Facies, Paleogeography, and Sedimentary History of the Southern Permian Basin in Europe

The structural position of the Southern Permian Basin (SPB) is controlled by the Caledonian and Variscan tectonic framework (Fig. 1). The basin is located between the mid-North Sea High and Ringkobing-Fyn High in the north, the East European Platform in the east and the Variscan tectogene in the south (Fig. 2). In the area of maximum subsidence (i.e. in the Variscan Foreland), the substrate is composed of consolidated Caledonian massifs. This consists of (1) the Netherlands-North German Massif (possibly a terrane), considered now (Hoffmann 1990) as a separate structural unit of Precambrian age which was established finally in Caledonian time, and (2) a part of the Holstein-Rugen-Pomorze Terrane (Caledonian fold zone; Franke 1990) limited by strike-slip faults from the North German-Polish Variscan orogenic belt. The Southern Permian Basin has several narrow connections with adjacent basins (for references, see Sorensen and Martinsen 1987) and possible temporary connections with the Tethys domain via the Polish-Dobrugea trough, along a rift zone (Ziegler 1987) and with small basins on the Inner Variscan domain. These connections and the SPB tectonic framework were induced by pre-Permian tectonics generally described as a subequatorial structural plan and submeridional deep fractures (Franke 1990)

Cytokinesis defects and cancer

Whole-genome and centrosome duplication as a consequence of cytokinesis failure can drive tumorigenesis in experimental model systems. However, whether cytokinesis failure is in fact an important cause of human cancers has remained unclear. In this Review, we summarize evidence that whole-genome-doubling events are frequently observed in human cancers and discuss the contribution that cytokinesis defects can make to tumorigenesis. We provide an overview of the potential causes of cytokinesis failure and discuss how tetraploid cells that are generated through cytokinesis defects are used in cancer as a transitory state on the route to aneuploidy. Finally, we discuss how cytokinesis defects can facilitate genetic diversification within the tumour to promote cancer development and could constitute the path of least resistance in tumour evolution