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1. 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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2. Kumar M, Tripathi K, Khanna R, Kumar M, Khanna AK: Hemangiopericytoma of the spleen: unusual presentation as multiple abscess. World J Surg Oncol; 2005;3:77

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  • BACKGROUND: Hemangiopericytoma is a soft tissue vascular neoplasm arising from capillary pericytes and is found throughout the body in soft tissues and bone.
  • Primary vascular neoplasm of the spleen constitutes the majority of nonhaematolymphoid splenic tumors like haemangioma, lymphangioma, hemangioendothelioma, hemangiopericytoma etc.
  • Splenic hemangiopericytoma is a rare tumor and probably first case was described in 1989.

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  • (PMID = 16359555.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1352359
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3. 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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  • (PMID = 16339405.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01-CA80124; United States / NCI NIH HHS / CA / R01-CA115767; United States / NCI NIH HHS / CA / R01-CA96915
  • [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 / Biomarkers
  • [Other-IDs] NLM/ PMC1895376
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4. 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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5. Perretta S, Guerrero V, Garcia-Aguilar J: Surgical treatment of rectal cancer: local resection. Surg Oncol Clin N Am; 2006 Jan;15(1):67-93
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  • Local treatment of rectal cancer aims to decrease the morbidity and the functional sequela associated with radical surgery without compromising local tumor control and long-term survival.
  • Selecting the optimal therapy for an individual patient with rectal cancer is crucial and requires consideration of both tumor and patient characteristics.
  • Only patients with well- or moderately differentiated T1 tumors without blood vessel or lymphatic vessel invasion are candidates for curative local excision as the only form of treatment.
  • Tumors penetrating the muscularis propria should not be treated by local excision alone.
  • The tumor should be removed by full-thickness local excision with an adequate normal margin for pathologic evaluation.
  • Intense, close follow-up is critical for early diagnosis of local recurrences as many of them may be surgically salvaged by radical resection.
  • Local treatment can also be used for palliation of patients with histological unfavorable or advanced tumors, and those who are medically unfit for radical surgery.
  • [MeSH-major] Colectomy / methods. Rectal Neoplasms / surgery. Rectum / surgery
  • [MeSH-minor] Combined Modality Therapy. Humans. Neoplasm Staging. Patient Selection. Preoperative Care

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  • (PMID = 16389151.001).
  • [ISSN] 1055-3207
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 110
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6. 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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7. Menon C, Ghartey A, Canter R, Feldman M, Fraker DL: Tumor necrosis factor-alpha damages tumor blood vessel integrity by targeting VE-cadherin. Ann Surg; 2006 Nov;244(5):781-91
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  • [Title] Tumor necrosis factor-alpha damages tumor blood vessel integrity by targeting VE-cadherin.
  • BACKGROUND: Isolated limb perfusion using high-dose human tumor necrosis factor-alpha with melphalan is effective therapy for bulky extremity in-transit melanoma and sarcoma.
  • OBJECTIVE: While it is widely accepted that melphalan is a DNA alkylating agent, the mechanism of selective antitumor effect of tumor necrosis factor-alpha is unclear.
  • METHODS AND RESULTS: Electron microscopic analyses of human melanoma biopsies, pre- and post-melphalan perfusion, showed that the addition of tumor necrosis factor-alpha caused gapping between endothelial cells by 3 to 6 hours post-treatment followed by vascular erythrostasis in treated tumors.
  • In human melanoma xenografts raised in mice, tumor necrosis factor-alpha selectively increased tumor vascular permeability by 3 hours and decreased tumor blood flow by 6 hours post-treatment relative to treated normal tissue.
  • In an in vitro tumor endothelial cell model, tumor necrosis factor-alpha caused vascular endothelial adherens junction protein, VE-cadherin, to relocalize within the cell membrane away from cell-cell junctions leading to gapping between endothelial cells by 3 to 6 hours post-treatment.
  • Clinical isolated limb perfusion tumor specimens, at 3 hours postperfusion, showed a discontinuous and irregular pattern of VE-cadherin expression at endothelial cell junctions when compared with normal (skin) or pretreatment tumor tissue.
  • CONCLUSIONS: Together, the data suggest that tumor necrosis factor-alpha selectively damages the integrity of tumor vasculature by disrupting VE-cadherin complexes at vascular endothelial cell junctions leading to gapping between endothelial cells, causing increased vascular leak and erythrostasis in tumors.
  • [MeSH-major] Antigens, CD / metabolism. Cadherins / metabolism. Endothelium, Vascular / drug effects. Melanoma, Experimental. Skin / blood supply. Skin Neoplasms. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Animals. Biopsy. Blood Flow Velocity. Cell Line, Tumor. Flow Cytometry. Humans. Mice. Mice, Nude. Microscopy, Electron. Neoplasm Transplantation. Transplantation, Heterologous. Treatment Outcome

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  • (PMID = 17060772.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cadherins; 0 / Tumor Necrosis Factor-alpha; 0 / cadherin 5
  • [Other-IDs] NLM/ PMC1856603
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8. Siemann DW, Horsman MR: Vascular targeted therapies in oncology. Cell Tissue Res; 2009 Jan;335(1):241-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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9. Jiang G, Jiang Y, Shen Y, Nam KH, Lee D, Gao Z: DNA loaded carrier preferential extravasation from tumor blood vessel. Int J Pharm; 2009 Mar 18;369(1-2):155-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA loaded carrier preferential extravasation from tumor blood vessel.
  • Non-viral gene delivery carriers were prepared by using DNA/polyethylenimine/polymethacrylic acid (DPP) polyplexes and its extravasation from tumor blood vessel was evaluated with mouse dorsal skin fold window chamber model.
  • The DNA/PEI (DP) complex with a ratio of N to P (10/1) was coated with polymethacrylic acid, and the ratio of PMA to DNA complex in DNA/PEI/PMA (DPP) polyplex was fixed 0.03 (w/w).
  • DPP polyplex penetrating through tumor blood vessel appeared fast and stayed longer in tumour interstitial, this fact was observed from mouse dorsal skin fold window chamber model.
  • [MeSH-minor] Animals. Cell Line, Tumor. Erythrocyte Aggregation. Flow Cytometry. Humans. Mice. Mice, Inbred C57BL. Neoplasms / blood supply. Particle Size. Skin Window Technique. Transfection / methods

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  • (PMID = 19027841.001).
  • [ISSN] 1873-3476
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Polymethacrylic Acids; 25087-26-7 / polymethacrylic acid; 9002-98-6 / Polyethyleneimine; 9007-49-2 / DNA
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10. Zalinski S, Goumard C, Scatton O, Terris B, Plantier F, Dupin N, Soubrane O: Liver recurrence of a subcutaneous temporal hemangiopericytoma: the index case. J Gastrointest Surg; 2009 Jun;13(6):1155-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liver recurrence of a subcutaneous temporal hemangiopericytoma: the index case.
  • INTRODUCTION: Hemangiopericytoma is an uncommon soft tissue vascular neoplasm.
  • Its natural history is mostly benign, but recurrences may occur and determining if these late-discovered tumors are distant metastases or synchronous slow and silent-growing locations is sometimes challenging.
  • The histopathological diagnosis and definition of hemangiopericytoma is based on its distinction with solitary fibrous tumors.
  • [MeSH-major] Hemangiopericytoma / pathology. Liver Neoplasms / pathology
  • [MeSH-minor] Breast Neoplasms / pathology. Female. Hepatectomy. Humans. Magnetic Resonance Imaging. Middle Aged. Neoplasm Recurrence, Local / pathology. Tomography, X-Ray Computed

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  • (PMID = 19148704.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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12. Kanthou C, Tozer GM: Tumour targeting by microtubule-depolymerizing vascular disrupting agents. Expert Opin Ther Targets; 2007 Nov;11(11):1443-57
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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13. Karakunnel JJ, Gulley JL, Arlen P, Mulquin M, Wright J, Turkbey IB, Choyke P, Figg WD, Dahut W: Cediranib (AZD2171) in docetaxel-resistant, castration-resistant prostate cancer (CRPC). J Clin Oncol; 2009 May 20;27(15_suppl):5141

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • VEGF is implicated in tumor blood vessel formation and in disease progression in several solid tumors.
  • RESULTS: Thirty-four of a planned 35 patients have been enrolled and 4 remain on active treatment (2-7 months).
  • There have been 13 of 23 evaluable patients with tumor shrinkage and 4 have met the criteria for partial response.
  • Targeted lesions included bone (17) and soft tissue (15).

