB Rep; 2008 Dec 31;41(12):833-9
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  • Angiogenesis in tumors is driven by multiple growth factors that activate receptor tyrosine kinases.
  • An important driving force of angiogenesis in solid tumors is signaling through vascular endothelial growth factor (VEGF) and its receptors (VEGFRs).
  • However, when used alone, inhibitors of VEGF/VEGFR signaling do not destroy all blood vessels in tumors and do not slow the growth of most human cancers.
  • One promising target is the signaling pathway of hepatocyte growth factor (HGF) and its receptor (HGFR, also known as c-Met), which plays important roles in angiogenesis and tumor growth.
  • The HGF/c-Met signaling pathway is now recognized as a promising target in cancer by inhibiting angiogenesis, tumor growth, invasion, and metastasis.

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  • (PMID = 19123972.001).
  • [ISSN] 1976-6696
  • [Journal-full-title] BMB reports
  • [ISO-abbreviation] BMB Rep
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL024136; United States / NCI NIH HHS / CA / R01 CA082923; United States / NHLBI NIH HHS / HL / HL59157; United States / NHLBI NIH HHS / HL / R01 HL059157; United States / NCI NIH HHS / CA / CA82923; United States / NHLBI NIH HHS / HL / HL24136
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
  • [Number-of-references] 76
  • [Other-IDs] NLM/ NIHMS561650; NLM/ PMC4417610
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43. Whitehurst B, Flister MJ, Bagaitkar J, Volk L, Bivens CM, Pickett B, Castro-Rivera E, Brekken RA, Gerard RD, Ran S: Anti-VEGF-A therapy reduces lymphatic vessel density and expression of VEGFR-3 in an orthotopic breast tumor model. Int J Cancer; 2007 Nov 15;121(10):2181-91
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  • [Title] Anti-VEGF-A therapy reduces lymphatic vessel density and expression of VEGFR-3 in an orthotopic breast tumor model.
  • Metastasis is facilitated by lymphangiogenesis, the growth of new intratumoral or peritumoral lymphatic vessels from pre-existing vessels.
  • Vascular endothelial growth factor A (VEGF-A) is a well-known angiogenic factor.
  • We examined the effect of the anti-VEGF-A neutralizing antibody 2C3 on tumor lymphangiogenesis and metastasis in an orthotopic breast carcinoma model using MDA-MB-231 cells and its luciferase-tagged derivative, 231-Luc(+) cells.
  • Anti-VEGF-A antibody therapy reduced blood and lymphatic vessel densities by 70% and 80%, respectively, compared with the control antibody.
  • Macrophage infiltration was reduced in 2C3-treated tumors by 32%, but VEGF-C expression was unchanged.
  • In contrast, neoplastic cells and blood vessels in tumors from 2C3-treated mice expressed significantly less angiopoietin-2 (Ang-2) than tumors from control mice.
  • These results suggest a novel mechanism by which anti-VEGF-A therapy may suppress tumor lymphangiogenesis and subsequent metastasis supporting the use of anti-VEGF-A therapy to control metastasis clinically.
  • [MeSH-major] Antibodies / immunology. Antibodies / therapeutic use. Breast Neoplasms / immunology. Breast Neoplasms / metabolism. Lymphatic Vessels. Vascular Endothelial Growth Factor A / immunology. Vascular Endothelial Growth Factor Receptor-3 / metabolism
  • [MeSH-minor] Angiopoietin-2 / metabolism. Animals. Biomarkers, Tumor. Cell Line, Tumor. Cell Proliferation. Disease Models, Animal. Female. Humans. Lung Neoplasms / immunology. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Macrophages / immunology. Mice. Mice, SCID. Vascular Endothelial Growth Factor C / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17597103.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiopoietin-2; 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
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44. Reynolds AR: Potential relevance of bell-shaped and u-shaped dose-responses for the therapeutic targeting of angiogenesis in cancer. Dose Response; 2009;8(3):253-84
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  • Tumor angiogenesis, the growth of new blood vessels into tumors, facilitates tumor growth and thus represents an attractive therapeutic target.
  • Recent work has focused on understanding the effects of anti-angiogenic agents on tumor biology and has revealed a number of new findings that may help to explain the limited efficacy of angiogenesis inhibitors.
  • Hormesis may also be relevant for drugs that target the vascular endothelial growth factor (VEGF) signalling pathway and for metronomic chemotherapy.

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  • (PMID = 20877487.001).
  • [ISSN] 1559-3258
  • [Journal-full-title] Dose-response : a publication of International Hormesis Society
  • [ISO-abbreviation] Dose Response
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2939687
  • [Keywords] NOTNLM ; angiogenesis / anti-angiogenic therapy / biphasic / chemotherapy / hormesis / pharmacodynamics
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45. Yu J, May L, Milsom C, Anderson GM, Weitz JI, Luyendyk JP, Broze G, Mackman N, Rak J: Contribution of host-derived tissue factor to tumor neovascularization. Arterioscler Thromb Vasc Biol; 2008 Nov;28(11):1975-81
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  • [Title] Contribution of host-derived tissue factor to tumor neovascularization.
  • OBJECTIVE: The role of host-derived tissue factor (TF) in tumor growth, angiogenesis, and metastasis has hitherto been unclear and was investigated in this study.
  • METHODS AND RESULTS: We compared tumor growth, vascularity, and responses to cyclophosphamide (CTX) of tumors in wild-type (wt) mice, or in animals with TF levels reduced by 99% (low-TF mice).
  • Global growth rate of 3 different types of transplantable tumors (LLC, B16F1, and ES teratoma) or metastasis were unchanged in low-TF mice.
  • However, several unexpected tumor/context-specific alterations were observed in these mice, including:.
  • (1) reduced tumor blood vessel size in B16F1 tumors;.
  • (3) aborted tumor growth after inoculation of TF-deficient tumor cells (ES TF(-/-)) in low-TF mice.
  • TF-deficient tumor cells grew readily in mice with normal TF levels and attracted exclusively host-related blood vessels (without vasculogenic mimicry).
  • We postulate that this complementarity may result from tumor-vascular transfer of TF-containing microvesicles, as we observed such transfer using human cancer cells (A431) and mouse endothelial cells, both in vitro and in vivo.
  • CONCLUSIONS: Our study points to an important but context-dependent role of host TF in tumor formation, angiogenesis and therapy.

