Abstract

Mutations of the retinoblastoma tumour suppressor gene (RB1) or components regulating the RB pathway have been identified in almost every human malignancy. The E2F transcription factors function in cell cycle control and are intimately regulated by RB. Studies of model organisms have revealed conserved functions for E2Fs during development, suggesting that the cancer-related proliferative roles of E2F family members represent a recent evolutionary adaptation. However, given that some human tumours have concurrent RB1 inactivation and E2F amplification and overexpression, we propose that there are alternative tumour-promoting activities for the E2F family, which are independent of cell cycle regulation.

Author affiliations

1. Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics and Department of Molecular Genetics;
2. Integrated Medical Scientist Program, College of Medicine and Public Health, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA.

Correspondence to: Gustavo Leone^1,2 Email: Gustavo.Leone@osumc.edu

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