Cold IPOs

Die vorliegende Dissertation beschäftigt sich mit den rechtlichen Erscheinungs- und Gestaltungsformen von Cold IPOs und den in diesem Zusammenhang bestehenden gesellschafts- und kapitalmarktrechtlichen Fragen in Deutschland und Österreich. Vor diesem Hintergrund werden die einzelnen Verfahrensschritte des Cold IPOs und die damit einhergehenden rechtlichen Fragen aufgezeigt. Aus gesellschaftsrechtlicher Sicht werden insbesondere die Auswirkungen der BGH-Rechtsprechung zur Mantelverwendung auf einen Cold IPO besprochen. In kapitalmarktrechtlicher Hinsicht wird die Frage behandelt, inwieweit die Börsenzulassungsvoraussetzungen mittels eines Cold IPOs umgangen werden und welche Konsequenzen eine etwaige Umgehung nach sich zieht. Zudem wird geklärt, ob im Zuge eines Cold IPOs die Pflicht zur Abgabe eines Übernahmeangebots entsteht. Darüber hinaus wird untersucht, ob die als Börsenvehikel dienende Gesellschaft im Vorfeld des Cold IPOs eine Ad-hoc-Meldung veröffentlichen muss und inwieweit sich eine entsprechende Veröffentlichung auf die Umsetzung der Transaktion auswirkt. Ferner wird die Frage behandelt, ob und unter welchen Voraussetzungen es im Zuge eines Cold IPOs zu übernahmerechtlichen Nachzahlungspflichten kommen kann. Abschließend werden die sog SPACs (Special Purpose Acquisition Companies) thematisiert. Dabei werden zunächst die typischen Wesensmerkmale eines SPACs und der Ablauf einer SPAC-Transaktion dargestellt. In rechtlicher Hinsicht wird insbesondere die Frage behandelt, ob ein SPAC in Deutschland und Österreich zur Börse zugelassen werden kann. Ferner wird geklärt, ob sich die spezifischen Merkmale einer SPAC-Gesellschaft auch mittels einer deutschen bzw österreichischen Aktiengesellschaft abbilden lassen

Characterization of gastric adenocarcinoma cell lines established from CEA424/SV40 T antigen-transgenic mice with or without a human CEA transgene

BACKGROUND: Gastric carcinoma is one of the most frequent cancers worldwide. Patients with gastric cancer at an advanced disease stage have a poor prognosis, due to the limited efficacy of available therapies. Therefore, the development of new therapies, like immunotherapy for the treatment of gastric cancer is of utmost importance. Since the usability of existing preclinical models for the evaluation of immunotherapies for gastric adenocarcinomas is limited, the goal of the present study was to establish murine in vivo models which allow the stepwise improvement of immunotherapies for gastric cancer. METHODS: Since no murine gastric adenocarcinoma cell lines are available we established four cell lines (424GC, mGC3, mGC5, mGC8) from spontaneously developing tumors of CEA424/SV40 T antigen (CEA424/Tag) mice and three cell lines derived from double-transgenic offsprings of CEA424/Tag mice mated with human carcinoembryonic antigen (CEA)-transgenic (CEA424/Tag-CEA) mice (mGC2(CEA), mGC4(CEA), mGC11(CEA)). CEA424/Tag is a transgenic C57BL/6 mouse strain harboring the Tag under the control of a -424/-8 bp CEA gene promoter which leads to the development of invasive adenocarcinoma in the glandular stomach. Tumor cell lines established from CEA424/Tag-CEA mice express the well defined tumor antigen CEA under the control of its natural regulatory elements. RESULTS: The epithelial origin of the tumor cells was proven by morphological criteria including the presence of mucin within the cells and the expression of the cell adhesion molecules EpCAM and CEACAM1. All cell lines consistently express the transgenes CEA and/or Tag and MHC class I molecules leading to their susceptibility to lysis by Tag-specific CTL in vitro. Despite the presentation of CTL-epitopes derived from the transgene products the tumor cell lines were tumorigenic when grafted into C57BL/6, CEA424/Tag or CEA424/Tag-CEA-transgenic hosts and no significant differences in tumor take and tumor growth were observed in the different hosts. Although no spontaneous tumor rejection was observed, vaccination of C57BL/6 mice with lysates from gastric carcinoma cell lines protected C57BL/6 mice from tumor challenge, demonstrating the tumorigenicity of the tumor cell lines in nontransgenic mice of the H-2(b )haplotype. CONCLUSION: These tumor cell lines grafted in different syngeneic hosts should prove to be very useful to optimize immunotherapy regimens to be finally tested in transgenic animals developing primary gastric carcinomas

Ceacam1 separates graft-versus-host-disease from graft-versus-tumor activity after experimental allogeneic bone marrow transplantation.

BACKGROUND: Allogeneic bone marrow transplantation (allo-BMT) is a potentially curative therapy for a variety of hematologic diseases, but benefits, including graft-versus-tumor (GVT) activity are limited by graft-versus-host-disease (GVHD). Carcinoembryonic antigen related cell adhesion molecule 1 (Ceacam1) is a transmembrane glycoprotein found on epithelium, T cells, and many tumors. It regulates a variety of physiologic and pathological processes such as tumor biology, leukocyte activation, and energy homeostasis. Previous studies suggest that Ceacam1 negatively regulates inflammation in inflammatory bowel disease models. METHODS: We studied Ceacam1 as a regulator of GVHD and GVT after allogeneic bone marrow transplantation (allo-BMT) in mouse models. In vivo, Ceacam1(-/-) T cells caused increased GVHD mortality and GVHD of the colon, and greater numbers of donor T cells were positive for activation markers (CD25(hi), CD62L(lo)). Additionally, Ceacam1(-/-) CD8 T cells had greater expression of the gut-trafficking integrin α(4)β(7), though both CD4 and CD8 T cells were found increased numbers in the gut post-transplant. Ceacam1(-/-) recipients also experienced increased GVHD mortality and GVHD of the colon, and alloreactive T cells displayed increased activation. Additionally, Ceacam1(-/-) mice had increased mortality and decreased numbers of regenerating small intestinal crypts upon radiation exposure. Conversely, Ceacam1-overexpressing T cells caused attenuated target-organ and systemic GVHD, which correlated with decreased donor T cell numbers in target tissues, and mortality. Finally, graft-versus-tumor survival in a Ceacam1(+) lymphoma model was improved in animals receiving Ceacam1(-/-) vs. control T cells. CONCLUSIONS: We conclude that Ceacam1 regulates T cell activation, GVHD target organ damage, and numbers of donor T cells in lymphoid organs and GVHD target tissues. In recipients of allo-BMT, Ceacam1 may also regulate tissue radiosensitivity. Because of its expression on both the donor graft and host tissues, this suggests that targeting Ceacam1 may represent a potent strategy for the regulation of GVHD and GVT after allogeneic transplantation