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  • (PMID = 18772494.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL095096-01; United States / NHLBI NIH HHS / HL / R01 HL095096; United States / NHLBI NIH HHS / HL / R01 HL095096-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide; 9035-58-9 / Thromboplastin
  • [Other-IDs] NLM/ NIHMS126028; NLM/ PMC2848475
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46. Huber MA, Kraut N, Schweifer N, Dolznig H, Peter RU, Schubert RD, Scharffetter-Kochanek K, Pehamberger H, Garin-Chesa P: Expression of stromal cell markers in distinct compartments of human skin cancers. J Cutan Pathol; 2006 Feb;33(2):145-55
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  • BACKGROUND: The importance of changes in the supporting tumor stroma for cancer initiation and progression is well established.
  • The characteristics of an activated tumor stroma, however, are not completely understood.
  • In an effort to better characterize the desmoplastic response to human skin tumors, we evaluated the expression pattern of three stromal cell markers, fibroblast-activation protein (FAP), endoglyx-1, and endosialin, in a series of melanocytic and epithelial skin tumors.
  • RESULTS: FAP-positive fibroblasts were detected in all tumor tissues tested, including cases of melanocytic nevi, melanoma metastases, basal cell carcinomas, and squamous cell carcinomas.
  • Endoglyx-1 expression was confined to normal and tumor blood vessel endothelium including 'hot spots' of neoangiogenesis within the cutaneous melanoma metastases.
  • Endosialin was selectively induced in subsets of small- and medium-sized tumor blood vessels in melanoma metastases and squamous cell carcinomas.
  • CONCLUSIONS: These data describe novel aspects of stromal marker expression in distinct compartments of human skin tumors and may point to potential targets for novel therapeutic strategies aimed at the tumor stroma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Skin Neoplasms / metabolism. Stromal Cells / metabolism
  • [MeSH-minor] Antigens, CD. Antigens, Neoplasm / biosynthesis. Antigens, Neoplasm / genetics. Antigens, Surface / biosynthesis. Antigens, Surface / genetics. Gelatinases. Gene Expression Profiling. Humans. Immunohistochemistry. Membrane Glycoproteins / biosynthesis. Membrane Glycoproteins / genetics. Membrane Proteins / biosynthesis. Membrane Proteins / genetics. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Serine Endopeptidases / biosynthesis. Serine Endopeptidases / genetics

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  • (PMID = 16420310.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / CD248 protein, human; 0 / EMILIN3 protein, human; 0 / Membrane Glycoproteins; 0 / Membrane Proteins; 0 / Neoplasm Proteins; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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47. Veeravagu A, Hou LC, Hsu AR, Cai W, Greve JM, Chen X, Tse V: The temporal correlation of dynamic contrast-enhanced magnetic resonance imaging with tumor angiogenesis in a murine glioblastoma model. Neurol Res; 2008 Nov;30(9):952-9
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  • [Title] The temporal correlation of dynamic contrast-enhanced magnetic resonance imaging with tumor angiogenesis in a murine glioblastoma model.
  • OBJECTIVE: Glioblastoma multiforme (GBM) is a WHO grade IV malignant brain tumor with poor prognosis, despite advances in surgical and adjuvant therapy.
  • GBM is characterized by areas of central necrosis and high levels of angiogenesis, during which increased vascular permeability allows for the extravasation of endothelial progenitor cells to support blood vessel and tumor growth.
  • The purpose of this study was to characterize changes in tumor vascular permeability, vascular density and vessel morphology in vivo during angiogenesis.
  • METHODS: An orthotropic murine (GL26) glioblastoma model was used in this study. in vivo serial dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) in combination with histologic and molecular genetic analyses was performed to correlate in vivo imaging of vascular development.
  • RESULTS: DCE-MRI revealed a significant change in tumor vessel permeability dependent upon tumor progression and size.
  • Time to max signal intensity displayed a stepwise increase between days 21 and 24 (p<0.05), a critical period before exponential tumor growth during which a significant increase in tumor vascular density and vessel caliber is observed on histology.
  • DISCUSSION: In vivo changes of orthotopic glioma blood vessel permeability as shown by DCE-MRI correlates with histologic quantification of vascular density and vessel caliber as well as with the molecular expression of angiogenic factors.
  • DCE-MRI is a useful tool for non-invasive in vivo monitoring of angiogenesis in pre-clinical tumor models.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Magnetic Resonance Imaging / methods. Neovascularization, Pathologic / pathology
  • [MeSH-minor] Analysis of Variance. Angiopoietin-1 / genetics. Angiopoietin-2 / genetics. Animals. Antigens, CD31 / metabolism. Carbocyanines / chemistry. Cell Line, Tumor. Contrast Media / chemistry. Disease Models, Animal. Disease Progression. Image Enhancement / methods. Immunohistochemistry. Mice. Mice, Inbred C57BL. Neoplasm Transplantation / methods. Neoplasms, Experimental / blood supply. Neoplasms, Experimental / pathology. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 18662497.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / Antigens, CD31; 0 / CY5.5 cyanine dye; 0 / Carbocyanines; 0 / Contrast Media; 0 / Vascular Endothelial Growth Factor A
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48. Dudley AC, Klagsbrun M: Tumor endothelial cells have features of adult stem cells. Cell Cycle; 2009 Jan 15;8(2):236-8
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  • [Title] Tumor endothelial cells have features of adult stem cells.
  • We recently reported that prostate tumor-specific endothelial cells had features of mesenchymal stem cells and could transdifferentiate to form cartilage and bone-like tissues.
  • Plasticity in the tumor vasculature may be related to well-known tumor blood vessel abnormalities and could underlie an intrinsic adaptive mechanism in tumor endothelial cells for circumventing anti-angiogenic strategies.

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  • (PMID = 19158490.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA45548; United States / NCI NIH HHS / CA / P01 CA045548-23; United States / NCI NIH HHS / CA / R56 CA037392; United States / NCI NIH HHS / CA / R37 CA037392-27; United States / NCI NIH HHS / CA / CA045548-23; United States / NCI NIH HHS / CA / CA37392; United States / NCI NIH HHS / CA / L30 CA117002; United States / NCI NIH HHS / CA / CA037392-27; United States / NCI NIH HHS / CA / R37 CA037392; United States / NCI NIH HHS / CA / P01 CA045548; United States / NCI NIH HHS / CA / R01 CA037392
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS211167; NLM/ PMC2901174
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49. Il'ina TS, Bashkirov VN: [Interaction of bacteria of the genus Bartonella with the host: inhibition of apoptosis, induction of proliferation, and formation of tumors]. Mol Gen Mikrobiol Virusol; 2008;(3):3-11
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  • [Title] [Interaction of bacteria of the genus Bartonella with the host: inhibition of apoptosis, induction of proliferation, and formation of tumors].
  • The bacteria of the genus Bartonella are the causative agents for earlier not diagnosed or re-emergent diseases of the humans, danger of which increases in relation with increasing number of persons with the disturbed immune status.
  • Bartonellae are intracellular parasites, the places of their habitation in the humans and animals are the endothelial cells of blood vessels and erythrocytes.
  • The induction of the type IV secretion system, effector protein transmission, inhibition of the endothelial cells apoptosis, and induction of their proliferation lead to formation of new blood vessels and tumors.
  • [MeSH-major] Apoptosis / physiology. Bartonella / physiology. Bartonella Infections / metabolism. Endothelial Cells / pathology. Erythrocytes / pathology. Host-Pathogen Interactions. Neovascularization, Pathologic / microbiology. Vascular Neoplasms / microbiology
  • [MeSH-minor] Cell Proliferation. Endothelium, Vascular / microbiology. Endothelium, Vascular / pathology. Humans. Virulence Factors / metabolism