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  • (PMID = 27964432.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Naidoo S, Raidoo DM: Tissue kallikrein and kinin receptor expression in an angiogenic co-culture neuroblastoma model. Metab Brain Dis; 2006 Sep;21(2-3):253-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue kallikrein and kinin receptor expression in an angiogenic co-culture neuroblastoma model.
  • The sprouting of new blood vessels from pre-existing vasculature (angiogenesis) is essential for tumour survival, influenced by tumour cell-endothelial cell interactions and is tightly regulated by biochemical cues including the kallikrein-kinin system (KKS).
  • Tissue kallikrein and the kinin B1R and B2R receptors were demonstrated on interacting neuroblastomas and HUVECs to varying degrees, as well as at actual heterogeneous contact zones in both 2-D and 3-D models.
  • The KKS, known to enhance DNA synthesis and process pro-angiogenic precursors of both tumour cells and the extra-cellular matrix, may, by its multi-functional activities at sites of tumour-blood vessel interactions, regulate aspects of both angiogenesis and tumourigenesis.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Kallikreins / biosynthesis. Kinins / metabolism. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Neuroblastoma / metabolism. Neuroblastoma / pathology. Receptors, Neuropeptide / biosynthesis
  • [MeSH-minor] Cell Differentiation / physiology. Coculture Techniques. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Humans. Immunohistochemistry. Kallikrein-Kinin System / physiology. Protein Transport. Tissue Distribution

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  • (PMID = 16865540.001).
  • [ISSN] 0885-7490
  • [Journal-full-title] Metabolic brain disease
  • [ISO-abbreviation] Metab Brain Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Kinins; 0 / Receptors, Neuropeptide; EC 3.4.21.- / Kallikreins
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15. El-Akra N, Noirot A, Faye JC, Souchard JP: Synthesis of estradiol-pheophorbide a conjugates: evidence of nuclear targeting, DNA damage and improved photodynamic activity in human breast cancer and vascular endothelial cells. Photochem Photobiol Sci; 2006 Nov;5(11):996-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synthesis of estradiol-pheophorbide a conjugates: evidence of nuclear targeting, DNA damage and improved photodynamic activity in human breast cancer and vascular endothelial cells.
  • The synthesis, physico-chemical properties, cellular localization and photocytotoxicity of estradiol-pheophorbide a conjugates in estrogen-dependent cancer and vascular endothelial cells are described with the aim of increasing the photodynamic activity by targeting the nucleus of both tumor and blood vessel cells.
  • [MeSH-major] Breast Neoplasms / pathology. Chlorophyll / analogs & derivatives. DNA Damage. Endothelium, Vascular / drug effects. Estradiol / chemical synthesis. Photochemotherapy
  • [MeSH-minor] Cell Line, Tumor. Humans. Reactive Oxygen Species. Spectrometry, Fluorescence. Spectrum Analysis / methods

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  • (PMID = 17077894.001).
  • [ISSN] 1474-905X
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 1406-65-1 / Chlorophyll; 15664-29-6 / pheophorbide a; 4TI98Z838E / Estradiol
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16. Sonveaux P: Provascular strategy: targeting functional adaptations of mature blood vessels in tumors to selectively influence the tumor vascular reactivity and improve cancer treatment. Radiother Oncol; 2008 Mar;86(3):300-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Provascular strategy: targeting functional adaptations of mature blood vessels in tumors to selectively influence the tumor vascular reactivity and improve cancer treatment.
  • Blood flow and flow-related microenvironmental parameters (tissue pO(2), pH, distribution, bioenergetic status, and nutrient supply) are important factors known to modulate the sensitivity of cancer cells to ionizing radiations and circulating anticancer agents.
  • Whereas tumor pO(2) and consequently tumor radiosensitivity are highly influenced by local perfusion ensuring oxygen supply, blood also serves as a vehicle for the delivery of anticancer agents to tumor cells.
  • In expanding tumors, blood flow is generally low due to the aberrant vascular architecture and to the altered microenvironment, leading to chronic hypoxia.
  • Different approaches have been developed aimed at transiently increasing blood flow and oxygen bioavailability in tumors at the time of treatment.
  • This review focuses on provascular approaches that exploit functional adaptations of mature vessels to the tumor microenvironment to sensitize tumors to radio- and chemotherapy.
  • Our contribution to the field has revealed that the stimulation of endogenous nitric oxide production and the systemic delivery of endothelin-1 inhibitors both achieve selective and transient tumor vasodilation.
  • [MeSH-major] Blood Vessels. Neoplasms / blood supply. Neoplasms / therapy. Neovascularization, Pathologic. Vasodilation
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Humans. Radiation Tolerance. Regional Blood Flow / physiology. Vasodilator Agents / pharmacology

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  • (PMID = 18313779.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vasodilator Agents
  • [Number-of-references] 150
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17. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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18. Zeng Q, Li S, Chepeha DB, Giordano TJ, Li J, Zhang H, Polverini PJ, Nor J, Kitajewski J, Wang CY: Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling. Cancer Cell; 2005 Jul;8(1):13-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling.
  • While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis.
  • Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo.
  • Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development.
  • Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Endothelium, Vascular / metabolism. Head and Neck Neoplasms / pathology. Membrane Proteins / metabolism. Mitogen-Activated Protein Kinases / metabolism. Neovascularization, Pathologic / pathology
  • [MeSH-minor] Animals. Calcium-Binding Proteins. Enzyme Activation. Female. Humans. Intercellular Signaling Peptides and Proteins. Ligands. Mice. Mice, SCID. Neoplasms / blood supply. Neoplasms / drug therapy. Neoplasms / pathology. RNA, Small Interfering / pharmacology. Receptors, Cell Surface / metabolism. Receptors, Notch. Signal Transduction

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  • (PMID = 16023595.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA100849; United States / NIDCR NIH HHS / DE / R01DE015964; United States / NIDCR NIH HHS / DE / R01DE13848
  • [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 / Calcium-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Ligands; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Cell Surface; 0 / Receptors, Notch; 134324-36-0 / Serrate proteins; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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19. Huang J, Tan Y, Tang Q, Liu X, Guan X, Feng Z, Zhu J: A high-affinity human/mouse cross-reactive monoclonal antibody, specific for VEGFR-2 linear and conformational epitopes. Cytotechnology; 2010 Jan;62(1):61-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Vascular endothelial growth factors receptor 2 (VEGFR-2) has been implicated in playing an important role in the formation of new blood vessels in tumors and other diseases.

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  • (PMID = 20387114.001).
  • [ISSN] 0920-9069
  • [Journal-full-title] Cytotechnology
  • [ISO-abbreviation] Cytotechnology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC3303004
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20. Yan Y, Xu W, Qian H, Zhu W, Mao F, Zhang X: Tumstatin45-132-TNFalpha suppresses tumour growth through anti-angiogenic effects and cytotoxicity. Biotechnol Appl Biochem; 2010 Jul;56(3):119-27
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  • [Title] Tumstatin45-132-TNFalpha suppresses tumour growth through anti-angiogenic effects and cytotoxicity.
  • Tumstatin45-132 is an 88-amino-acid fragment possessing the equivalent ability of full-length tumstatin to block new tumour blood-vessel formation and suppress tumour growth.
  • TNFalpha (tumour necrosis factor alpha), an antitumour agent, is used in clinical therapy, but is limited by its strong systemic toxicity.
  • In-vivo antitumour activities were examined in tumour-bearing mice.
  • We observed that tumstatin45-132-TNFalpha inhibited angiogenesis and tumour-cell viability in vitro.
  • In-vivo experiments showed that intratumoural injection of tumstatin45-132-TNFalpha significantly inhibited the growth of xenograft tumours in mice.
  • MRI analysis revealed that tumstatin45-132-TNFalpha treatment also decreased mean blood-vessel density in vivo.
  • Tumstatin45-132-TNFalpha exerted antitumour activities by decreasing proliferation, inducing apoptosis in tumour cells and anti-angiogenesis.
  • In conclusion, our findings suggest that tumstatin45-132-TNFalpha has significant activity against F6 tumour cells and that it may be a potential approach for cancer therapy.
  • [MeSH-minor] Animals. Apoptosis. Baculoviridae. Cell Line, Tumor. Humans. Mice. Mice, Inbred BALB C. Xenograft Model Antitumor Assays

