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  • 1
    Language: English
    In: Cancer Letters, Oct 28, 2010, Vol.296(2), p.160(8)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.canlet.2010.04.010 Byline: Wolf-Dietrich C. Beecken (a), Eva Maria Ringel (a), Jan Babica (b), Elsie Oppermann (c), Dietger Jonas (a), Roman A. Blaheta (a) Keywords: Angiogenesis; [beta].sub.2-Glycoprotein-I; Cell cycle; Cyclins; HUVEC Abstract: [beta].sub.2-Glycoprotein-I ([beta].sub.2gpI), an abundant plasma glycoprotein, functions as a regulator of thrombosis. Previously, we demonstrated that plasmin-clipped [beta].sub.2gpI (c[beta].sub.2gpI) exerts an anti-angiogenic effect on human umbilical vein endothelial cells (HUVEC). The present study was focused on the molecular background responsible for this phenomenon. c[beta].sub.2gpI strongly reduced HUVEC growth and proliferation as evidenced by the MTT and BrdU assay and delayed cell cycle progression arresting HUVEC in the S-and G2/M-phase. Western blot analysis indicated that c[beta].sub.2gpI inhibited cyclin A, B and D1, and enhanced p21 and p27 expression. Activity of p38 was down-regulated independently from the c[beta].sub.2gpI incubation time. Phosphorylation of ERK1/2 was not changed early (30 and 60min) but became enhanced later (90min, 4h). JNK activity was reduced rapidly after c[beta].sub.2gpI treatment but compared to controls, increased thereafter. Annexin II blockade prevented growth inhibition and cell cycle delay evoked by c[beta].sub.2gpI. We assume that c[beta].sub.2gpI's effects on HUVEC growth is mediated via cyclin A, B and D1 suppression, up-regulation of p21 and p27 and coupled to modifications of the mitogen-activated protein (MAP) kinase signalling pathway. c[beta].sub.2gpI may represent a potential endogenous angiogenesis-targeted compound, opening the possibility of a novel tool to treat cancer. Author Affiliation: (a) Department of Urology, J.W. Goethe-University, Frankfurt am Main, Germany (b) Institute of Biochemistry II, J.W. Goethe-University, Frankfurt am Main, Germany (c) Department of General and Visceral Surgery, J.W. Goethe-University, Frankfurt am Main, Germany Article History: Received 3 September 2009; Revised 19 March 2010; Accepted 6 April 2010
    Keywords: Endothelium -- Growth ; Endothelium -- Analysis
    ISSN: 0304-3835
    Source: Cengage Learning, Inc.
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  • 2
    Language: English
    In: The Journal of Urology, 2002, Vol.167(4), pp.1794-1794
    Description: Byline: Alexander Mosner, Michael Probst, Dietger Jonas, Wolf-Dietrich Beecken Keywords: intestinal fistula; bladder fistula; balloon catheterization, Foley Author Affiliation: From the Clinic for Urology and Pediatric Urology, J. W. Goethe University, Frankfurt/Main, Germany Article History: Accepted 16 November 2001
    Keywords: Intestinal Fistula ; Bladder Fistula ; Balloon Catheterization, Foley ; Medicine
    ISSN: 0022-5347
    E-ISSN: 1527-3792
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  • 3
    Language: English
    In: World Journal of Urology, 2010, Vol.28(4), pp.465-471
    Description: Byline: Eva Juengel (1), Wolf-Dietrich C. Beecken (1), Santhosh Mundiyanapurath (1), Tobias Engl (1), Dietger Jonas (1), Roman A. Blaheta (1) Keywords: Adhesion; Bladder carcinoma; HUVEC; Maspin; Valproic acid Abstract: Purpose Maspin belongs to the serpin family and has been shown to suppress tumor growth and metastasis in several tumor types. The role of maspin in bladder carcinoma has not been fully elucidated, and the object of this study was to investigate whether maspin contributes to bladder tumor adhesion to vascular endothelial cells (HUVEC). Methods Expression of maspin-coding mRNA was evaluated in a panel of bladder carcinoma cell lines. Maspin distribution in maspin mRNA.sup.high versus maspin mRNA.sup.low cells was further analyzed by flow cytometry and confocal microscopy. Adhesion to HUVEC was measured in a coculture model and correlated with the surface-bound maspin. Results