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  • (PMID = 18763333.001).
  • [ISSN] 0208-0613
  • [Journal-full-title] Molekuliarnaia genetika, mikrobiologiia i virusologiia
  • [ISO-abbreviation] Mol. Gen. Mikrobiol. Virusol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Virulence Factors
  • [Number-of-references] 86
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51. Horn L, Sandler A: Chemotherapy and antiangiogenic agents in non-small-cell lung cancer. Clin Lung Cancer; 2007 Feb;8 Suppl 2:S68-73
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  • Angiogenesis, the growth of new vessels from preexisting vessels, is a fundamental step in tumor growth and progression.
  • Tumor-related angiogenesis has become an attractive target for anticancer therapy.
  • Vascular endothelial growth factor (VEGF) is a key angiogenic factor implicated in tumor blood vessel formation and permeability.
  • There is emerging evidence that inhibition of a single target leads to upregulation of other angiogenic signaling cascades.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Clinical Trials as Topic. Humans. Neovascularization, Pathologic / drug therapy. Protein Kinase Inhibitors / therapeutic use. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / drug effects

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  • (PMID = 17382027.001).
  • [ISSN] 1525-7304
  • [Journal-full-title] Clinical lung cancer
  • [ISO-abbreviation] Clin Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 57
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52. Shankar S, Ganapathy S, Chen Q, Srivastava RK: Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis. Mol Cancer; 2008;7:16
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  • METHODS: Prostate cancer TRAIL-resistant LNCaP cells were implanted in Balb c nude mice to examine the effects of curcumin and/or TRAIL on tumor growth and genes related to apoptosis, metastasis and angiogenesis.
  • RESULTS: Curcumin inhibited growth of LNCaP xenografts in nude mice by inducing apoptosis (TUNEL staining) and inhibiting proliferation (PCNA and Ki67 staining), and sensitized these tumors to undergo apoptosis by TRAIL.
  • In xenogrfated tumors, curcumin upregulated the expression of TRAIL-R1/DR4, TRAIL-R2/DR5, Bax, Bak, p21/WAF1, and p27/KIP1, and inhibited the activation of NFkappaB and its gene products such as cyclin D1, VEGF, uPA, MMP-2, MMP-9, Bcl-2 and Bcl-XL.
  • Curcumin also inhibited number of blood vessels in tumors, and circulating endothelial growth factor receptor 2-positive endothelial cells in mice.
  • CONCLUSION: The ability of curcumin to inhibit tumor growth, metastasis and angiogenesis, and enhance the therapeutic potential of TRAIL suggests that curcumin alone or in combination with TRAIL can be used for prostate cancer prevention and/or therapy.
  • [MeSH-major] Apoptosis / drug effects. Curcumin / pharmacology. Drug Resistance, Neoplasm / drug effects. Neoplasm Metastasis. Neovascularization, Pathologic / pathology. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclooxygenase 2 / metabolism. Drug Screening Assays, Antitumor. Humans. Interleukin-2 / metabolism. Mice. Mice, Nude. NF-kappa B / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Receptors, Death Domain / metabolism

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  • (PMID = 18226269.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Interleukin-2; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Death Domain; 0 / TNF-Related Apoptosis-Inducing Ligand; 136601-57-5 / Cyclin D1; EC 1.14.99.1 / Cyclooxygenase 2; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2249593
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53. Doukas CN, Maglogiannis I, Chatziioannou A, Papapetropoulos A: Automated angiogenesis quantification through advanced image processing techniques. Conf Proc IEEE Eng Med Biol Soc; 2006;1:2345-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Angiogenesis, the formation of blood vessels in tumors, is an interactive process between tumor, endothelial and stromal cells in order to create a network for oxygen and nutrients supply, necessary for tumor growth.
  • According to this, angiogenic activity is considered a suitable method for both tumor growth or inhibition detection.
  • The angiogenic potential is usually estimated by counting the number of blood vessels in particular sections.
  • One of the most popular assay tissues to study the angiogenesis phenomenon is the developing chick embryo and its chorioallantoic membrane (CAM), which is a highly vascular structure lining the inner surface of the egg shell.
  • The aim of this study was to develop and validate an automated image analysis method that would give an unbiased quantification of the micro-vessel density and growth in angiogenic CAM images.
  • The results indicate the high accuracy of the tool, which has been thus extensively used for tumor growth detection at different stages of embryonic development.
  • [MeSH-major] Angiography / methods. Blood Vessels / cytology. Blood Vessels / growth & development. Image Interpretation, Computer-Assisted / methods. Imaging, Three-Dimensional / methods. Neovascularization, Physiologic / physiology. Pattern Recognition, Automated / methods

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  • (PMID = 17946107.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
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54. Shibuya K, Nakajima T, Fujiwara T, Chiyo M, Hoshino H, Moriya Y, Suzuki M, Hiroshima K, Nakatani Y, Yoshino I: Narrow band imaging with high-resolution bronchovideoscopy: a new approach for visualizing angiogenesis in squamous cell carcinoma of the lung. Lung Cancer; 2010 Aug;69(2):194-202
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: We investigated the ability of a high-resolution bronchovideoscopy system with narrow band imaging (NBI) to detect blood vessel structures in squamous cell carcinoma (SCC) of bronchi, as well as squamous dysplasia.
  • RESULTS: The following were clearly observed with NBI with high-resolution bronchovideoscopy: increased vessel growth and complex networks of tortuous vessels of various sizes, in squamous dysplasia; some dotted vessels, in addition to increased vessel growth and complex networks of tortuous vessels, in ASD; several dotted vessels and spiral or screw type tumor vessels of various sizes and grades, in SCC.
  • Capillary blood vessel and/or tumor vessel mean diameters of ASD, CIS, microinvasive and invasive carcinoma were 41.4+/-9.8 microm, 63.7+/-8.2 microm, 136.5+/-29.9 microm and 259.4+/-29.6 microm, respectively.
  • These results indicated a statistically significant increase of mean vessel diameters in the four groups (P<0.0001).
  • CONCLUSION: NBI with high-resolution bronchovideoscopy was useful for detecting the increased vessel growth and complex networks of tortuous vessels, dotted vessels and spiral or screw type tumor vessels of bronchial mucosa.
  • [MeSH-major] Bronchi / blood supply. Bronchoscopy. Carcinoma, Squamous Cell / diagnosis. Lung Neoplasms / diagnosis. Neovascularization, Pathologic

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • [CommentIn] Lung Cancer. 2010 Aug;69(2):131-2 [20554344.001]
  • (PMID = 20541831.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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55. Wehbe K, Pineau R, Eimer S, Vital A, Loiseau H, Déléris G: Differentiation between normal and tumor vasculature of animal and human glioma by FTIR imaging. Analyst; 2010 Dec;135(12):3052-9
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  • [Title] Differentiation between normal and tumor vasculature of animal and human glioma by FTIR imaging.
  • Malignant gliomas are very aggressive tumors, highly angiogenic and invading heterogeneously the surrounding brain parenchyma, making their resection very difficult.
  • To overcome the limits of current diagnostic imaging techniques used for gliomas, we proposed using FTIR imaging, with a spatial resolution from 6 to 10 μm, to provide molecular information for their histological examination, based on discrimination between normal and tumor vasculature.
  • Differentiation between normal and tumor blood vessel spectra by hierarchical cluster analysis was performed on tissue sections obtained from xenografted brain tumors of Rag-gamma mice 28 days after intracranial implantation of glioma cells, as well as for human brain tumors obtained in clinics.
  • First on the animal model, classification of FTIR spectra of blood vessels could be performed using spectral intervals based on fatty acyl (3050-2800 cm(-1)) and carbohydrate (1180-950 cm(-1)) absorptions, with the formation of two clusters corresponding to healthy and tumor parts of the tissue sections.
  • Further data treatments on these two spectral intervals provided interpretable information about the molecular contents involved in the differentiation between normal and tumor blood vessels, the latter presenting a higher level of fatty acyl chain unsaturation and an unexpected loss of absorption from osidic residues.
  • This classification method was further successfully tested on human glioma tissue sections.
  • These findings demonstrate that FTIR imaging could highlight discriminant molecular markers to distinguish between normal and tumor vasculature, and help to delimitate areas of corresponding tissue.
  • [MeSH-major] Brain Neoplasms / pathology. Capillaries / anatomy & histology. Capillaries / pathology. Diagnostic Imaging / methods. Glioma / pathology. Spectroscopy, Fourier Transform Infrared / methods
  • [MeSH-minor] Animals. Carbohydrates / analysis. Cell Line, Tumor. Cluster Analysis. Fatty Acids / analysis. Humans. Male. Mice. Mice, Inbred Strains. Neoplasm Transplantation. Neovascularization, Pathologic. Transplantation, Heterologous