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  • (PMID = 20569201.001).
  • [ISSN] 1470-8744
  • [Journal-full-title] Biotechnology and applied biochemistry
  • [ISO-abbreviation] Biotechnol. Appl. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Recombinant Fusion Proteins; 0 / tumstatin45-132-TNF
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21. Ryan AJ, Wedge SR: ZD6474--a novel inhibitor of VEGFR and EGFR tyrosine kinase activity. Br J Cancer; 2005 Jun;92 Suppl 1:S6-13
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  • Angiogenesis is crucial for maintaining the supply of oxygen and nutrients required to support solid tumour growth.
  • Inhibitors of tumour blood vessel formation are therefore being sought, in particular, inhibitors of vascular endothelial growth factor-A (VEGF)-signalling, which has a pivotal role in stimulating neovascular growth and survival.
  • ZD6474 is an orally bioavailable inhibitor of VEGF receptor-2 tyrosine kinase activity that in preclinical studies has been shown to inhibit both VEGF-induced signalling in endothelial cells and tumour-induced angiogenesis.
  • Consistent with inhibition of angiogenesis, once-daily oral dosing of ZD6474 produced significant broad-spectrum antitumour activity in a panel of histologically diverse human tumour xenografts.
  • In addition to its antiangiogenic properties, ZD6474 also has activity against the epidermal growth factor receptor (EGFR) tyrosine kinase, which could impart a direct inhibitory effect on tumour cell growth and survival.
  • This may be particularly relevant in tumours with a dependency upon EGFR signalling, for example in certain tumours harbouring activating mutations in EGFR.
  • [MeSH-major] Neoplasms / physiopathology. Neovascularization, Pathologic. Piperidines / pharmacology. Piperidines / therapeutic use. Quinazolines / pharmacology. Quinazolines / therapeutic use
  • [MeSH-minor] Administration, Oral. Biological Availability. Cell Survival. Drug Administration Schedule. Humans. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / genetics. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / genetics. Signal Transduction

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  • (PMID = 15928657.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 65
  • [Other-IDs] NLM/ PMC2362058
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22. Shchors K, Evan G: Tumor angiogenesis: cause or consequence of cancer? Cancer Res; 2007 Aug 1;67(15):7059-61
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  • [Title] Tumor angiogenesis: cause or consequence of cancer?
  • Both tumors and normal tissues need a blood supply for oxygen, nutrients, and waste removal.
  • However, whereas normal vasculature is hierarchically assembled into efficient networks of arteries, capillaries, and veins, the blood vessels of tumors are a mess-chaotic, leaky, inefficient, and barely making do.
  • Do tumor vessels lack the signals to mature or, instead, is their maturation actively suppressed?
  • What triggers and maintains tumor vasculature?
  • In a recent study using a switchable Myc-driven mouse tumor model, we addressed these fundamental questions.
  • We identified the inflammatory cytokine interleukin-1beta as an essential initiating trigger of vascular endothelial growth factor-dependent angiogenesis.
  • Here, we consider how kinetic studies using regulatable forms of Myc or other oncogenes can shed new light on the way tumors initiate and maintain their aberrant blood supplies.
  • [MeSH-major] Angiogenesis Inducing Agents / therapeutic use. Angiogenesis Inhibitors / therapeutic use. Neoplasms / blood supply. Neovascularization, Pathologic / drug therapy

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  • (PMID = 17671171.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA098018; United States / NCI NIH HHS / CA / F32 CA106039
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Angiogenesis Inhibitors
  • [Number-of-references] 19
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23. 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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24. 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
Hazardous Substances Data Bank. 3-Methylcholanthrene .

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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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25. 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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26. Hajitou A: Targeted systemic gene therapy and molecular imaging of cancer contribution of the vascular-targeted AAVP vector. Adv Genet; 2010;69:65-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted systemic gene therapy and molecular imaging of cancer contribution of the vascular-targeted AAVP vector.
  • We have reported a new generation of vascular-targeted systemic hybrid prokaryotic-eukaryotic vectors as chimeras between an adeno-associated virus (AAV) and targeted bacteriophage (termed AAV/phage; AAVP).
  • As a proof of concept, we assessed the in vivo efficacy of vector in animal models of cancer by displaying on the phage capsid the cyclic Arg-Gly-Asp (RGD-4C) ligand that binds to alphav integrin receptors specifically expressed on the angiogenic blood vessels of tumors.
  • The ligand-directed vector was able to specifically deliver imaging and therapeutic transgenes to tumors in mice, rats, and dogs while sparing the normal organs.
  • This chapter reviews some gene transfer strategies and the potential of the vascular-targeted AAVP vector for enhancing the effectiveness of existing systemic gene delivery and genetic-imaging technologies.
  • [MeSH-major] Bacteriophages / genetics. Dependovirus / genetics. Endothelium, Vascular / drug effects. Genetic Therapy / methods. Genetic Vectors / therapeutic use

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20807602.001).
  • [ISSN] 0065-2660
  • [Journal-full-title] Advances in genetics
  • [ISO-abbreviation] Adv. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0701159
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Receptors, Virus
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27. Kucera T, Lammert E: Ancestral vascular tube formation and its adoption by tumors. Biol Chem; 2009 Oct;390(10):985-94
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  • [Title] Ancestral vascular tube formation and its adoption by tumors.
  • Similar to growing and metabolically active tissues, tumors require a dense vasculature to gain access to oxygen and nutrients.
  • However, blood vessels in tumors differ from vessels in normal tissues in many respects.
  • In particular, the tumor vasculature is in an active state of angiogenesis or vasculogenesis, and it is immature and leaky.
  • Blood vessels are multicellular tubes formed by polarized endothelial cells, which face the patent vascular lumen with their apical cell surface, whereas their basal cell surface faces extracellular matrix on the outside of the vessels.
  • In contrast, blood vessels in invertebrates often have a vascular lumen lined by basal cell surfaces.
  • These vessels are often formed by a process named 'ancestral vascular tube formation'.
  • Here, we discuss the hypothesis that the supply of tumors with blood can be achieved by both endothelial cell-lined tubes as well as tubes formed by the tumor cells themselves using the ancestral vascular tube formation mechanism.
  • We discuss this hypothesis with a particular focus on gastrointestinal tumors.
  • [MeSH-major] Neoplasms / blood supply. Neovascularization, Pathologic. Neovascularization, Physiologic
  • [MeSH-minor] Animals. Endothelium, Vascular / cytology. Endothelium, Vascular / metabolism. Extracellular Matrix / metabolism. Gastrointestinal Neoplasms / blood supply. Gastrointestinal Neoplasms / metabolism. Gastrointestinal Neoplasms / physiopathology. Humans

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  • (PMID = 19642872.001).
  • [ISSN] 1437-4315
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 85
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28. 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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  • [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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29. 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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30. 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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31. 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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32. Ran YL, Zhong X, Hu H, Yu L, Lou JN, Yang ZH: [Establishment and application of engrafted tumor models with humanized tumor blood vessel]. Ai Zheng; 2006 Nov;25(11):1323-8
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  • [Title] [Establishment and application of engrafted tumor models with humanized tumor blood vessel].
  • BACKGROUND & OBJECTIVE: Animal models are indispensable in the studies of tumor endothelial genes and anti-angiogenic therapy.
  • This study was to build a new engrafted tumor model with humanized blood vessels.
  • The mice inoculated with only tumor cells were used as controls.
  • Tumor growth was observed.
  • The tumor-bearing mice were treated by anti-HLSEC monoclonal antibody 2B6 to observe its effect on tumor growth.
  • RESULTS: Tumor growth was significantly enhanced by the co-inoculation of HLSECs with BEL7402 cells in NOD/SCID mice; tumor weight was increased by 5.1 folds as compared with that of control.
  • GFP-labeled vessels could easily be observed in the tumors from co-inoculation of HLSECs with BEL7402 cells.
  • When treated with 2B6 antibody, humanized MVD was decreased by 65.1% in the engrafted tumors and the tumor weight lost 71.8%.
  • CONCLUSIONS: When co-inoculate with human tumor cell lines into mice, HLSECs could survive, proliferate, and contribute to tumor angiogenesis, which may enhance tumor growth.
  • The engrafted tumor in vivo model with humanized vessels can be widely used in the research of functional genes in tumor angiogenesis and anti-angiogenic therapies.
  • [MeSH-major] Endothelial Cells / transplantation. Liver Neoplasms / pathology. Neovascularization, Pathologic
  • [MeSH-minor] Animals. Cell Line, Tumor. Cells, Cultured. Disease Models, Animal. Female. Humans. Liver / cytology. Mice. Mice, Inbred NOD. Mice, Nude. Mice, SCID. Microcirculation / pathology. Neoplasm Transplantation

