W Dippold

Johannes Gutenberg-Universität Mainz, Mayence, Rheinland-Pfalz, Germany

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Publications (105)481.83 Total impact

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    ABSTRACT: ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
    ChemInform 06/2010; 33(22). DOI:10.1002/chin.200222281
  • [Show abstract] [Hide abstract]
    ABSTRACT: ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
    ChemInform 01/2010; 33(4). DOI:10.1002/chin.200204203
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    ABSTRACT: The ganglioside GD3 has a variety of biological functions. These include stimulatory effects is on proliferation, natural killer activity and cytokine production by freshly isolated peripheral T cells. In this study we have characterized anti-GD3 antibody (MoAb Z21) mediated effects on T cell clones. Our data indicate that α/β TCR CD4+ and CD8+ as well as γ/δ TCR positive T cells can be stimulated resulting in proliferation and cytokine production. This effect could be blocked by cyclosporin A and did not involve the LFA-3 or CD4 molecule. Apart from IFN-γ and IL-2 production by T helper I and T helper 0 cells we have observed production of IL-4 and IL-10 by T helper 2 cells indicating that the GD3 molecule is not a marker for a certain functional T cell subset. In contrast to anti-CD3 mediated activation, the responsiveness of T cells to stimulation via GD3 was dependent on the cell surface expression of the molecule and could be enhanced by costimulation via CD2, CD3, CD26 or CD28. In addition, anti-GD3 antibodies delivered a potent costimulatory signal for antigen-induced proliferation of CD4+ T lymphocytes. In summary, our experiments illuminate the mechanisms of anti-GD3 antibody induced T cell activation.
    Scandinavian Journal of Immunology 06/2006; 41(5):475 - 480. DOI:10.1111/j.1365-3083.1995.tb03595.x · 1.88 Impact Factor
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    ABSTRACT: E-selectin mediated tumor cell adhesion plays an important role in metastasis. Here we show that ionizing radiation (IR) induces E-selectin gene and protein expression in human endothelial cells at therapeutically relevant dose level. E-selectin expression is accompanied by an increase in the adhesion of human colon carcinoma cells to primary human umbilical vein endothelial cells (HUVEC). The HMG-CoA reductase inhibitor lovastatin impairs IR-stimulated E-selectin expression as analyzed at the level of the protein, mRNA and promoter. Inactivation of Rho GTPases either by use of Clostridium difficile toxin A or by co-expression of dominant-negative Rho blocked IR-induced E-selectin gene induction, indicating Rho GTPases to be essential. Radiation-induced expression of E-selectin was also blocked by all-trans retinoic acid (at-RA), whereas 9-cis retinoic acid was ineffective. Abrogation of IR-stimulated E-selectin expression by lovastatin and at-RA reduced tumor cell adhesion in a dose-dependent manner. Combined treatment with lovastatin and at-RA exerted additive inhibitory effects on radiation-induced E-selectin expression and tumor cell adhesion. Therefore, application of statins and at-RA might have clinical impact in protecting against E-selectin-promoted metastasis, which might arise as an unwanted side effect from radiation treatment.
    Carcinogenesis 09/2004; 25(8):1335-44. DOI:10.1093/carcin/bgh133 · 5.27 Impact Factor
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    ABSTRACT: E-selectin mediated cell-cell adhesion plays an important role in inflammatory processes and extravasation of tumor cells. Tumor necrosis factor-alpha (TNF-alpha) induces E-selectin gene and protein expression in primary human endothelial cells (HUVEC) and in an endothelial cell line (EA.hy-926). As shown by ELISA and FACS analyses, HMG-CoA reductase inhibitors (e.g., lovastatin) impair the TNF-alpha stimulated increase in E-selectin protein expression. Similar results were obtained for E-selectin mRNA expression and promoter activity, indicating that the effect of lovastatin is based on inhibition of gene expression. The effective inhibitory concentration of lovastatin was in a physiologically relevant range (IC50<0.1 microM). Lovastatin-mediated block of TNF-alpha induced E-selectin expression is due to inhibition of protein geranylgeranylation rather than farnesylation. Down-regulation of Rho signaling by coexpression of dominant-negative Rho mutants (i.e RhoA, RhoB and Rac) impaired TNF-alpha driven E-selectin gene expression, indicating Rho signaling to be essential for transcriptional activation of the E-selectin gene. Inhibition of E-selectin expression by lovastatin gives rise to a significant reduction in TNF-alpha stimulated adhesion of colon carcinoma cells to HUVEC. Furthermore, low concentration of lovastatin (i.e., < or =1 microM) attenuated TNF-alpha induced tumor cell invasion in vitro. The data support the view that statins might be clinically useful in protection against E-selectin mediated metastasis.