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  • (PMID = 20927459.001).
  • [ISSN] 1364-5528
  • [Journal-full-title] The Analyst
  • [ISO-abbreviation] Analyst
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carbohydrates; 0 / Fatty Acids
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56. Wood PA, Bove K, You S, Chambers A, Hrushesky WJ: Cancer growth and spread are saltatory and phase-locked to the reproductive cycle through mediators of angiogenesis. Mol Cancer Ther; 2005 Jul;4(7):1065-75
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  • Tumor metastases are 2- to 3-fold more frequent when the resection is done during diestrus as compared with estrus.
  • Tumor angiogenesis is essential for both cancer growth and lethal metastatic cancer spread.
  • The balance between vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) modulates new blood vessel formation and blood vessel permeability.
  • We, therefore, asked whether the estrous cycle modulates the density of CD31-positive vessels within the tumor, the permeability of tumor blood vessels, levels of VEGF and bFGF immunoreactive protein in normal breast and breast cancer, and whether expression of these genes are modulated by the estrous cycle stage in C(3)HeB/FeJ mice.
  • We find that tumor blood vessel density and blood volume do not vary throughout the cycle; however, tumor capillary permeability is regulated by the estrous cycle being highest in diestrus, the cycle stage associated with the highest cancer growth rate and the highest frequency of post-resection cancer metastasis.
  • VEGF protein in this mammary tumor varies with the estrus cycle with highest levels in proestrus.
  • In a non-breast tumor, methylcholantrenene A sarcoma, from CD(2)F(1) mice, tumor VEGF protein also varies with the estrus cycle with highest levels in proestrus and diestrus.
  • VEGF gene expression in the mammary tumor does not change significantly across the cycle, but is modulated by the cycle in normal breast tissue. bFGF protein concentration is 6-fold higher in normal breast than in breast cancer. bFGF protein pattern in both tumor and breast are similar, opposite to VEGF, and affected by oophorectomy. bFGF message is modulated by the cycle in both breast cancer and normal breast.
  • The changes in breast cancer capillary permeability, VEGF, and bFGF that occur during each fertility cycle, in breast tissue and breast cancer, putatively in response to cyclical changes in sex hormones, might contribute, at least in part, to both the modulation of cancer growth and post-resection breast cancer spread by the fertility cycle.
  • These fertility cycle-induced effects on tumor biology also seem to extend to non-breast cancer biology.
  • [MeSH-major] Estrous Cycle / physiology. Fibroblast Growth Factor 2 / metabolism. Mammary Neoplasms, Animal / pathology. Neovascularization, Pathologic. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Blood Vessels / anatomy & histology. Blood Vessels / physiology. Capillary Permeability. Female. Gonadal Steroid Hormones / blood. Male. Mammary Glands, Animal / blood supply. Mammary Glands, Animal / metabolism. Methylcholanthrene / toxicity. Mice. Mice, Inbred Strains. Ovariectomy. RNA, Messenger / metabolism. Reference Values. Sarcoma / blood supply. Sarcoma / chemically induced. Sarcoma / metabolism

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  • (PMID = 16020664.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 50749; United States / NCI NIH HHS / CA / R01 CA31635
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 56-49-5 / Methylcholanthrene
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57. Koskinen WJ, Bono P, Leivo I, Vaheri A, Aaltonen LM, Joensuu H: Lymphatic vessel density in vocal cord carcinomas assessed with LYVE-1 receptor expression. Radiother Oncol; 2005 Nov;77(2):172-5
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  • [Title] Lymphatic vessel density in vocal cord carcinomas assessed with LYVE-1 receptor expression.
  • We investigated whether the lymphatic vessel density (LVD) of vocal cord carcinomas differs from that of other head and neck carcinomas.
  • PATIENTS AND METHODS: Deparaffinized tissue from tumors of 60 patients diagnosed with head and neck squamous cell carcinoma (HNSCC) were immunostained for LYVE-1, a novel lymphatic vessel marker.
  • Tumor blood vessel density (BVD) was assessed using immunostaining for CD31.
  • RESULTS: Tumor overall LVD, including both intra- and peritumoral lymph vessels, was 10-fold lower than the BVD (5 counts/mm2 vs. 52 mm(-2), respectively).
  • A high LVD was associated with a high BVD (P = .002), but neither was associated with the tumor size.
  • Both tumor LVD and BVD were lower in vocal cord carcinomas than in HNSCCs arising at other sites (median, 0 vs. 7 mm(-2), P=.016; and median, 36 vs. 52 mm(-2), P = .006, respectively).
  • Only one vocal cord carcinoma was associated with a regional metastasis at the time of the diagnosis.
  • Among the rest of the cases tumor size was a better predictor for the presence of regional metastases than tumor BVD or LVD in a logistic regression model (odds ratio 2.2, 95% CI 1.1-4.5).
  • CONCLUSION: Vocal cord carcinomas have a low lymph vessel density as compared with HNSCCs arising at other sites.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Gene Expression Regulation, Neoplastic. Glycoproteins / metabolism. Head and Neck Neoplasms / pathology. Lymphatic Vessels / pathology. Vocal Cords / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Biopsy, Needle. Cohort Studies. Female. Humans. Immunohistochemistry. Laryngeal Neoplasms / genetics. Laryngeal Neoplasms / mortality. Laryngeal Neoplasms / pathology. Logistic Models. Lymph Nodes / pathology. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Probability. Prognosis. Sensitivity and Specificity. Statistics, Nonparametric. Survival Rate. Vesicular Transport Proteins