Maspin.sup.high (RT-4, RT-112) cell lines strongly attached to HUVEC, whereas maspin.sup.low (UMUC-3, MGH-U1) cell lines poorly adhered to HUVEC. Distinct cytoplasmic maspin accumulation and moderate surface-bound maspin was found in RT-4 cells. Blocking maspin surface receptors prevented tumor cell attachment to HUVEC, indicating that surface-bound maspin is responsible for triggering cell adhesion. PMA-triggered elevation of surface-bound maspin was accompanied by an enhanced adhesion capacity of RT-4 cells, compared to controls. Finally, exposing the bladder carcinoma cells to the differentiation-inducing agent valproic acid led to a surface-bound (but not cytoplasmic) maspin decrease, paralleled by a significant reduction in tumor cell binding to HUVEC. Conclusion Surface-bound maspin directly controls bladder carcinoma cell adhesion to the vascular wall. Blocking this process may prevent transendothelial migration and tumor cell dissemination. Therefore, therapeutic down-regulation of surface-bound maspin might become an option to prevent tumor spread into distant organs. Author Affiliation: (1) Klinik fur Urologie und Kinderurologie, Zentrum der Chirurgie, Johann Wolfgang Goethe-Universitatsklinik, Klinik fur Urologie und Kinderurologie, Interdisziplinares Forschungs- und Laborgebaude, Chirurgische Forschung, Haus 25, Zi 204, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany Article History: Registration Date: 12/03/2010 Received Date: 12/10/2009 Accepted Date: 11/03/2010 Online Date: 25/03/2010
    Keywords: Adhesion ; Bladder carcinoma ; HUVEC ; Maspin ; Valproic acid
    ISSN: 0724-4983
    E-ISSN: 1433-8726
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  • 4
    In: Journal of the National Cancer Institute, 2001, Vol.93(3), pp.208-213
    Description: Background: Tumors commonly outgrow their blood supply, thereby creating hypoxic conditions, which induce apoptosis and increase expression of angiogenic growth factors. The bcl-2 oncogene inhibits apoptosis induced by a variety of stimuli, including hypoxia. On the basis of bcl-2's role in regulating apoptosis in response to hypoxia, we hypothesized that this oncogene might affect other responses to hypoxia, such as the expression of angiogenic growth factors. Methods: Three prostate carcinoma cell lines, PC3, LNCaP, and DU-145, were stably transfected with a bcl-2 complementary DNA (cDNA), and transfectants were analyzed in vitro for the expression of angiogenic factors after exposure to either normoxic (19% O 2 ) or hypoxic (1% O 2 ) conditions. The in vivo angiogenic potential of the transfected cells was determined by analyzing vessel density in xenografts derived from them and by measuring the ability of these xenografts to induce neovascularization when implanted in mouse corneal micropockets. Statistical tests were two-sided. Results: When exposed to hypoxic conditions, prostate carcinoma cells overexpressing bcl-2 expressed statistically significantly higher levels of vascular endothelial growth factor (VEGF), an angiogenic factor, than control-transfected cells ( P = .001 for PC3, P = .04 for DU-145 after 48 hours). This effect of bcl-2 was independent of its antiapoptotic activity because increased expression of VEGF was detected in PC3 cells overexpressing bcl-2 even though PC3 cells are inherently resistant to hypoxia-induced apoptosis. In vivo , xenograft tumors derived from the bcl-2-overexpressing prostate carcinoma cell lines displayed increased angiogenic potential and grew more aggressively than tumors derived from the control cell lines ( P = .03 for PC3). Treatment of bcl-2-overexpressing and control tumors with the antiangiogenic drug TNP-470 neutralized the aggressive angiogenesis in bcl-2-overexpressing tumors ( P = .04 for PC3, P = .004 for DU-145) and the moderate angiogenesis in control tumors ( P = .01 for PC3, P = .05 for DU-145), resulting in similar growth rates for both tumors. Conclusions: bcl-2 may play a dual role in tumorigenesis by suppressing apoptosis and by stimulating angiogenesis.
