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Milestone 12

Death defying

Apoptosis and cancer

Nature Reviews Cancer volume 6, pages S14–S15 (2006)Cite this article

Kerr, Wyllie and Currie suggested that, unlike necrosis, apoptosis might represent a genetically regulated cell-suicide programme, and, importantly, they stated: “We should now like to speculate that hyperplasia might sometimes result from decreased apoptosis rather than increased mitosis, although we emphasize that we know of no definitive studies to support such a hypothesis.”

Importantly, in 1988, David Vaux, Suzanne Cory and Jerry Adams showed that expression of the B-cell lymphoma 2 ( BCL2 ) gene, which had been identified by others as being translocated in follicular lymphoma (see Milestone 10), could promote the survival of haematopoietic cells after the removal of growth factors (Gwyn Williams and co-workers were later to show that these growth factors suppressed apoptosis). Vaux and colleagues also showed that the oncogene Myc cooperated with Bcl2 to produce tumours in immunocompromised mice. They suggested that BCL2 provided a distinct survival signal that might contribute to neoplasia by allowing a clone to persist until other oncogenes, such as Myc, became activated. This and subsequent work provided evidence that cell survival was regulated independently of cell proliferation, and that impaired cell death, similar to enhanced proliferation, was indeed a key step in tumour development. In the same year, John Reed and colleagues found that overexpression of BCL2 in an immortalized mouse cell line did not induce proliferation or transformation in vitro. Although these cells did produce tumours in mice, further mutational events were required. In 1989, Tim McDonnell, Stanley Korsmeyer and colleagues reported that the expression of a BCL2–immunoglobulin fusion protein in B cells prolonged their survival — an event that this group also showed was tumorigenic.

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References

ORIGINAL RESEARCH PAPERS

  1. Kerr, J. F., Wyllie, A. H. & Currie, A. R. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br. J. Cancer 26, 239–257 (1972)

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  2. Vaux, D. L., Cory, S. & Adams, J. M. Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells. Nature 335, 440–442 (1988)

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FURTHER READING

  1. Reed, J. C., Cuddy, M., Slabiak, T., Croce, C. M. & Nowell, P. C. Oncogenic potential of bcl-2 demonstrated by gene transfer. Nature 336, 259–261 (1988)

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  2. McDonnell, T. M. et al. bcl-2–immunoglobulin transgenic mice demonstrate extended B cell survival and follicular lymphoproliferation. Cell 57, 79–88 (1989)

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  3. Williams, G. T., Smith, C. A., Spooncer, E., Dexter, T. M. & Taylor, D. R. Haemopoietic colony stimulating factors promote cell survival by suppressing apoptosis. Nature 343, 76–79 (1990)

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  4. Askew, D. S., Ashmun, R. A., Simmons, B. C. & Cleveland, J. L. Constitutive c-myc expression in an IL-3-dependent myeloid cell line suppresses cell cycle arrest and accelerates apoptosis. Oncogene 6, 1915–1922 (1991)

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  5. Evan, G. I. et al. Induction of apoptosis in fibroblasts by c-myc protein. Cell 69, 119–128 (1992)

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  1. Senior Editor, Nature Reviews Cancer,

    Nicola McCarthy

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  1. Nicola McCarthy
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McCarthy, N. Death defying. Nat Rev Cancer 6 (Suppl 1), S14–S15 (2006). https://doi.org/10.1038/nrc1854

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