MacInnes Group

Translation and cancer

The focus of the MacInnes lab is to unravel the molecular mechanisms by which mutations in genes involved in the translation machinery result in cancer.  It has been well established that several human bone marrow failure diseases (which all predispose individuals to acute myeloid leukemia) are linked to mutations in genes encoding proteins that are involved in the synthesis and function of the most fundamental element of protein synthesis in the living cell, the ribosome.  Using both zebrafish models and cells derived from human patients we aim to understand how these mutations result in malfunctioning ribosomes, and how these malfunctions results in malignancies.

About the research

Key publications
MacInnes, A., Amsterdam, A., Lees, J., Hopkins, N. (2009) Cancer: The Outlaw Cell, 3rd edition. Chapter on Zebrafish models of cancer (in press).

MacInnes, A., Amsterdam, A., Hopkins, N., Lees, J. (2008) Loss of p53 protein synthesis in zebrafish tumors with ribosomal protein gene mutations. Proc. Natl. Acad.Sci. UA 105: 10408-10413.

Fralish, G.,, Philipp, M,, Meloni, A,, Chen, W,, MacInnes, A,, Barak, L,, Caron, M. (2008) Smoothened signaling in vertebrates is facilitated by a G-protein coupled receptor kinase. Mol. Biol. Cell 19: 5478-5489.

Wilbanks, A., Fralish, G., Kirby, M., Barak., L, Li, Y., Caron, M. (2004) ß-arrestin2 regulates zebrafish development through the Hedgehog signaling pathway. Science 306: 2264-2267.

Publication list