    Keywords: Prostate Cancer -- Development And Progression ; Vascular Endothelial Growth Factor -- Measurement;
    ISSN: 1460-2105
    ISSN: 00278874
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  • 5
    In: Journal of the National Cancer Institute, 2001, Vol.93(14), pp.1075-1081
    Description: Background: Tumor cells are known to be heterogeneous with respect to their metastatic activity, proliferation rate, and activity of several enzymes. However, little is known about the heterogeneity of tumor angiogenic activity. We investigated whether heterogeneity of angiogenic activity could be responsible for the well-known observation of no take of human tumors transplanted into immunodeficient mice. Methods: Severe combined immunodeficient (SCID) mice were xenotransplanted subcutaneously with tumor tissue (n = 55) or cell suspension of a human liposarcoma cell line (SW-872) or subclones (n = 28), with varying cell proliferation rates. Xenograft tumor growth was recorded for up to 6 months. Tumor tissues were then removed and analyzed for tumor cell apoptosis, microvessel density, and cell proliferation. All statistical tests were two-sided. Results: Pieces of tumor derived from the parental cell line or its clones gave rise to three kinds of tumors: 1) highly angiogenic and fast-growing (aggressive) tumors, 2) weakly angiogenic and slow-growing tumors, and 3) nonangiogenic and stable tumors. Most tumors retained the original phenotype of their parental tumor. Tumor volume correlated positively with microvessel density (Spearman correlation coefficient [ r ] = .89; P .0001) and inversely with tumor cell apoptosis (Spearman r = .68; P = .002). Tumor volume was less strongly but still positively correlated with tumor cell proliferation in vivo (Spearman r = .55; P = .02). Conclusions: Human liposarcoma cells appear to be heterogeneous in their angiogenic activity. When tumor cells with little or no angiogenic activity are transplanted into SCID mice, a microscopic, dormant tumor results that may not grow further. Because such tiny tumors are neither grossly visible nor palpable, they have previously been called no take. The finding that an angiogenic tumor can contain subpopulations of tumor cells with little or no angiogenic activity may provide a novel mechanism for dormant micrometastases, late recurrence, and changes in rate of tumor progression.
    Keywords: Neovascularization -- Physiological Aspects ; Cancer Invasiveness -- Physiological Aspects ; Carcinogenesis ; Sarcoma;
    ISSN: 0027-8874
    E-ISSN: 1460-2105
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  • 6
    Language: English
    In: The Journal of Urology, 04/2002, p.1794
    ISSN: 0022-5347
    Source: Wolters Kluwer - Ovid - Lippincott Williams & Wilkins (via CrossRef)
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  • 7
    In: Journal of the National Cancer Institute, 2001, Vol.93(5), pp.382-387
    Description: Background: Angiogenesis is essential for tumor growth and progression. Therefore, inhibition of angiogenesis is being studied as a new anticancer therapy. Because cytotoxic chemotherapy is more effective on rapidly growing tumors than on slowly growing tumors, it has been assumed that antiangiogenic therapy will also be effective only on rapidly growing, highly vascularized tumors. We compared the effects of two angiogenesis inhibitors, TNP-470 and angiostatin, on slowly growing, poorly vascularized and rapidly growing, highly vascularized human tumors in mice. Methods: Slowly growing (RT-4) and rapidly growing (MGH-U1) human bladder carcinoma cell lines were grown in severe combined immunodeficiency mice. Established tumors were treated with one of the two angiogenesis inhibitors. Tumor volumes, vascularity, and proliferation indices were determined. The in vitro effects of TNP-470 and of angiostatin on the proliferation of RT-4 and MGH-U1 cells were also investigated. All statistical tests were two-sided. Results: RT-4 and MGH-U1 tumor growth was statistically significantly inhibited by both angiogenesis inhibitors ( P .001). Both inhibitors decreased the blood vessel density in both tumor types but did not alter the in vivo proliferation indices of the tumors. TNP-470, but not angiostatin, marginally decreased the in vitro proliferation of MGH-U1 cells. Conclusion: Slowly growing, poorly vascularized tumors in animal models respond as well as rapidly growing, highly vascularized tumors to therapy with the angiogenesis inhibitors TNP-470 and angiostatin.