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  • (PMID = 16229916.001).
  • [ISSN] 0167-8140
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / LYVE1 protein, human; 0 / Vesicular Transport Proteins
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58. Dudek AZ, Zwolak P, Jasinski P, Terai K, Gallus NJ, Ericson ME, Farassati F: Protein kinase C-beta inhibitor enzastaurin (LY317615.HCI) enhances radiation control of murine breast cancer in an orthotopic model of bone metastasis. Invest New Drugs; 2008 Feb;26(1):13-24
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  • Radiation therapy is a widely used treatment for metastatic bone cancer, but the rapid onset of tumor radioresistance is a major problem.
  • We investigated the radiosensitizing effect of enzastaurin, a protein kinase Cbeta (PKCbeta) inhibitor, on bone tumor growth and tumor-related pain.
  • Using an orthotopic model of bone metastasis, we observed that a combination of enzastaurin and localized radiation treatment reduced tumor blood vessel density, bone destruction and pain compared to single modality treatment.
  • In conclusion, we demonstrate that inhibition of PKCbeta in combination with localized radiation treatment suppresses tumor growth and alleviates pain as compared to radiation-only treatment.
  • We also show that the radiosensitizing effect of enzastaurin is associated with suppression of tumor cell proliferation and tumor-induced angiogenesis possibly through inhibition of the Ras pathway.
  • [MeSH-major] Indoles / pharmacology. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / radiotherapy. Protein Kinase C / antagonists & inhibitors. Radiation-Sensitizing Agents / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / radiation effects. Bone Neoplasms / drug therapy. Bone Neoplasms / radiotherapy. Bone Neoplasms / secondary. Caspases / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Combined Modality Therapy. Disease Models, Animal. Dose-Response Relationship, Drug. Endothelial Cells / drug effects. Endothelial Cells / radiation effects. Female. Mice. Mice, Inbred C3H. Mice, SCID. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / radiotherapy. Osteoclasts / drug effects. Osteoclasts / metabolism. Osteoclasts / radiation effects. Pain / drug therapy. Pain / radiotherapy. Protein Kinase C beta. Radiotherapy, Adjuvant / methods. Signal Transduction / drug effects. Tumor Burden / drug effects. Tumor Burden / radiation effects. ras Proteins / metabolism

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  • (PMID = 17805485.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indoles; 0 / Radiation-Sensitizing Agents; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C beta; EC 3.4.22.- / Caspases; EC 3.6.5.2 / ras Proteins; UC96G28EQF / enzastaurin
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59. Nguyen VA, Kutzner H, Fürhapter C, Tzankov A, Sepp N: Infantile hemangioma is a proliferation of LYVE-1-negative blood endothelial cells without lymphatic competence. Mod Pathol; 2006 Feb;19(2):291-8
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  • [Title] Infantile hemangioma is a proliferation of LYVE-1-negative blood endothelial cells without lymphatic competence.
  • Infantile hemangiomas are common benign vascular tumors that exhibit a characteristic history of rapid proliferation in the first year of life and slow spontaneous involution during early childhood.
  • The recent discovery of an immature phenotype of proliferating hemangioma endothelial cells due to the exclusive expression of the lymphatic endothelial hyaluronan receptor LYVE-1 led to the proposal that infantile hemangiomas are the result of a primary defect in endothelial cell maturation.
  • In immunohistochemical and immunofluorescent stains, hemangioma vessels were negative for all lymphatic endothelial cell-specific markers tested during both proliferation and involution.
  • In addition, the lack of lymphatic endothelial cell-specific markers implies that infantile hemangiomas are tumors of blood vessels without lymphatic competence.

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  • (PMID = 16424896.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / HLA-DR Antigens; 0 / LYVE1 protein, human; 0 / Vesicular Transport Proteins; 0 / von Willebrand Factor
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60. di Tomaso E, Capen D, Haskell A, Hart J, Logie JJ, Jain RK, McDonald DM, Jones R, Munn LL: Mosaic tumor vessels: cellular basis and ultrastructure of focal regions lacking endothelial cell markers. Cancer Res; 2005 Jul 1;65(13):5740-9
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  • [Title] Mosaic tumor vessels: cellular basis and ultrastructure of focal regions lacking endothelial cell markers.
  • Endothelial cells of blood vessels in tumors may be thin, fragile, and defective in barrier function.
  • We found previously that the endothelium of vessels in human colon carcinoma xenografts in mice is a mosaic structure.
  • Approximately 85% of tumor vessels have uniform CD31 and/or CD105 immunoreactivity, but the remainder have focal regions that lack these common endothelial markers.
  • The present study assessed the ultrastructure of the vessel lining and the integrity of the basement membrane in these regions.
  • Using immunolabeling and confocal microscopy, we identified blood vessels that lacked CD31 and CD105 immunoreactivity and then analyzed the ultrastructure of these vessels by transmission electron microscopy.
  • Eleven percent of vessels in orthotopic tumors and 24% of vessels in ectopic tumors had defects in CD31 and CD105 staining measuring on average 10.8 microm (range, 1-41.2 microm).
  • Ultrastructural studies identified endothelial cells at 92% of CD31- and CD105-negative sites in orthotopic tumors and 70% of the sites in ectopic tumors.
  • Thus, most regions of tumor vessels that lack CD31 and CD105 immunoreactivity represent attenuated endothelial cells with abnormal expression of endothelial cell markers, but some are gaps between endothelial cells.
  • [MeSH-major] Antigens, CD31 / analysis. Colonic Neoplasms / blood supply. Vascular Cell Adhesion Molecule-1 / analysis
  • [MeSH-minor] Animals. Antigens, CD. Basement Membrane / immunology. Basement Membrane / ultrastructure. Blood Vessels / immunology. Blood Vessels / ultrastructure. Cell Line, Tumor. Female. Humans. Immunohistochemistry. Mice. Mice, SCID. Microscopy, Confocal. Microscopy, Electron. Neoplasm Transplantation. Neovascularization, Pathologic / immunology. Neovascularization, Pathologic / pathology. Receptors, Cell Surface. Transplantation, Heterologous

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  • (PMID = 15994949.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA80124; United States / NHLBI NIH HHS / HL / P01-HL24136; United States / NCI NIH HHS / CA / P50-CA90270; United States / NCI NIH HHS / CA / R01-CA82923; United States / NHLBI NIH HHS / HL / R01-HL59157
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD31; 0 / ENG protein, human; 0 / Receptors, Cell Surface; 0 / Vascular Cell Adhesion Molecule-1
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61. Renner O, Carnero A: Mouse models to decipher the PI3K signaling network in human cancer. Curr Mol Med; 2009 Jun;9(5):612-25
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  • Combining tissue-specific expression of PI3K and AKT with a secondary oncogenic event, for example, leads to the development of specific tumors.
  • Such models are more accurate for growth studies of human tumors than those involving xenograft tumors, due to the interconnection of the tumors with blood vessels.
  • With the discovery of oncogenic mutations in members of the PI3K pathway, mouse lines harboring these mutations are being developed in order to imitate the molecular features of a human tumor.
  • [MeSH-major] Neoplasms / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Signal Transduction