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  • (PMID = 17094895.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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33. 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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34. Maeda H, Bharate GY, Daruwalla J: Polymeric drugs for efficient tumor-targeted drug delivery based on EPR-effect. Eur J Pharm Biopharm; 2009 Mar;71(3):409-19
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  • [Title] Polymeric drugs for efficient tumor-targeted drug delivery based on EPR-effect.
  • Under these circumstances tumor-targeted delivery of anticancer drugs is perhaps one of the most important steps for cancer chemotherapy.
  • We reported such a drug for the first time, styrene-maleic acid copolymer-conjugated neocarzinostatin (SMANCS) in 1979, and it eventually led to formulate the concept of the enhanced permeability and retention (EPR) effect of solid tumors in 1986.
  • The EPR-effect appears as a universal phenomenon in solid tumors which warrants the development of other polymeric drugs or nanomedicine.
  • The drug concentration in tumor compared to that of the blood (T/B ratio) can be usually as high as 10-30 times.
  • In case of SMANCS/Lipiodol given via tumor feeding artery, the T/B ratio can be as high as 2000, a real pin-point targeting.
  • EPR-effect is not just passive targeting for momentary tumor delivery, but it means prolonged drug retention for more than several weeks or longer.
  • This review describes the pathophysiological mechanisms of the EPR-effect, architectural difference of tumor blood vessel, various factors involved and artificial augmentation of EPR-effect with respect to tumor-selective delivery, and then advantages and problems of macromolecular drugs.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Delayed-Action Preparations. Drug Carriers / chemistry. Humans. Polymers / chemistry. Tissue Distribution

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  • (PMID = 19070661.001).
  • [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; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Delayed-Action Preparations; 0 / Drug Carriers; 0 / Polymers
  • [Number-of-references] 122
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35. 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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36. 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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37. Stollman TH, Ruers TJ, Oyen WJ, Boerman OC: New targeted probes for radioimaging of angiogenesis. Methods; 2009 Jun;48(2):188-92
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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 new blood vessels, is a multi-step process regulated by pro- and anti-angiogenic factors.
  • In order to grow and metastasize, tumors need a constant supply of oxygen and nutrients.
  • For their growth beyond the size of 1-2 mm tumors are dependent on angiogenesis.
  • Recently, various new anti-cancer agents (e.g. bevacizumab, sorafenib and sunitinib) have become available that specifically inhibit angiogenesis in tumors.
  • To evaluate the effects of these new anti-angiogenic agents it would be of interest to scintigraphically image the process of angiogenesis in tumors.
  • 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, Robo-4).
  • Several ligands targeting these markers have been tested as a radiotracer for imaging angiogenesis in tumors.
  • Here the preclinical and clinical studies with these new tracers to image angiogenesis in tumors are reviewed.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neoplasms / diagnosis. Neovascularization, Pathologic / diagnosis
  • [MeSH-minor] Animals. Antigens, Surface. Biomarkers, Tumor / metabolism. Extracellular Matrix Proteins. Glutamate Carboxypeptidase II. Humans. Integrin alphaVbeta3 / metabolism. Matrix Metalloproteinases. Oligopeptides / metabolism. Radiopharmaceuticals. Receptors, Vascular Endothelial Growth Factor / metabolism. Vascular Endothelial Growth Factor A

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  • (PMID = 19318127.001).
  • [ISSN] 1095-9130
  • [Journal-full-title] Methods (San Diego, Calif.)
  • [ISO-abbreviation] Methods
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 0 / Radiopharmaceuticals; 0 / Vascular Endothelial Growth Factor A; 99896-85-2 / arginyl-glycyl-aspartic acid; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 71
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38. 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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39. 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

  • [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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40. 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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41. Sartippour MR, Pietras R, Marquez-Garban DC, Chen HW, Heber D, Henning SM, Sartippour G, Zhang L, Lu M, Weinberg O, Rao JY, Brooks MN: The combination of green tea and tamoxifen is effective against breast cancer. Carcinogenesis; 2006 Dec;27(12):2424-33
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  • Studies in our laboratory have provided evidence that green tea extract inhibits breast cancer growth by a direct anti-proliferative effect on the tumor cells, as well as by indirect suppressive effects on the tumor-associated endothelial cells.
  • In this study, we asked whether concurrent administration of green tea may add to the anti-tumor effects of standard breast cancer therapy.
  • In animal experiments, mice treated with both green tea and tamoxifen had the smallest MCF-7 xenograft tumor size, and the highest levels of apoptosis in tumor tissue, as compared with either agent administered alone.
  • Moreover, the suppression of angiogenesis in vivo correlated with larger areas of necrosis and lower tumor blood vessel density in treated xenografts.
  • Green tea decreased levels of ER-alpha in tumors both in vitro and in vivo.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Plant Extracts / pharmacology. Tamoxifen / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Beverages. Cell Division / drug effects. Cell Line, Tumor. Estrogen Receptor alpha / drug effects. Estrogen Receptor alpha / metabolism. Female. Humans. Mice. Mice, Nude. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Transcription, Genetic / drug effects. Transplantation, Heterologous


42. 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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43. 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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  • 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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44. Shen R, Ye Y, Chen L, Yan Q, Barsky SH, Gao JX: Precancerous stem cells can serve as tumor vasculogenic progenitors. PLoS One; 2008;3(2):e1652
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precancerous stem cells can serve as tumor vasculogenic progenitors.
  • Tumor neo-vascularization is critical for tumor growth, invasion and metastasis, which has been considered to be mediated by a mechanism of angiogenesis.
  • However, histopathological studies have suggested that tumor cells might be the progenitor for tumor vasculature.
  • Therefore, we investigated whether pCSCs serve as progenitors for tumor vasculogenesis.
  • Herein, we report that in the pCSC-derived tumors, most blood vessels were derived from pCSCs.
  • The pCSCs are much more potent in tumor vasculogenesis than the differentiated tumor monocytic cells (TMCs) from the same tumor, which had comparable or even higher capacity to produce some vascular growth factors, suggesting that the potent tumor vasculogenesis of pCSCs is associated with their intrinsic stem-like property.
  • Consistently tumor vasculogenesis was also observed in human cancers such as cervical cancer and breast cancer and xenograft lymphoma.
  • Our studies indicate that pCSCs can serve as tumor vasculogenic stem/progenitor cells (TVPCs), and may explain why anti-angiogenic cancer therapy trials are facing challenge.
  • [MeSH-major] Neoplasms / blood supply. Neovascularization, Pathologic. Precancerous Conditions / pathology. Stem Cells / pathology
  • [MeSH-minor] Angiogenic Proteins / pharmacology. Anoxia. Cell Differentiation. Cytokines / pharmacology. Humans. Up-Regulation / genetics. Vascular Endothelial Growth Factor Receptor-2 / genetics

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  • (PMID = 18286204.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Cytokines; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC2242848
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45. 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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46. Derleth C, Mayer IA: Antiangiogenic therapies in early-stage breast cancer. Clin Breast Cancer; 2010;10 Suppl 1:E23-31
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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47. Blasiak B, Tomanek B, Abulrob A, Iqbal U, Stanimirovic D, Albaghdadi H, Foniok T, Lun X, Forsyth P, Sutherland GR: Detection of T(2) changes in an early mouse brain tumor. Magn Reson Imaging; 2010 Jul;28(6):784-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of T(2) changes in an early mouse brain tumor.
  • The aim of the study was to determine the effect of early tumor growth on T(2) relaxation times in an experimental glioma model.
  • The imaging studies were performed from Day 10 through Day 13 following tumor inoculation.
  • Tumor blood vessel density was determined using quantitative immunochemistry.
  • Tumor volume was measured daily using MR images.
  • T(2) values of the tumor were measured in five areas across the tumor and calculated using a single exponential fitting of the echo train.
  • The measurements on Days 10 and 13 after tumor inoculation showed a 20% increase in T(2).
  • The changes in T(2) correlated with the size of the tumor.
  • Statistically significant differences in T(2) values were observed between the edge of the tumor and the brain tissue on Days 11, 12 and 13 (P=.014, .008, .001, respectively), but not on Day 10 (P=.364).
  • T(2) increases in growing glioma and varies heterogenously across the tumor.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Analysis of Variance. Animals. Brain / pathology. Disease Models, Animal. Disease Progression. Male. Mice. Mice, Nude. Tumor Burden

