Histology and histopathology Vol.11, nº 1 (1996)

Permanent URI for this collection

http://hdl.handle.net/10201/177552

Browse

Browsing Histology and histopathology Vol.11, nº 1 (1996) by Subject "Apoptosis"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Open Access
    Cell rounding with «Rip off» detachment
    (Murcia : F. Hernández, 1996) Sit, K.H.
    The «rounding up» characteristic of mitotic, apoptotic, transformed and non-transformed cells appears to be initiated by various causative factors. Cytoskeletal and adhesion modulations have been implicated. Endocytic intemalization via large channels seen in the rounding of arnoeba and human cells alike, implicate a third mechanism, viz. membrane flow and fusion, where «rip off» detachment sheds parts of the cell to achieve freedom. Mutilation as a means for detachment is also used by moving fibroblasts, linking shape change with movement via a distinct mechanism. While rounding may follow detachment and detachment may follow rounding, «rip off» mutilation, whether selfinflicted or imposed, and modulation of stickiness are fundamentally different processes
  • Thumbnail Image
    Publication
    Open Access
    Elimination of transformed cells by normal cells: a novel concept for the control of carcinogenesis
    (Murcia : F. Hernández, 1996) Bauer, G.
    Control of transformed cells by neighbouring normal cells is known since the beginning of transformation studies in vitro. The classical explanation for this phenomenon is based on proliferation inhibition of transformed cells by normal cells. We extend this model by presenting data that show that TGF-B-treated normal cells can eliminate transformed cells by induction of apoptosis. Both the TGF-8-induced signal pathway in normal cells, leading to the production of a short-lived apoptosis-inducing factor, as well as the specific interaction of this factor with transformed cells depend on the action of reactive oxygen species. Sensitivity to induction of apoptosis seems to be a common feature associated with the transformed state, independent of the originally transforming principle. Therefore, tumor development should require either interference with the process of elimination or acquisition of resistance against it. We discuss experimental evidence for interfering substances, such as antioxidants, as well as for genetic systems that protect transformed cells from the negative effects of their cellular environment, such as Bcl-2 or papilloma viruses. These findings, as well as the general resistance of exvivo tumor cells against induction of apoptosis are in line with the novel model of control of tumor progression presented by us in this review.