    Keywords: Neovascularization -- Prevention ; Antineoplastic Agents -- Evaluation ; Tumors ; Chemotherapy;
    ISSN: 1460-2105
    ISSN: 00278874
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  • 8
    Language: English
    In: Cancer Letters, 2010, Vol.296(2), pp.160-167
    Description: β -Glycoprotein-I (β gpI), an abundant plasma glycoprotein, functions as a regulator of thrombosis. Previously, we demonstrated that plasmin-clipped β gpI (cβ gpI) exerts an anti-angiogenic effect on human umbilical vein endothelial cells (HUVEC). The present study was focused on the molecular background responsible for this phenomenon. cβ gpI strongly reduced HUVEC growth and proliferation as evidenced by the MTT and BrdU assay and delayed cell cycle progression arresting HUVEC in the S-and G2/M-phase. Western blot analysis indicated that cβ gpI inhibited cyclin A, B and D1, and enhanced p21 and p27 expression. Activity of p38 was down-regulated independently from the cβ gpI incubation time. Phosphorylation of ERK1/2 was not changed early (30 and 60 min) but became enhanced later (90 min, 4 h). JNK activity was reduced rapidly after cβ gpI treatment but compared to controls, increased thereafter. Annexin II blockade prevented growth inhibition and cell cycle delay evoked by cβ gpI. We assume that cβ gpI’s effects on HUVEC growth is mediated via cyclin A, B and D1 suppression, up-regulation of p21 and p27 and coupled to modifications of the mitogen-activated protein (MAP) kinase signalling pathway. cβ gpI may represent a potential endogenous angiogenesis-targeted compound, opening the possibility of a novel tool to treat cancer.
    Keywords: Angiogenesis ; Β 2-Glycoprotein-I ; Cell Cycle ; Cyclins ; Huvec ; Medicine
    ISSN: 0304-3835
    E-ISSN: 1872-7980
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  • 9
    Language: English
    In: The American Journal of the Medical Sciences, April 2010, Vol.339(4), pp.341-344
    Description: In this study, we aimed to determine those clinical and pathologic features that are associated with pelvic lymph node metastasis in patients with transitional cell cancer of the bladder. Unlike previous studies, we particularly focused on intravesical tumor location. We included 173 patients who underwent radical cystectomy and bilateral pelvic lymphadenectomy for muscle-invasive or high-risk superficial bladder cancer. Fifty patients (28.9%) presented with lymph node metastases. Tumor-related and personal characteristics were analyzed. Lymph node positive disease occurred in association with an increasing pathologic tumor stage ( 〈 10 ) and with a decreasing differentiation status ( = 0.008). The rate of pelvic lymph node metastasis differed in primary tumors growing on different intravesical locations. Cancers located exclusively on the lateral bladder walls ( 〈 10 ) and tumors involving the lateral walls ( = 0.042) were highly correlated with lymph node positive disease. Posterior wall tumors were least associated with lymph node metastases compared with other tumor locations ( = 0.015). Focal tumor growths located on the lateral bladder wall and an increasing pathologic tumor stage and decreasing differentiation-status were identified as independent risk factors for the pelvic lymph node status. For the first time we present the association of intravesical tumor location and the rate of lymph node metastasis in transitional cell cancer of the bladder. Our findings may ultimately contribute to a more individualized patient management.
    Keywords: Lymph Node Metastases ; Tumor Location ; Risk Factors ; Transitional Cell Carcinoma ; Medicine
    ISSN: 0002-9629
    E-ISSN: 1538-2990
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  • 10
    Language: English
    In: Cancer research, 15 April 2003, Vol.63(8), pp.1990-3
    Description: The observation that radiation treatment to a local area of the body results in an antitumor effect for tumors distant to the radiation site has been termed the "abscopal effect." To understand the mechanism of this unusual phenomenon, we examined whether the effect was mediated through p53, a protein complex up-regulated in irradiated cells. Non-tumor-bearing legs of C57BL/6 (wild-type p53) and p53 null B6.129S2-Trp53(tm1Tyj) mice were irradiated to determine whether an abscopal effect could be observed against Lewis lung carcinoma (LLC) and T241 (fibrosarcoma) implanted at a distant site. In mice with wild-type p53, both LLC and T241 tumors implanted into the midline dorsum grew at a significantly slower rate when the leg of the animal was exposed to five 10-Gy fractions of radiation compared with sham-irradiated animals, suggesting that the abscopal effect is not tumor specific. When the radiation dose to the leg was reduced (twelve fractions of 2 Gy each), the inhibition of LLC tumor growth was decreased indicating a radiation-dose dependency for the abscopal effect. In contrast, when the legs of p53 null animals or wild-type p53 mice treated with pifithrin-alpha (a p53 blocker) were irradiated (five 10-Gy fractions), tumor growth was not delayed. These data implicate p53 as a key mediator of the radiation-induced abscopal effect and suggest that pathways downstream of p53 are important in eliciting this response.
    Keywords: Carcinoma, Lewis Lung -- Radiotherapy ; Fibrosarcoma -- Radiotherapy ; Tumor Suppressor Protein P53 -- Physiology
    ISSN: 0008-5472
    E-ISSN: 15387445
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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