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  • [Copyright] Crown Copyright 2010. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20395097.001).
  • [ISSN] 1873-5894
  • [Journal-full-title] Magnetic resonance imaging
  • [ISO-abbreviation] Magn Reson Imaging
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / RMF-79031
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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48. Reardon DA, Egorin MJ, Desjardins A, Vredenburgh JJ, Beumer JH, Lagattuta TF, Gururangan S, Herndon JE 2nd, Salvado AJ, Friedman HS: Phase I pharmacokinetic study of the vascular endothelial growth factor receptor tyrosine kinase inhibitor vatalanib (PTK787) plus imatinib and hydroxyurea for malignant glioma. Cancer; 2009 May 15;115(10):2188-98
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I pharmacokinetic study of the vascular endothelial growth factor receptor tyrosine kinase inhibitor vatalanib (PTK787) plus imatinib and hydroxyurea for malignant glioma.
  • BACKGROUND: This study determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, vatalanib, when administered with imatinib and hydroxyurea on a continuous daily schedule among recurrent malignant glioma patients.
  • Strategies to target tumor blood vessel endothelial cells and pericytes by inhibiting VEGFR and platelet-derived growth factor, respectively, were safe among recurrent malignant glioma patients and may enhance antiangiogenesis activity.

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  • (PMID = 19248046.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108786; United States / NINDS NIH HHS / NS / 5P50-NS20023; United States / NCRR NIH HHS / RR / M01 RR 30; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NCI NIH HHS / CA / 2P30 CA47904; United States / NCI NIH HHS / CA / P30 CA047904; United States / NINDS NIH HHS / NS / NS020023-250020; United States / NCI NIH HHS / CA / 5 R37 CA11898; United States / NCI NIH HHS / CA / 5 P50 CA 108786-4; United States / NINDS NIH HHS / NS / P50 NS020023-250020; United States / NCI NIH HHS / CA / R37 CA011898
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Phthalazines; 0 / Piperazines; 0 / Pyridines; 0 / Pyrimidines; 5DX9U76296 / vatalanib; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
  • [Other-IDs] NLM/ NIHMS113633; NLM/ PMC2691174
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49. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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50. 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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51. 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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52. 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.

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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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53. 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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54. 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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55. Duncan FJ, Wulff BC, Tober KL, Ferketich AK, Martin J, Thomas-Ahner JM, Allen SD, Kusewitt DF, Oberyszyn TM, Vanbuskirk AM: Clinically relevant immunosuppressants influence UVB-induced tumor size through effects on inflammation and angiogenesis. Am J Transplant; 2007 Dec;7(12):2693-703
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  • [Title] Clinically relevant immunosuppressants influence UVB-induced tumor size through effects on inflammation and angiogenesis.
  • The mechanisms by which CsA, MMF, tacrolimus (TAC) or sirolimus (SRL), alone or in dual combinations, influence tumor development and progression are not completely understood.
  • In the current study, chronically UV-exposed mice treated with SRL alone or in combination with CsA or TAC developed more tumors than mice treated with vehicle or other immunosuppressants, but the tumors were significantly smaller and less advanced.
  • Mice treated with CsA or TAC developed significantly larger tumors than vehicle-treated mice, and a larger percentage in the CsA group were malignant.
  • The addition of MMF to CsA, but not to TAC, significantly reduced tumor size.
  • Immunosuppressant effects on UVB-induced inflammation and tumor angiogenesis may explain these findings.
  • CsA enhanced both UVB-induced inflammation and tumor blood vessel density, while MMF reduced inflammation.
  • Addition of MMF to CsA reduced tumor size and vascularity.
  • SRL did not affect inflammation, but significantly reduced tumor vascularity.
  • Thus the choice of immunosuppressants has important implications for tumor number, size and progression, likely due to the influence of immunosuppressants on UVB-induced inflammation and angiogenesis.
  • [MeSH-major] Carcinoma, Squamous Cell / etiology. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / pharmacology. Neoplasms, Radiation-Induced / pathology. Neovascularization, Pathologic / pathology. Skin Neoplasms / etiology. Ultraviolet Rays / adverse effects
  • [MeSH-minor] Animals. Blood Vessels / drug effects. Blood Vessels / pathology. Cyclosporine / adverse effects. Cyclosporine / pharmacology. Disease Models, Animal. Drug Therapy, Combination. Female. Inflammation / drug therapy. Inflammation / etiology. Inflammation / pathology. Mice. Mice, Hairless. Mycophenolic Acid / adverse effects. Mycophenolic Acid / analogs & derivatives. Mycophenolic Acid / pharmacology. Sirolimus / adverse effects. Sirolimus / pharmacology. Tacrolimus / adverse effects. Tacrolimus / pharmacology

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  • (PMID = 17941958.001).
  • [ISSN] 1600-6135
  • [Journal-full-title] American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
  • [ISO-abbreviation] Am. J. Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16058; United States / NCI NIH HHS / CA / R01 CA 109204; United States / NCI NIH HHS / CA / R03 CA 110054
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
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56. 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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57. Lu ZR, Mohs AM, Zong Y, Feng Y: Polydisulfide Gd(III) chelates as biodegradable macromolecular magnetic resonance imaging contrast agents. Int J Nanomedicine; 2006;1(1):31-40
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  • Macromolecular gadolinium (Gd)(III) complexes have a prolonged blood circulation time and can preferentially accumulate in solid tumors, depending on the tumor blood vessel hyperpermeability, resulting in superior contrast enhancement in magnetic resonance (MR) cardiovascular imaging and cancer imaging as shown in animal models.
  • Polydisulfide Gd(III) complexes have relatively long blood circulation time and gradually degrade into small Gd(III) complexes, which are rapidly excreted via renal filtration.
  • These agents result in effective and prolonged in vivo contrast enhancement in the blood pool and tumor tissue in animal models, yet demonstrate minimal Gd(III) tissue retention as the clinically used low-molecular-weight agents.

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  • (PMID = 17722260.001).
  • [ISSN] 1176-9114
  • [Journal-full-title] International journal of nanomedicine
  • [ISO-abbreviation] Int J Nanomedicine
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB000489; United States / NCI NIH HHS / CA / R33 CA095873; United States / NIBIB NIH HHS / EB / R01 EB00489
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Chelating Agents; 0 / Contrast Media; 0 / Disulfides; 0 / Macromolecular Substances; AU0V1LM3JT / Gadolinium
  • [Number-of-references] 47
  • [Other-IDs] NLM/ PMC2426761
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58. 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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59. 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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60. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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61. Jordan BF, Runquist M, Raghunand N, Baker A, Williams R, Kirkpatrick L, Powis G, Gillies RJ: Dynamic contrast-enhanced and diffusion MRI show rapid and dramatic changes in tumor microenvironment in response to inhibition of HIF-1alpha using PX-478. Neoplasia; 2005 May;7(5):475-85
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dynamic contrast-enhanced and diffusion MRI show rapid and dramatic changes in tumor microenvironment in response to inhibition of HIF-1alpha using PX-478.
  • PX-478 is a new agent known to inhibit the hypoxia-responsive transcription factor, HIF-1alpha, in experimental tumors.
  • Dynamic contrast-enhanced (DCE) and diffusion-weighted (DW) magnetic resonance imaging (MRI) were used to monitor acute effects on tumor hemodynamics and cellularity, respectively.
  • For DCE-MRI, a macromolecular contrast reagent, BSA-Gd-DTPA, was used to determine vascular permeability and vascular volume fractions.
  • PX-478 induced a dramatic reduction in tumor blood vessel permeability within 2 hours after treatment, which returned to baseline by 48 hours.
  • The anti-VEGF antibody, Avastin, reduced both the permeability and vascular volume.
  • PX-478 had no effect on the perfusion behavior of a drug-resistant tumor system, A-549.
  • Tumor cellularity, estimated from ADCw, was significantly decreased 24 and 36 hours after treatment.