    The FASEB Journal 02/2004; 18(1):140-2. DOI:10.1096/fj.03-0261fje · 5.48 Impact Factor
  • Angewandte Chemie International Edition 11/2001; 40(20):3836-3839. · 11.34 Impact Factor
  • Angewandte Chemie 10/2001; 113(20):3954-3957. DOI:10.1002/1521-3757(20011015)113:203.0.CO;2-R
  • Angewandte Chemie International Edition 02/2001; 40(2):366-369. · 11.34 Impact Factor
  • Angewandte Chemie 01/2001; 113(2):379-382. DOI:10.1002/1521-3757(20010119)113:23.0.CO;2-S
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    ABSTRACT: The membrane-bound complement inhibitors CD46 (membrane cofactor protein), CD55 (decay-accelerating factor) and CD59 (protectin) protect tumour cells against lysis by activated complement. In this study, a total of 14 (3 gastric, 3 colonic and 8 pancreatic) gastrointestinal tumour cell lines were examined for the expression of CD46, CD55 and CD59 with respect to the regulatory efficacy of interferon-gamma (IFN-gamma). The effects of IFN-gamma on mRNA and protein expression levels of CD46, CD55 and CD59 were evaluated by Northern blot hybridisation, RT-PCR, flow cytometry and immunostaining. In unstimulated cell lines, CD46 and CD59 transcripts were expressed at comparable levels, whereas the basal expression of CD55 mRNA was heterogeneous. The complement inhibitor proteins were detected in all cell lines using specific antibodies. Additional immunohistochemical stainings of gastrointestinal tissue specimens supported these findings. IFN-gamma evoked a weak induction of certain transcripts in a subset of the cell lines. Upregulation of protein expression was only observed in HT29 cells for CD55 and CD59 and was accompanied by a marked increase of the corresponding transcripts. We conclude that membrane-bound complement inhibitors are broadly expressed in gastrointestinal tumour cells and vary in their susceptibility to IFN-gamma. Thus, they may be involved in tumour escape mechanisms in gastric, pancreatic and colorectal cancer.
    European Journal of Cancer 02/1999; 35(1):117-24. DOI:10.1016/S0959-8049(98)00290-1 · 4.82 Impact Factor
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    ABSTRACT: Protein expression of the putative tumour-suppressor gene DCC on chromosome 18q was evaluated in a panel of 16 matched colorectal cancer and normal colonic tissue samples together with DCC mRNA expression and allelic deletions (loss of heterozygosity, LOH). Determined by a polymerase chain reaction (PCR)-LOH assay, 12 of the 16 (75%) cases were informative with LOH occurring in 2 of the 12 cases. For DCC mRNA, transcripts could be detected in all analysed normal tissues (eight out of eight) by RT-PCR, whereas 6 of the 15 tumours were negative. DCC protein expression, investigated by immunohistochemistry using the monoclonal antibody 15041 A directed against the intracellular domain, was homogeneously positive in all normal tissue samples. In tumour tissues, no DCC protein was seen in 11 out of 16 samples (69%). For the DCC codon 201, we found a loss of a wild-type codon sequence caused by mutation or LOH in at least 8 out of 15 cases (53%) compared with the corresponding normal tissue. DCC protein expression was undetectable in eight of the nine tumours missing both wild-type codons. Only one of the five tumours with retained DCC protein expression had no detectable wild-type codon 201. In addition, 9 out of 15 normal tissue specimens were mutated in codon 201. In two out of three cases with homozygous wild-type codons in peripheral blood lymphocyte (PBL) DNA, mutations were already observed in the tumour adjacent normal colonic mucosa. We conclude that DCC immunostaining should be introduced in the clinicopathological routine because of its strong correlation with the known prognostic markers 18q LOH and mutation of codon 201. Images Figure 1 Figure 2 Figure 3 Figure 4
    British Journal of Cancer 03/1998; 77(4):588-94. DOI:10.1038/bjc.1998.95 · 4.82 Impact Factor
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    ABSTRACT: Gangliosides with a terminal 9-O-acetylated disialosyl group (CDw60 structures) show a restricted surface expression on human leukocytes. Hithereto, they have only been detected on subpopulations of human T lymphocytes. Using the defined CDw60 antibody UM4D4 and two new antibodies with preferential CDw60 activities, F6 and Z17, we demonstrate for the first time that CDw60 is an activation marker on human B lymphocytes. In vitro phorbol ester-stimulated human peripheral blood B lymphocytes as well as in vivo activated tonsillar B lymphocytes became CDw60 positive. CDw60 expression of these cells exceeds that of resting and activated T-lymphocytes.
