Myc: A weapon of mass destruction

Julie Secombe; Sarah B. Pierce; Robert N. Eisenman

doi:10.1016/S0092-8674(04)00336-8

Myc: A weapon of mass destruction

Julie Secombe, Sarah B. Pierce, Robert N. Eisenman

Research output: Contribution to journal › Review article › peer-review

109 Scopus citations

Abstract

Growth and proliferation potentiated by deregulated myc oncogene expression is balanced by myc-induced apoptosis. Abrogation of this apoptotic pathway in Myc overexpressing cells leads to cancer progression. Recent work has shown that cell clones in the Drosophila wing disc with higher dMyc expression levels act as supercompetitors to potentiate the programmed death of surrounding normal cells. Yet another paper identifies dE2F1 as a critical component of pathways that normally restrict the ability of growth perturbing genes like dMyc to cause organ overgrowth.

Original language	English (US)
Pages (from-to)	153-156
Number of pages	4
Journal	Cell
Volume	117
Issue number	2
DOIs	https://doi.org/10.1016/S0092-8674(04)00336-8
State	Published - Apr 16 2004
Externally published	Yes

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0092-8674(04)00336-8

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AU - Pierce, Sarah B.

AU - Eisenman, Robert N.

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N2 - Growth and proliferation potentiated by deregulated myc oncogene expression is balanced by myc-induced apoptosis. Abrogation of this apoptotic pathway in Myc overexpressing cells leads to cancer progression. Recent work has shown that cell clones in the Drosophila wing disc with higher dMyc expression levels act as supercompetitors to potentiate the programmed death of surrounding normal cells. Yet another paper identifies dE2F1 as a critical component of pathways that normally restrict the ability of growth perturbing genes like dMyc to cause organ overgrowth.

AB - Growth and proliferation potentiated by deregulated myc oncogene expression is balanced by myc-induced apoptosis. Abrogation of this apoptotic pathway in Myc overexpressing cells leads to cancer progression. Recent work has shown that cell clones in the Drosophila wing disc with higher dMyc expression levels act as supercompetitors to potentiate the programmed death of surrounding normal cells. Yet another paper identifies dE2F1 as a critical component of pathways that normally restrict the ability of growth perturbing genes like dMyc to cause organ overgrowth.

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Myc: A weapon of mass destruction

Abstract

ASJC Scopus subject areas

UN SDGs

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