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  • (PMID = 19601810.001).
  • [ISSN] 1875-5666
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 191
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62. Ogasawara S, Yano H, Momosaki S, Akiba J, Nishida N, Kojiro S, Moriya F, Ishizaki H, Kuratomi K, Kojiro M: Growth inhibitory effects of IFN-beta on human liver cancer cells in vitro and in vivo. J Interferon Cytokine Res; 2007 Jun;27(6):507-16
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  • After HAK-1B cells were transplanted into nude mice, various doses of IFN-beta were administered, and the tumor volume, weight, histology, tumor blood vessel, and angiogenesis factor expression were examined.
  • IFN-beta induced a dose-dependent decrease in tumor volume and weight and a significant increase of apoptosis in the tumor.
  • Both basic fibroblast growth factor (bFGF) and blood vessel number in the tumor decreased only in mice receiving the lowest dose (1000 IU) of IFN-beta.
  • [MeSH-major] Interferon-beta / pharmacology. Liver Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. Disease Progression. Female. Fluorouracil / pharmacology. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Receptor, Interferon alpha-beta / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 17572015.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 156986-95-7 / Receptor, Interferon alpha-beta; 77238-31-4 / Interferon-beta; U3P01618RT / Fluorouracil
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63. Zhou S, Xu S, Zhang H, Liu Z, Liang Z, Song X, Jiang Y, Zhao D: [Prognostic significance of angiogenesis and blood vessel invasion in stage I non-small cell lung cancer after complete surgical resection]. Zhongguo Fei Ai Za Zhi; 2007 Feb 20;10(1):29-33
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  • [Title] [Prognostic significance of angiogenesis and blood vessel invasion in stage I non-small cell lung cancer after complete surgical resection].
  • The aim of this study is to evaluate the prognostic implications of angiogenesis and tumor blood vessel invasion (BVI) in stage I NSCLC patients who underwent complete resection.
  • Angiogenesis was assessed by vascular endothelial growth factor (VEGF) and microvessel density (MVD), BVI was assessed by examining the direct invasion of tumor cells marked by CD34 within vessel lumen.
  • CONCLUSIONS: Tumor vessel invasion and high VEGF expression are independent prognostic factors for overall survival of postoperative stage I NSCLC.

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  • (PMID = 21110929.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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64. Dineen SP, Sullivan LA, Beck AW, Miller AF, Carbon JG, Mamluk R, Wong H, Brekken RA: The Adnectin CT-322 is a novel VEGF receptor 2 inhibitor that decreases tumor burden in an orthotopic mouse model of pancreatic cancer. BMC Cancer; 2008;8:352
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  • [Title] The Adnectin CT-322 is a novel VEGF receptor 2 inhibitor that decreases tumor burden in an orthotopic mouse model of pancreatic cancer.
  • Angiogenesis is required for tumor growth, and subsequently, mediators of angiogenesis are attractive targets for therapy.
  • Vascular endothelial growth factor (VEGF) is a well-characterized mediator of tumor angiogenesis that functions primarily by binding and activating VEGF receptor 2 (VEGFR2).
  • METHODS: The efficacy of CT-322 was evaluated in vivo using two orthotopic pancreatic tumor models.
  • The first model was a human tumor xenograft where MiaPaCa-2 cells were injected into the tail of the pancreas of nude mice.
  • The second model was a syngeneic tumor using Pan02 cells injected into pancreas of C57BL/6J mice.
  • In both models, therapy was initiated once primary tumors were established.
  • Mice bearing MiaPaCa-2 tumors were treated with vehicle or CT-322 alone.
  • Gemcitabine alone or in combination with CT-322 was added to the treatment regimen of mice bearing Pan02 tumors.
  • Therapy was given twice a week for six weeks, after which the animals were sacrificed and evaluated (grossly and histologically) for primary and metastatic tumor burden.
  • Primary tumors were also evaluated by immunohistochemistry for the level of apoptosis (TUNEL), microvessel density (MECA-32), and VEGF-activated blood vessels (Gv39M).
  • RESULTS: Treatment with CT-322 was effective at preventing pancreatic tumor growth and metastasis in orthotopic xenograft and syngeneic models of pancreatic cancer.
  • Additionally, CT-322 treatment increased apoptosis, reduced microvessel density and reduced the number of VEGF-activated blood vessels in tumors.
  • Finally, CT-322, in combination with gemcitabine was safe and effective at controlling the growth of syngeneic pancreatic tumors in immunocompetent mice.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Neovascularization, Pathologic / drug therapy. Pancreatic Neoplasms / drug therapy. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Line, Tumor. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Deoxycytidine / therapeutic use. Disease Models, Animal. Female. Humans. Mice. Mice, Inbred C57BL. Mice, Nude. Necrosis. Neoplasm Metastasis / drug therapy. Treatment Outcome. Xenograft Model Antitumor Assays


65. Burton JB, Priceman SJ, Sung JL, Brakenhielm E, An DS, Pytowski B, Alitalo K, Wu L: Suppression of prostate cancer nodal and systemic metastasis by blockade of the lymphangiogenic axis. Cancer Res; 2008 Oct 1;68(19):7828-37
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  • Our group, along with others, has shown that initial tumor cell dissemination to regional lymph nodes via lymphatics also promotes systemic metastasis in mouse models.
  • The aim of this study was to investigate the efficacy of suppressive therapies targeting either the angiogenic or lymphangiogenic axis in inhibiting regional lymph node and systemic metastasis in subcutaneous and orthotopic prostate tumor xenografts.
  • Both androgen-dependent and more aggressive androgen-independent prostate tumors were used in our investigations.
  • Interestingly, we observed that the threshold for dissemination is lower in the vascular-rich prostatic microenvironment compared with subcutaneously grafted tumors.
  • Both vascular endothelial growth factor-C (VEGF-C) ligand trap (sVEGFR-3) and antibody directed against VEGFR-3 (mF4-31C1) significantly reduced tumor lymphangiogenesis and metastasis to regional lymph nodes and distal vital organs without influencing tumor growth.
  • Conversely, angiogenic blockade by short hairpin RNA against VEGF or anti-VEGFR-2 antibody (DC101) reduced tumor blood vessel density, significantly delayed tumor growth, and reduced systemic metastasis, although it was ineffective in reducing lymphangiogenesis or nodal metastasis.
  • Collectively, these data clarify the utility of vascular therapeutics in prostate tumor growth and metastasis, particularly in the context of the prostate microenvironment.

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  • (PMID = 18829538.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA092131-07; United States / NCI NIH HHS / CA / P50 CA86306; United States / NCI NIH HHS / CA / P50 CA086306; United States / NCI NIH HHS / CA / CA101904-05; United States / NCI NIH HHS / CA / CA122693-02; United States / NCI NIH HHS / CA / P50 CA092131; United States / NCI NIH HHS / CA / R21 CA122693-02; United States / NCI NIH HHS / CA / R01 CA101904; United States / NCI NIH HHS / CA / R21 CA122693; United States / NCI NIH HHS / CA / R01 CA101904-05
  • [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 / Vascular Endothelial Growth Factor C; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
  • [Other-IDs] NLM/ NIHMS165537; NLM/ PMC2800077
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66. Bielawska-Pohl A, Blesson S, Benlalam H, Trenado A, Opolon P, Bawa O, Rouffiac V, Dus D, Kieda C, Chouaib S: The anti-angiogenic activity of IL-12 is increased in iNOS-/- mice and involves NK cells. J Mol Med (Berl); 2010 Aug;88(8):775-84
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  • We have previously reported that the in vivo transfer of murine interleukin-12 (IL-12) gene using a Semliki Forest virus vector induced tumor regression through inhibition of tumor blood vessel formation.
  • To examine whether IL-12 anti-angiogenic activity interferes with the NO pathway, we used inducible nitric oxide synthase-deficient mice (iNOS-/-) and demonstrated that the anti-tumor effect of IL-12 is more pronounced in these mice.
  • In addition, despite the increased level of intratumoral VEGF in iNOS-/- mice, IL-12 induced a stronger inhibition of blood vessel formation.
  • Histological analysis of SFV-IL-12-treated tumors showed an increase in natural killer (NK) perivascular infiltration in iNOS-/- as compared to control mice.
  • [MeSH-minor] Animals. Endothelial Cells / pathology. Gene Knockout Techniques. Mice. Mice, Inbred C57BL. Nitric Oxide / immunology. Vascular Endothelial Growth Factor A / immunology