    Immunology Letters 12/1997; 59(3):151-157. DOI:10.1016/S0165-2478(97)00116-8 · 2.37 Impact Factor
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    ABSTRACT: Inhibitors of factor VIII are a rare condition in non-hemophiliacs, but they are frequently responsible for life threatening hemorrhage. Acquired factor VIII:C inhibitors represent the spontaneous development of autoantibodies that partially or completely neutralize the plasma coagulant activity of the clotting factor. The autoantibodies can arise in diverse clinical settings, in older adults they are frequently associated with immunologic disorders or malignancies. We report of a 75-year-old man with acquired factor VIII:C inhibitor associated with adenocarcinoma of the prostate and a successful treatment of a severe bleeding complication with porcine factor VIII. A 75-year-old man was admitted because of a hematoma of his right cheek and an isolated prolonged aPTT. Acquired factor VIII:C inhibitor was identified as the cause and immuno-suppressive therapy was begun. In the clinical course severe hemorrhaging occurred and was successfully treated with porcine factor VIII (Hyate:C). The initially high inhibitor titer of 32 Bethesda Units (BU) disappeared. As the cause of acquired factor VIII:C inhibitor a newly diagnosed adenocarcinoma of the prostate is likely. After complete remission of acquired factor VIII:C inhibitor radiation therapy was begun. Six months after severe hemorrhaging the patient was clinically stable and PSA levels were normal. This case demonstrates the necessity of a precise diagnosis and therapy regimen of this coagulopathy based on clinical and laboratory data. In the absence of hemorrhage immuno-suppressive therapy with corticosteroids is indicated, in a patient with severe bleeding and high inhibitor titer (> or = 5 BU) porcine factor VIII should be administered.
    Medizinische Klinik 05/1997; 92(4):241-5. · 0.27 Impact Factor
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    ABSTRACT: Die spontane Hemmkörperhämophilie ist eine extrem seltene, aber durch schwere Blutungskomplikationen häufig lebensbedrohliche Erkrankung. Ursächlich sind Autoantikörper gegen den Faktor VIII:C, die zu einer partiellen oder kompletten Inhibierung der Gerinnungsfunktion führen. Bei ungefähr der Hälfte der betroffenen Patienten ist das Auftreten der Autoantikörper mit anderen Erkrankungen assoziiert, bei älteren Patienten sind es häufig Autoimmunerkrankungen oder Malignome. Wir berichten über einen 75jährigen Patienten mit spontaner Hemmkörperhämophilie, der Assoziation mit einem Adenokarzinom der Prostata und der erfolgreichen Therapie einer lebensbedrohlichen Blutungskomplikation mit porzinem Faktor VIII:C (Hyate:C≿). Ein 75 Jahre alter Patient wurde wegen eines Hämatoms der rechten Wange sowie einer isolierten PTT-Verlängerung stationär aufgenommen. Als Ursache fand sich die Hemmkörperhämophilie gegen den Faktor VIII:C. Zunächst wurde eine immunsuppressive Therapie mit Prednisolon und Cyclophosphamid eingeleitet. Im weiteren Verlaufkam es zu lebensbedrohlichen Weichteilblutungen, die schließlich erfolgreich mit porzinem Faktor VIII:C (Hyate:C≿) zum Stillstand gebracht werden konnten. Der initial hohe Inhibitortiter von 32 Bethesda-Einheiten sank auf Null. Als Ursache der Hemmkörperhämophilie ist ein neu diagnostiziertes Adenokarzinom der Prostata anzunehmen. Nach kompletter Remission der Hemmkörperhämophilie wurde eine Strahlentherapie durchgeführt. Ein halbes Jahr nach der schweren Blutungskomplikation ist der Patient weiter gerinnungsstabil und das PSA wieder normwertig. Dieser Fall verdeutlicht die Notwendigkeit einer schnellen Diagnose der Koagulopathie und die Bedeutung der individuelle Auswahl der medikamentösen Therapiestrategie in Abhängigkeit vom Vorliegen oder Fehlen einer aktiven Blutung. Bei fehlender Blutung ist eine immunsuppressive Therapie mit Corticosteroiden angezeigt, bei einer akuten, schweren Blutung mit einem Hemmkörpertiter von ≧5 BU eine initiale Therapie mit porzinem Faktor VIII. Inhibitors of factor VIII are a rare condition in non-hemophiliacs, but they are frequently responsible for life threatening hemorrhage. Acquired factor VIII:C inhibitors represent the spontaneous development of autoantibodies that partially or completely neutralize the plasma coagulant activitiy of the clotting factor. The autoantibodies can arise in diverse clinical settings, in older adults they are frequently associated with