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Cell death and cancer: an introduction

Oncogene volume 23, pages 2744–2745 (2004)Cite this article

The omission or repression of cell death has a dual impact on medical oncology. First, disabling the signal transduction mechanisms leading to cell death and/or suppression of the biochemical program involved in cell death execution is likely to play a primordial role in the process of oncogenesis. Death resistance thus enables the Darwinian selection of clones whose vital needs for external growth factors, nutrients and contact-dependent survival signals progressive diminish, thereby increasing the autonomy of tumor cells and enabling them to spread and to metastasize to sites at which, in normal conditions, they could not subsist. Second, conventional therapy with chemotherapeutic agents or ionizing irradiation aims at killing tumor cells, usually by triggering a latent biochemical death program. In the standard scenario, however, after an initial response, resistant tumor cells are selected and ‘escape’ from death induction, thus determining subsequent therapeutic failure. It is plausible that increased death resistance of tumor cells thus participates in sealing the patient's inexorable fate.

Death pathways can follow different subroutines, which, unfortunately enough, are classified according to mere morphological criteria. Apoptosis, the most preponderant type of cell death (‘type 1 cell death’) can be opposed to other types of cell death such as autophagic (‘type 2’) cell death, mitotic catastrophe, as well as necrosis (oncosis), according to morphological criteria such as chromatin condensation (present in apoptosis), accumulation of autophagic vacuoles (exclusive for type 2 cell death), mitotic features (as observable in mitotic catastrophe), or massive swelling of cytoplasmic organelles (oncosis) (Jaattela, 2004). Nonetheless, this clear distinction is probably not relevant in functional terms because the same lethal stimuli can trigger different subroutines of cell death, depending on the cellular context, for instance, the ATP content (Melino and Nicotera, 2004). Moreover, regulators of the apoptotic pathway can also act on other cell death subroutines, and mitotic catastrophe is probably executed through the activation of caspases and mitochondrial membrane permeabilization, two processes that are generally considered to be pathognomic for apoptosis (Castedo et al., 2004).

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  1. CNRS-UMR 8125, Institut Gustave Roussy, 39 rue Camille-Desmoulins, Villejuif, F-94805, France

    Guido Kroemer

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Kroemer, G. Cell death and cancer: an introduction. Oncogene 23, 2744–2745 (2004). https://doi.org/10.1038/sj.onc.1207531

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