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  • (PMID = 20383693.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 187348-17-0 / Interleukin-12; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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67. Jassar AS, Suzuki E, Kapoor V, Sun J, Silverberg MB, Cheung L, Burdick MD, Strieter RM, Ching LM, Kaiser LR, Albelda SM: Activation of tumor-associated macrophages by the vascular disrupting agent 5,6-dimethylxanthenone-4-acetic acid induces an effective CD8+ T-cell-mediated antitumor immune response in murine models of lung cancer and mesothelioma. Cancer Res; 2005 Dec 15;65(24):11752-61
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  • [Title] Activation of tumor-associated macrophages by the vascular disrupting agent 5,6-dimethylxanthenone-4-acetic acid induces an effective CD8+ T-cell-mediated antitumor immune response in murine models of lung cancer and mesothelioma.
  • 5,6-Dimethylxanthenone-4-acetic acid (DMXAA) is a small molecule in the flavanoid class that has antitumor activity thought to be due to ability to induce high local levels of tumor necrosis factor (TNF)-alpha that disrupt established blood vessels within tumors.
  • Although characterized as a "vascular disrupting agent," there are some studies suggesting that DMXAA also has effects on the immune system that are important for its efficacy.
  • We show that DMXAA efficiently activated tumor-associated macrophages to release a variety of immunostimulatory cytokines and chemokines, including TNF-alpha; IFN-inducible protein-10; interleukin-6; macrophage inflammatory protein-2; monocyte chemotactic protein-1; and regulated on activation, normal T-cell expressed, and secreted.
  • DMXAA treatment was highly effective in both small and large flank tumors.
  • Animals cured of tumors by DMXAA generated a systemic memory response and were resistant to tumor cell rechallenge.
  • DMXAA treatment led to initial tumor infiltration with macrophages that was followed by an influx of CD8(+) T cells.
  • These CD8(+) T cells were required for antitumor efficacy because tumor inhibitory activity was lost in nude mice, mice depleted of CD8(+) T cells, and perforin knockout mice, but not in CD4(+) T-cell-depleted mice.
  • These data show that activation of tumor-associated macrophages by DMXAA is an efficient way to generate a CD8(+) T-cell-dependent antitumor immune response even in animals with relatively nonimmunogenic tumors.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. CD8-Positive T-Lymphocytes / immunology. Disease Models, Animal. Lung Neoplasms. Macrophages / metabolism. Mesothelioma. Neovascularization, Pathologic / therapy. Xanthones / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. CD4-Positive T-Lymphocytes / immunology. Carcinoma, Lewis Lung / blood supply. Carcinoma, Lewis Lung / immunology. Carcinoma, Lewis Lung / therapy. Chemokines / metabolism. Cytokines / metabolism. Immunotherapy. Membrane Glycoproteins / genetics. Membrane Glycoproteins / physiology. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Mice, Nude. Perforin. Pore Forming Cytotoxic Proteins

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  • (PMID = 16357188.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 66726
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Chemokines; 0 / Cytokines; 0 / Membrane Glycoproteins; 0 / Pore Forming Cytotoxic Proteins; 0 / Xanthones; 0829J8133H / vadimezan; 126465-35-8 / Perforin
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68. Huang K, Pradhan A, Nahar S, Montenegro M, Yan K, Yu Y: Geant4 estimation model of high Z atom concentration for tumor vessel ablation. Conf Proc IEEE Eng Med Biol Soc; 2009;2009:3060-3
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  • [Title] Geant4 estimation model of high Z atom concentration for tumor vessel ablation.
  • In our novel technique of tumor vessels treatment, High Z (HZ) contrast atoms are injected into the blood vessel and the tumor region is irradiated with "narrowband" fluorescence photon (FP) beam tuned to the "resonance energies".
  • The results also showed that the minimum molar concentration required for apoptosis of tumor endothelial cells (ECs) for Gd, Pt, Au and U in normal experimental condition were 220.44 nmol/ml, 55.57 nmol/ml, 49.78 nmol/ml and 9.05 nmol/ml, respectively.
  • [MeSH-major] Endothelial Cells / pathology. Neoplasms / pathology. Neoplasms / radiotherapy. Radiotherapy Dosage. Radiotherapy Planning, Computer-Assisted / methods

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  • (PMID = 19964608.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 49DFR088MY / Platinum; 4OC371KSTK / Uranium; 7440-57-5 / Gold; AU0V1LM3JT / Gadolinium
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69. Fannon M, Forsten-Williams K, Nugent MA, Gregory KJ, Chu CL, Goerges-Wildt AL, Panigrahy D, Kaipainen A, Barnes C, Lapp C, Shing Y: Sucrose octasulfate regulates fibroblast growth factor-2 binding, transport, and activity: potential for regulation of tumor growth. J Cell Physiol; 2008 May;215(2):434-41
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  • [Title] Sucrose octasulfate regulates fibroblast growth factor-2 binding, transport, and activity: potential for regulation of tumor growth.
  • There are, however, many potent growth factors involved in tumor and blood vessel growth that bind to heparin with high affinity and their regulation by heparin may play a role in heparin's efficacy.
  • We therefore chose to study the activity of a heparin analog, sucrose octasulfate (SOS), which has been similarly shown to interact with heparin-binding growth factors.
  • Using mouse melanoma and lung carcinoma models, we demonstrate in vivo inhibition of tumor growth by SOS.
  • Studies were then performed to assess the effect of SOS on basic fibroblast growth factor (FGF-2) activity, a growth factor which promotes tumor and blood vessel growth and is produced by B16 melanoma cells.
  • Our results suggest that molecules such as SOS have the potential to remove growth factors from tumor microenvironments and the approach offers an attractive area for further study.

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
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  • (PMID = 18163458.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL086644-02; United States / NHLBI NIH HHS / HL / R01 HL056200; United States / NHLBI NIH HHS / HL / R01 HL086644; United States / NHLBI NIH HHS / HL / HL086644; United States / NHLBI NIH HHS / HL / HL56200; United States / NHLBI NIH HHS / HL / HL086644-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 103107-01-3 / Fibroblast Growth Factor 2; 57-50-1 / Sucrose; P7V86EYZ5L / sucrose octasulfate
  • [Other-IDs] NLM/ NIHMS78241; NLM/ PMC2585800
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70. Foillard S, Jin ZH, Garanger E, Boturyn D, Favrot MC, Coll JL, Dumy P: Synthesis and biological characterisation of targeted pro-apoptotic peptide. Chembiochem; 2008 Sep 22;9(14):2326-32
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  • We generated a peptide scaffold comprising two functional domains, one a tumour blood vessel "homing" motif and the other a programmed cell-death-inducing peptide sequence.
  • RGD peptides were selected to direct the molecular conjugate to alpha(V)beta(3) integrin-containing tumour cells.
  • We show that one compound displays significant biological effect in alpha(V)beta(3) integrin-containing tumour cells.