immunologic disorders or malignancies. We report of a 75-year-old man with acquired factor VIII:C inhibitor associated with adenocarcinoma of the prostate and a successful treatment of a severe bleeding complication with porcine factor VIII. A 75-year-old man was admitted because of a hematoma of his right cheek and an isolated prolonged aPTT. Acquired factor VIII:C inhibitor was identified as the cause and immunosuppressive therapy was begun. In the clinical course severe hemorrhaging occurred and was successfully treated with porcine factor VIII (Hyate:C≿). The initially high inhibitor titer of 32 Bethesda Units (BU) disappeared. As the cause of acquired factor VIII:C inhibitor a newly diagnosed adenocarcinoma of the prostate is likely. After complete remission of acquired factor VIII:C inhibitor radiation therapy was begun. Six months after severe hemorrhaging the patient was clinically stable and PSA levels were normal. This case demonstrates the necessity of a precise diagnosis and therapy regimen of this coagulopathy based on clinical and laboratory data. In the absence of hemorrhage immunosuppressive therapy with corticosteroids is indicated, in a patient with severe bleeding and high inhibitor titer (≧5 BU) porcine factor VIII should be administered.
    04/1997; 92(4):241-245. DOI:10.1007/BF03043266
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    European Heart Journal 04/1997; 18(3):524-5. DOI:10.1093/oxfordjournals.eurheartj.a015275 · 14.72 Impact Factor
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    ABSTRACT: Patients with advanced adenocarcinomas of the pancreas have an exceptionally poor prognosis. Modest activity has been demonstrated with single agents (response rates of 25% at best with 5-fluorouracil [5-FU] and mitomycin). Better results have not been obtained by combination chemotherapy. Improvements in the palliation have been achieved by treatment with 5-FU, folinic acid (FA), and interferon-alpha-2A (IFN-α) weekly in the context of a phase II trial. Of 57 evaluable patients, eight (14%) had a partial response (PR), eight (14%) a minor response (MR), and 28 (49%) had no change of disease (NC). The median survival time was 10 mo for patients with progressive disease. Twenty-two out of 36 patients with tumor-related pain whose tumors were affected in terms of PR, MR, and NC became free of pain during treatment. Fever (56%), nausea (37%), and diarrhea (33%) were common toxicities observed. Therefore, biochemical modulation of 5-FU with FA and IFN-α shows some positive effects in the treatment of pancreatic cancer with moderate toxicity.
    International Journal of Gastrointestinal Cancer 01/1997; 21(1):39-41. DOI:10.1007/BF02785918
  • Journal of Hepatology 08/1996; 25(1):122. DOI:10.1016/S0168-8278(96)80337-0 · 10.40 Impact Factor
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    ABSTRACT: E-selectin recognizes the oncofetal antigen sialyl-Lewis X, which is highly expressed in adenocarcinoma. Five alpha(1,3)fucosyltransferases (FT) have been cloned that confer cell-surface expression of sialyl-Lewis X on transfected cells. We show here that 12/18 gastrointestinal-tumor cell lines bind specifically to immobilized E-selectin and that in sialyl-Lewis-X-positive cells binding is inhibited with a monoclonal antibody against sialyl-Lewis X. Using RT-PCR, we determined the expression of the alpha(1,3)fucosyltransferases III, IV, V, VI and VII in gastrointestinal tumor cells. Transcripts of FT IV and FT VII are abundantly expressed in all tested cells. Therefore no single fucosyltransferase could be correlated with the expression of sialyl-Lewis X and the ability of the tumor cells to bind to E-selectin. The data suggest that in gastrointestinal-tumor cells sialyl-Lewis X is necessary but not sufficient for E-selectin binding.
    International Journal of Cancer 08/1996; 67(1):80-5. DOI:10.1002/(SICI)1097-0215(19960703)67:1<80::AID-IJC14>3.0.CO;2-G · 5.01 Impact Factor
  • Mutation Research/Environmental Mutagenesis and Related Subjects 08/1996; 360(3):215-215. DOI:10.1016/S0165-1161(96)90043-6

Publication Stats

2k Citations
481.83 Total Impact Points

Institutions

  • 1984–2010
    • Johannes Gutenberg-Universität Mainz
      • • Institute of Organic Chemistry
      • • I. Department of Medicine
      • • III. Department of Medicine
      Mayence, Rheinland-Pfalz, Germany
  • 1999
    • Sankt Elisabeth Hospital
      Bielefeld, North Rhine-Westphalia, Germany
  • 1995
    • Krankenhaus Nordwest
      Frankfurt, Hesse, Germany
  • 1981
    • Memorial Sloan-Kettering Cancer Center
      New York City, New York, United States
    • National Institutes of Health
      • Laboratory of Molecular Biology
      Maryland, United States