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  • (PMID = 15967100.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U54 CA90821; United States / NCI NIH HHS / CA / R01 CA098920; United States / NCI NIH HHS / CA / U54 CA090821; United States / NCI NIH HHS / CA / P30 CA03074; United States / NCI NIH HHS / CA / CA077575; United States / NCI NIH HHS / CA / R24 CA083148; United States / NCI NIH HHS / CA / R01 CA077575; United States / NCI NIH HHS / CA / CA98920
  • [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 / 2-amino-3-(4'-N,N-bis(2-chloroethyl)amino)phenylpropionic acid N-oxide; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Contrast Media; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Mustard Compounds; 0 / Phenylpropionates; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC1501160
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62. 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
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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63. Yagi N, Manabe I, Tottori T, Ishihara A, Ogata F, Kim JH, Nishimura S, Fujiu K, Oishi Y, Itaka K, Kato Y, Yamauchi M, Nagai R: A nanoparticle system specifically designed to deliver short interfering RNA inhibits tumor growth in vivo. Cancer Res; 2009 Aug 15;69(16):6531-8
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

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  • [Title] A nanoparticle system specifically designed to deliver short interfering RNA inhibits tumor growth in vivo.
  • Moreover, siRNA/WS leaked from blood vessels within tumors into the tumor tissue, where it accumulated and was subsequently transfected into the tumor cells.
  • Because the transcription factor KLF5 is known to play a role in tumor angiogenesis, we designed KLF5-siRNA to test the antitumor activity of siRNA/WS.
  • KLF5-siRNA/WS exhibited significant antitumor activity, although neither WS containing control scrambled-siRNA nor saline containing KLF5-siRNA affected tumor growth.
  • KLF5-siRNA/WS inhibited Klf5 expression within tumors at both mRNA and protein levels, significantly reducing angiogenesis, and we detected no significant acute or long-term toxicity.
  • Our findings support the idea that siRNA/WS can be used to knock down specific genes within tumors and thereby exert therapeutic effects against cancers.
  • [MeSH-major] Cell Proliferation / drug effects. Drug Delivery Systems / methods. Nanoparticles / therapeutic use. Neoplasms / drug therapy. Neoplasms / pathology. RNA, Small Interfering / administration & dosage
  • [MeSH-minor] Animals. Carbocyanines / administration & dosage. Gene Transfer Techniques. Half-Life. Humans. Kruppel-Like Transcription Factors / antagonists & inhibitors. Kruppel-Like Transcription Factors / genetics. Male. Mice. Mice, Inbred C57BL. Models, Biological. RNA Stability. Tumor Cells, Cultured. Whole Body Imaging / methods

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  • (PMID = 19654315.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbocyanines; 0 / KLF5 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / RNA, Small Interfering; 0 / cyanine dye 5
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64. Shinde Patil VR, Friedrich EB, Wolley AE, Gerszten RE, Allport JR, Weissleder R: Bone marrow-derived lin(-)c-kit(+)Sca-1+ stem cells do not contribute to vasculogenesis in Lewis lung carcinoma. Neoplasia; 2005 Mar;7(3):234-40
Hazardous Substances Data Bank. 8-HYDROXYQUINOLINE .

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  • The development of tumor vasculature is thought to occur through two complementary processes: sprouting angiogenesis from preexisting blood vessels of the host, and vasculogenesis, which involves the spontaneous development of vessels through specific recruitment, differentiation, and vascular incorporation of circulating endothelial cells (EC), endothelial progenitor cells (EPC), or potentially bone marrow-derived cells.
  • Recent reports, however, have challenged the belief that bone marrow-derived cells contribute to tumor neovascularization, claiming an exclusive role for sprouting angiogenesis in tumor blood vessel development.
  • We observed that although lin(-)c-kit(+)Sca-1+ and their derived cells demonstrate significant recruitment to carcinomas in vivo, they do not appear to functionally contribute to tumor neovascularization.
  • Furthermore, our results support the hypothesis that new vessel formation in carcinomas occurs primarily through endothelialization from adjacent and preexisting vasculature.

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  • (PMID = 15799823.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA85240; United States / NCI NIH HHS / CA / T32 CA079443; United States / NCI NIH HHS / CA / P50 CA086355; United States / NCI NIH HHS / CA / CA86355; United States / NCI NIH HHS / CA / CA96978; United States / NCI NIH HHS / CA / R01 CA096978; United States / NHLBI NIH HHS / HL / HL65584; United States / NHLBI NIH HHS / HL / R01 HL065584; United States / NCI NIH HHS / CA / CA79443; United States / NCI NIH HHS / CA / R01 CA085240
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Ly; 0 / Ly6a protein, mouse; 0 / Membrane Proteins; 0 / Organometallic Compounds; 14514-42-2 / indium oxine; 5UTX5635HP / Oxyquinoline; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC1501134
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65. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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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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66. Kamat AA, Sood AK: The merits of vascular targeting for gynecologic malignancies. Curr Oncol Rep; 2005 Nov;7(6):444-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The merits of vascular targeting for gynecologic malignancies.
  • Neovascularization is an early and critical step in tumor development and progression.
  • Tumor vessels are distinct from their normal counterparts morphologically as well as at a molecular level.
  • Recent studies on factors involved in tumor vascular development have identified new therapeutic targets for inhibiting tumor neovascularization and thus tumor progression.
  • However, the process of tumor blood vessel formation is complex, and each tumor exhibits unique features in its vasculature.
  • An understanding of the relative contribution of various pathways in the development of tumor vasculature is critical for developing effective and selective therapeutic approaches.
  • In this review, the mechanisms and factors involved in tumor blood vessel formation are discussed.
  • In addition, selected novel classes of antivascular therapies, including those targeting tumor endothelial cells and other components of the tumor vasculature, are summarized.

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  • (PMID = 16221381.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA110793-01; United States / NCI NIH HHS / CA / CA110793-01; United States / NCI NIH HHS / CA / R01 CA109298; United States / NCI NIH HHS / CA / CA 11079301; United States / NCI NIH HHS / CA / 1P50CA83639; United States / NCI NIH HHS / CA / R01 CA110793; United States / NCI NIH HHS / CA / R01 CA109298-01A1; United States / NCI NIH HHS / CA / P50 CA083639; United States / NCI NIH HHS / CA / P50 CA083639-02; United States / NCI NIH HHS / CA / CA10929801; United States / NCI NIH HHS / CA / CA083639-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 61
  • [Other-IDs] NLM/ NIHMS311223; NLM/ PMC3139990
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67. Dalrymple SL, Becker RE, Isaacs JT: The quinoline-3-carboxamide anti-angiogenic agent, tasquinimod, enhances the anti-prostate cancer efficacy of androgen ablation and taxotere without effecting serum PSA directly in human xenografts. Prostate; 2007 May 15;67(7):790-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • EXPERIMENTAL DESIGN: The tumor growth of a series of human prostate cancer xenografts (CWR-22Rv1, CWR-22R-H, LAPC-4, LNCaP, PC-3 and DU-145) in male nude mice given nothing versus tasquinimod alone or in combination with androgen ablation or with androgen ablation plus taxotere were evaluated as model systems to resolve these issues.
  • RESULTS: These studies documented that daily oral treatment with tasquinimod consistently, statistically (P < 0.05) inhibited the tumor growth of each of the xenografts in a dose-dependent manner via an anti-angiogenic response as monitored by a significant (P < 0.05) decrease in the tumor blood vessel density.
  • In addition, tasquinimod also enhanced the tumor growth inhibition and survival when combined with androgen ablation plus taxotere.
  • CONCLUSIONS: These results documented that differences in serum PSA in tasquinimod-treated hosts are related to inhibition in tumor growth.
  • [MeSH-major] Androgens / physiology. Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Prostate-Specific Antigen / blood. Prostatic Neoplasms / drug therapy. Quinolines / therapeutic use. Taxoids / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Synergism. Drug Therapy, Combination. Humans. Male. Mice. Mice, Nude. Survival Analysis. Xenograft Model Antitumor Assays


68. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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  • (PMID = 19038046.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC2627916
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69. Jordan BF, Runquist M, Raghunand N, Gillies RJ, Tate WR, Powis G, Baker AF: The thioredoxin-1 inhibitor 1-methylpropyl 2-imidazolyl disulfide (PX-12) decreases vascular permeability in tumor xenografts monitored by dynamic contrast enhanced magnetic resonance imaging. Clin Cancer Res; 2005 Jan 15;11(2 Pt 1):529-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The thioredoxin-1 inhibitor 1-methylpropyl 2-imidazolyl disulfide (PX-12) decreases vascular permeability in tumor xenografts monitored by dynamic contrast enhanced magnetic resonance imaging.
  • PURPOSE: The purpose of this study was to use dynamic contrast enhanced magnetic resonance imaging (DCE-MRI) to measure changes in tumor xenograft permeability produced by the antitumor thioredoxin-1 (Trx-1) inhibitor 1-methylpropyl 2-imidazolyl disulfide (PX-12) and to assess the relationship to Trx-1 and vascular endothelial growth factor (VEGF) levels.
  • Blood vessel permeability was estimated from the slope of the enhancement curves, and tumor vascular volume fraction from the ordinate.
  • Tumor Trx-1 and VEGF was also measured.
  • RESULTS: PX-12 caused a rapid 63% decrease in the average tumor blood vessel permeability within 2 hours of administration.
  • The changes in vascular permeability were not accompanied by alterations in average tumor vascular volume fraction.
  • There was a decrease in tumor and tumor-derived VEGF in plasma at 24 hours after treatment with PX-12, but not at earlier time points.
  • However, tumor redox active Trx-1 showed a rapid decline within 2 hours following PX-12 administration that was maintained for 24 hours.
  • CONCLUSION: The rapid decrease in tumor vascular permeability caused by PX-12 administration coincided with a decrease in tumor redox active Trx-1 and preceded a decrease in VEGF.
  • DCE-MRI responses to PX-12 in patients of Trx-1 inhibition at early time points and decreased VEGF at later times, may be useful to follow tumor response and even therapeutic benefit.
  • [MeSH-major] Capillary Permeability / drug effects. Colonic Neoplasms / blood supply. Disulfides / pharmacology. Imidazoles / pharmacology. Magnetic Resonance Imaging. Thioredoxins / antagonists & inhibitors
  • [MeSH-minor] Albumins. Animals. Contrast Media. Female. Gadolinium DTPA. Humans. Mice. Mice, SCID. Oxidation-Reduction. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15701837.001).
  • [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 / P30 CA Q3074; United States / NCI NIH HHS / CA / R01 CA 077204; United States / NCI NIH HHS / CA / R01 CA 077575; United States / NCI NIH HHS / CA / R24 CA 083148; United States / NCI NIH HHS / CA / U54 CA 090821
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Albumins; 0 / Contrast Media; 0 / Disulfides; 0 / IV 2 compound; 0 / Imidazoles; 0 / TXN protein, human; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / albumin-(gadolinium-DTPA); 52500-60-4 / Thioredoxins; K2I13DR72L / Gadolinium DTPA
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70. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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71. 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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72. 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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73. Schomber T, Zumsteg A, Strittmatter K, Crnic I, Antoniadis H, Littlewood-Evans A, Wood J, Christofori G: Differential effects of the vascular endothelial growth factor receptor inhibitor PTK787/ZK222584 on tumor angiogenesis and tumor lymphangiogenesis. Mol Cancer Ther; 2009 Jan;8(1):55-63
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  • [Title] Differential effects of the vascular endothelial growth factor receptor inhibitor PTK787/ZK222584 on tumor angiogenesis and tumor lymphangiogenesis.
  • Halting tumor growth by interfering with tumor-induced angiogenesis is an attractive therapeutic approach.
  • Such treatments include humanized antibodies blocking the activity of vascular endothelial growth factor (VEGF)-A (bevacizumab), soluble VEGF receptor (VEGFR) constructs (VEGF-Trap), or small-molecule inhibitors of VEGFR signaling, including PTK787/ZK222584 (PTK/ZK), sorafenib, and sunitinib.
  • PTK/ZK has been shown previously to specifically block VEGF-induced phosphorylation of VEGFR-1, -2 and -3 and thereby to inhibit endothelial cell proliferation, differentiation, and tumor angiogenesis.
  • We have investigated the effect of PTK/ZK on tumor angiogenesis and tumor lymphangiogenesis using the Rip1Tag2 transgenic mouse model of pancreatic beta cell carcinogenesis.
  • In Rip1Tag2 mice, tumor angiogenesis is predominantly mediated by VEGF-A, and as expected, PTK/ZK efficiently impaired tumor blood vessel angiogenesis and tumor growth.
  • Double-transgenic Rip1Tag2;Rip1VEGF-C and Rip1Tag2;Rip1VEGF-D mice not only exhibit VEGF-A-dependent blood vessel angiogenesis but also tumor lymphangiogenesis induced by the transgenic expression of VEGF-C or -D.
  • In these mouse models, PTK/ZK also repressed tumor blood vessel angiogenesis and tumor growth yet failed to affect tumor lymphangiogenesis and lymphogenic metastasis.
  • Adenoviral delivery of soluble VEGFR-3 also did not prevent tumor lymphangiogenesis in these mice.
  • In contrast, spontaneous tumor lymphangiogenesis, as observed by the stochastic expression of VEGF-C and -D in tumors of neural cell adhesion molecule-deficient Rip1Tag2 mice, was repressed by PTK/ZK and soluble VEGFR-3.
  • The results indicate that the time of onset and the levels of VEGF-C/D expression may be critical variables in efficiently repressing tumor lymphangiogenesis and that pathways other than VEGFR signaling may be involved in tumor lymphangiogenesis.
  • [MeSH-major] Lymphangiogenesis / drug effects. Neoplasms / drug therapy. Neoplasms / pathology. Neovascularization, Pathologic / drug therapy. Phthalazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors

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  • (PMID = 19139113.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phthalazines; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 5DX9U76296 / vatalanib; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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74. Borgne-Sanchez A, Dupont S, Langonné A, Baux L, Lecoeur H, Chauvier D, Lassalle M, Déas O, Brière JJ, Brabant M, Roux P, Péchoux C, Briand JP, Hoebeke J, Deniaud A, Brenner C, Rustin P, Edelman L, Rebouillat D, Jacotot E: Targeted Vpr-derived peptides reach mitochondria to induce apoptosis of alphaVbeta3-expressing endothelial cells. Cell Death Differ; 2007 Mar;14(3):422-35
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  • We have designed a peptide, TEAM-VP, composed of two functional domains, one a tumor blood vessel RGD-like 'homing' motif and the other an MMP-inducing sequence derived from Vpr.
  • Hence, this chimeric peptide constitutes the first example of a virus-derived mitochondriotoxic compound as a candidate to kill selectively tumor neo-endothelia.

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  • (PMID = 16888644.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, vpr; 0 / Integrin alphaVbeta3; 0 / Peptides
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75. Larina IV, Evers BM, Ashitkov TV, Bartels C, Larin KV, Esenaliev RO: Enhancement of drug delivery in tumors by using interaction of nanoparticles with ultrasound radiation. Technol Cancer Res Treat; 2005 Apr;4(2):217-26
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  • [Title] Enhancement of drug delivery in tumors by using interaction of nanoparticles with ultrasound radiation.
  • Efficacy and safety of cancer chemo- and biotherapy are limited by poor penetration of anti-cancer drugs from blood into tumor cells.
  • Tumor blood vessel wall, slow diffusion in the interstitium, and cancer cell membrane create physiological barriers for anti-cancer drugs, in particular promising macromolecular agents.
  • Recently, we proposed to use selective accumulation of exogenous nano- and microparticles in tumors followed by ultrasound-induced cavitation for safe and efficient drug and gene delivery.
  • The experiments were performed in athymic nude mice bearing human colon KM20 tumors, which are highly resistant to chemotherapy.
  • Our studies demonstrated that ultrasound irradiation in combination with the nanoparticle and drug injections significantly decreased tumor volume and resulted in complete tumor regression at optimal irradiation conditions, while the volume of control (non-irradiated) tumors increased despite drug injections.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Colonic Neoplasms / therapy. Drug Delivery Systems / methods. Nanostructures. Ultrasonography