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  • (PMID = 18712748.001).
  • [ISSN] 1439-7633
  • [Journal-full-title] Chembiochem : a European journal of chemical biology
  • [ISO-abbreviation] Chembiochem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cross-Linking Reagents; 0 / Drug Carriers; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 0 / Peptides; 99896-85-2 / arginyl-glycyl-aspartic acid
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71. Dhar K, Dhar G, Majumder M, Haque I, Mehta S, Van Veldhuizen PJ, Banerjee SK, Banerjee S: Tumor cell-derived PDGF-B potentiates mouse mesenchymal stem cells-pericytes transition and recruitment through an interaction with NRP-1. Mol Cancer; 2010;9:209
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  • [Title] Tumor cell-derived PDGF-B potentiates mouse mesenchymal stem cells-pericytes transition and recruitment through an interaction with NRP-1.
  • BACKGROUND: New blood vessel formation, or angiogenic switch, is an essential event in the development of solid tumors and their metastatic growth.
  • Tumor blood vessel formation and remodeling is a complex and multi-step processes.
  • The differentiation and recruitment of mural cells including vascular smooth muscle cells and pericytes are essential steps in tumor angiogenesis.
  • However, the role of tumor cells in differentiation and recruitment of mural cells has not yet been fully elucidated.
  • This study focuses on the role of human tumor cells in governing the differentiation of mouse mesenchymal stem cells (MSCs) to pericytes and their recruitment in the tumor angiogenesis process.
  • RESULTS: We show that C3H/10T1/2 mouse embryonic mesenchymal stem cells, under the influence of different tumor cell-derived conditioned media, differentiate into mature pericytes.
  • These differentiated pericytes, in turn, are recruited to bind with capillary-like networks formed by endothelial cells on the matrigel under in vitro conditions and recruited to bind with blood vessels on gel-foam under in vivo conditions.
  • The degree of recruitment of pericytes into in vitro neo-angiogenesis is tumor cell phenotype specific.
  • We identified tumor cell-secreted platelet-derived growth factor-B (PDGF-B) as a crucial factor controlling the differentiation and recruitment processes through an interaction with neuropilin-1 (NRP-1) in mesenchymal stem cells.
  • CONCLUSION: These new insights into the roles of tumor cell-secreted PDGF-B-NRP-1 signaling in MSCs-fate determination may help to develop new antiangiogenic strategies to prevent the tumor growth and metastasis and result in more effective cancer therapies.

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  • (PMID = 20687910.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Proto-Oncogene Proteins c-sis; 144713-63-3 / Neuropilin-1
  • [Other-IDs] NLM/ PMC2922194
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72. Xu Y, Choi J, Hylander B, Sen A, Evans SS, Kraybill WG, Repasky EA: Fever-range whole body hyperthermia increases the number of perfused tumor blood vessels and therapeutic efficacy of liposomally encapsulated doxorubicin. Int J Hyperthermia; 2007 Sep;23(6):513-27
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  • [Title] Fever-range whole body hyperthermia increases the number of perfused tumor blood vessels and therapeutic efficacy of liposomally encapsulated doxorubicin.
  • (1) Can fever-range whole body hyperthermia (FR-WBH) affect the number of perfused tumor blood vessels?
  • (2) Can pre-treatment with FR-WBH improve accumulation or anti-tumor efficacy of doxorubicin or DOXIL (liposomal doxorubicin)?
  • MATERIALS AND METHODS: Perfused blood vessels were visualized by intravenous injection of the fluorescent dye (DiOC7(3)) and the number of labeled vessels in tumors and normal organs of unheated mice and those previously heated to 39.5 degrees C for 6 hours were compared.
  • Using three animal tumor models (one syngeneic murine model and two human tumor xenografts in SCID mice) we also compared tumor growth and amount of intratumoral doxorubicin (given as free drug or as DOXIL) in control mice or those given pre-treatment with FR-WBH.
  • RESULTS: FR-WBH had no effect on the number of CD-31 labeled blood vessels.
  • However, in tumors, but not in normal organs of the same animals, FR-WBH resulted in a significant increase in those blood vessels which could take up dye over a prolonged period of time after heating.
  • There was also an increase in DOXIL uptake in the tumors of mice given FR-WBH prior to drug injection as well as enhanced therapeutic efficacy in all three tumor models.
  • CONCLUSIONS: FR-WBH increases the number of perfused blood vessels in tumors over a prolonged period following FR-WBH and thus may be useful for improving tumor targeting of cancer therapeutics.
  • We discuss these data in relation to long-conserved thermoregulatory features in normal vasculature, which may be deficient in tumor vasculature.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Colonic Neoplasms / drug therapy. Doxorubicin / therapeutic use. Hyperthermia, Induced / methods. Neoplasms / blood supply. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Case-Control Studies. Cell Line, Tumor / transplantation. Combined Modality Therapy. Disease Models, Animal. Female. Fever. Humans. Mice. Mice, SCID. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy

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  • (PMID = 17952765.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA094045; United States / NCI NIH HHS / CA / CA71599
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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73. Wu M, Kodani I, Dickinson D, Huff F, Ogbureke KU, Qin H, Arun S, Dulebohn R, Al-Shabrawey M, Tawfik A, Prater S, Lewis J, Wataha J, Messer R, Hsu S: Exogenous expression of caspase-14 induces tumor suppression in human salivary cancer cells by inhibiting tumor vascularization. Anticancer Res; 2009 Oct;29(10):3811-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exogenous expression of caspase-14 induces tumor suppression in human salivary cancer cells by inhibiting tumor vascularization.
  • To determine the tumorigenicity, tumor volume, tumor pathology and vascularization were analyzed in vivo.
  • Importantly, a significant decrease in tumor blood vessel formation was observed.
  • CONCLUSION: Salivary gland cancer cells underwent growth inhibition, cell death, and reduced tumorigenicity in vivo when exogenous caspase-14 was expressed, which could be due, in part, to an inhibitory effect of caspase-14 on tumor vascularization.

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  • (PMID = 19846913.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / DE017791-03; United States / NIDCR NIH HHS / DE / K23 DE017791; United States / NIDCR NIH HHS / DE / K23 DE017791-03
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 3.4.22.- / Caspase 14
  • [Other-IDs] NLM/ NIHMS167354; NLM/ PMC2810004
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74. Duda DG, Cohen KS, Kozin SV, Perentes JY, Fukumura D, Scadden DT, Jain RK: Evidence for incorporation of bone marrow-derived endothelial cells into perfused blood vessels in tumors. Blood; 2006 Apr 1;107(7):2774-6
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  • [Title] Evidence for incorporation of bone marrow-derived endothelial cells into perfused blood vessels in tumors.
  • Recent studies have demonstrated that the cellular contribution of the bone marrow to tumor neovascularization is highly complex.
  • In this context, the extent to which bone marrow-derived cells incorporate as bona fide endothelial (nonhematopoietic) cells into perfused tumor vessels, or any new vessels formed postnatally (vasculogenesis), is unclear.
  • To this end, we developed models to characterize local vessel-derived and bone marrow-derived endothelial cells (BMD-ECs).
  • Finally, we quantified their contribution to perfused blood vessels in tumors using transplanted as well as spontaneous primary and metastatic tumor models.
  • We demonstrate that BMD-ECs incorporate in perfused tumor vessels, and that this contribution varies with organ site and mouse strain.

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