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  • (PMID = 15773791.001).
  • [ISSN] 1533-0346
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104748
  • [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 / Antimetabolites, Antineoplastic; 0 / Polystyrenes; U3P01618RT / Fluorouracil
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76. 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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77. Xuan JW, Bygrave M, Valiyeva F, Moussa M, Izawa JI, Bauman GS, Klibanov A, Wang F, Greenberg NM, Fenster A: Molecular targeted enhanced ultrasound imaging of flk1 reveals diagnosis and prognosis potential in a genetically engineered mouse prostate cancer model. Mol Imaging; 2009 Jul-Aug;8(4):209-20
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  • [Title] Molecular targeted enhanced ultrasound imaging of flk1 reveals diagnosis and prognosis potential in a genetically engineered mouse prostate cancer model.
  • This report aimed at testing the possibility that Flk1+ (vascular endothelial growth factor receptor 2), a crucial angiogenesis factor of most tumor cells, could be a molecular targeted imaging marker for the diagnosis and prognosis of cancer.
  • We performed Flk1-targeted microbubble-enhanced ultrasound (US) imaging of prostate cancer in a genetically engineered mouse model with normal-appearing intact US (negative) prostates and with three different tumor sizes (small, medium, and large).
  • After this peak accumulation stage of Flk1+ molecules, lower and stabilized levels of Flk1+ signals were maintained together with tumor growth from small, to medium, to large size.
  • In a longitudinal observation in a subset (n = 5) of mice with established tumors, elevated Flk1+ signals were observed in tissues surrounding the prostate cancer, for example, the ipsilateral boundary zones between two developing tumor lobes, new tumor blood vessel recruits, the urethra border, and the pelvic node basin.
  • The results of the application in a genetically engineered mouse model with prostate cancer of molecular Flk1-targeted US imaging support the contention that Flk1 can be used as a molecular imaging marker for small tumors undetectable by microimaging and as a molecular diagnostic and prognosis marker for tumor metastasis and progression.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Contrast Media / administration & dosage. Prostatic Neoplasms / ultrasonography. Vascular Endothelial Growth Factor Receptor-2 / metabolism
  • [MeSH-minor] Animals. Drug Delivery Systems / methods. Early Detection of Cancer. Image Processing, Computer-Assisted / methods. Imaging, Three-Dimensional / methods. Male. Mice. Mice, Inbred C57BL. Mice, Inbred CBA. Mice, Transgenic. Neoplasm Metastasis. Neovascularization, Pathologic / ultrasonography. Prognosis

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  • (PMID = 19728975.001).
  • [ISSN] 1535-3508
  • [Journal-full-title] Molecular imaging
  • [ISO-abbreviation] Mol Imaging
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2 U01 CA084296-06
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Contrast Media; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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78. 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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79. 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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80. Lenz G, Wright G, Dave SS, Xiao W, Powell J, Zhao H, Xu W, Tan B, Goldschmidt N, Iqbal J, Vose J, Bast M, Fu K, Weisenburger DD, Greiner TC, Armitage JO, Kyle A, May L, Gascoyne RD, Connors JM, Troen G, Holte H, Kvaloy S, Dierickx D, Verhoef G, Delabie J, Smeland EB, Jares P, Martinez A, Lopez-Guillermo A, Montserrat E, Campo E, Braziel RM, Miller TP, Rimsza LM, Cook JR, Pohlman B, Sweetenham J, Tubbs RR, Fisher RI, Hartmann E, Rosenwald A, Ott G, Muller-Hermelink HK, Wrench D, Lister TA, Jaffe ES, Wilson WH, Chan WC, Staudt LM, Lymphoma/Leukemia Molecular Profiling Project: Stromal gene signatures in large-B-cell lymphomas. N Engl J Med; 2008 Nov 27;359(22):2313-23
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  • By contrast, the prognostically unfavorable stromal-2 signature reflected tumor blood-vessel density.
  • CONCLUSIONS: Survival after treatment of diffuse large-B-cell lymphoma is influenced by differences in immune cells, fibrosis, and angiogenesis in the tumor microenvironment.


81. 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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82. Isaacs JT, Pili R, Qian DZ, Dalrymple SL, Garrison JB, Kyprianou N, Björk A, Olsson A, Leanderson T: Identification of ABR-215050 as lead second generation quinoline-3-carboxamide anti-angiogenic agent for the treatment of prostate cancer. Prostate; 2006 Dec 1;66(16):1768-78
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  • RESULTS: Based upon its superior potency (i.e., 30- to 60-fold more potent than linomide) in these assays and its lack of a proinflammation in the Beagle-dog, ABR-215050 (tasquinimod), Figure 1, was characterized for dose-response ability to inhibit the growth of a series of four additional human and rodent prostate cancer models in mice.
  • Pharmacokinetic analysis following oral dosing documented that blood and tumor tissue levels of ABR-215050 as low as 0.5-1 microM are therapeutically effective.
  • This efficacy is correlated with inhibition of angiogenesis in a variety of assays (endothelial capillary tube formation, aortic ring assay, chorioallantoic membrane assay, real-time tumor blood flow and PO(2) measurements, tumor blood vessel density, and tumor hypoxic and apoptotic fractions).
  • CONCLUSIONS: Based upon its robust and consistent anti-angiogenic activity and thus tumor growth, ABR-215050 has entered clinical trials for the treatment of prostate cancer.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Prostatic Neoplasms / blood supply. Prostatic Neoplasms / drug therapy. Quinolines / pharmacology
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cell Line, Tumor. Dogs. Humans. Hydroxyquinolines / pharmacology. Male. Mice. Neovascularization, Pathologic / drug therapy. Rats. Xenograft Model Antitumor Assays

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  • (PMID = 16955399.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Hydroxyquinolines; 0 / Quinolines; 372T2944C0 / roquinimex; 756U07KN1R / tasquinimod
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83. 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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84. 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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85. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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86. Davis CJ, Barton JH, Sesterhenn IA: Cystic angiomyolipoma of the kidney: a clinicopathologic description of 11 cases. Mod Pathol; 2006 May;19(5):669-74
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  • This report deals with 11 examples of renal angiomyolipomas (AML) which appear to include an epithelial element as a part of the neoplasm in the form of gross or microscopic cysts-usually both.
  • Three of these were known to be symptomatic: intermittent flank pain and gross hematuria for 2 months; recurrent hematuria both before and after flank trauma and a third patient with acute abdomen due to a ruptured tumor blood vessel.
  • Seven tumors were in the right kidney and four in the left.
  • Microscopically, virtually all of the tumors included multiple smaller cysts and these were lined by flat, cuboidal or columnar epithelium and occasionally hobnail epithelium.
  • There was usually a subepithelial collar of poorly differentiated cells, but the solid element of all tumors was myomatous angiomyolipoma; only one case had any adipose tissue.
  • Immunohistochemically, all tumors tested were reactive with actin, desmin and HMB-45, with the latter being more intensely positive in the subepithelial collars.
  • [MeSH-major] Angiomyolipoma / pathology. Cysts / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Actins / analysis. Adult. Aged. Antigens, Neoplasm. Desmin / analysis. Female. Humans. Immunohistochemistry. MART-1 Antigen. Male. Melanoma-Specific Antigens. Middle Aged. Muscle, Smooth / chemistry. Neoplasm Proteins / analysis. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis

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  • (PMID = 16528375.001).
  • [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 / Actins; 0 / Antigens, Neoplasm; 0 / Desmin; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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87. 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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88. Zhao X, Hu J, Huang R, Yang L: Identification of one vasculature specific phage-displayed peptide in human colon cancer. J Exp Clin Cancer Res; 2007 Dec;26(4):509-14

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  • Blood vessels of tumors might carry specific markers that are usually related to angiogenesis.
  • Investigating these heterogeneous molecules in different tumor vessels might be beneficial for promoting antiangiogenic therapy.
  • The peptide might then be a potential candidate for targeted drug delivery in antivascular therapy and diagnosis of colon cancer.
  • [MeSH-major] Colonic Neoplasms / blood supply. Peptide Library. Peptides, Cyclic / chemistry

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  • (PMID = 18365546.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CPHSKPCLC peptide; 0 / Peptide Library; 0 / Peptides, Cyclic
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89. 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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90. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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91. Ciric E, Sersa G: Radiotherapy in combination with vascular-targeted therapies. Radiol Oncol; 2010 Jun;44(2):67-78

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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