Weakening link to colorectal cancer?

M. Barbier, S. Attoub, R. Calvez, M. Laffargue, A. Jarry, M. Mareel, F. Altruda, C. Gespach, D. Wu, B. Lu, E. Hirsch and M. P. Wymann ()
Additional contact information
M. Barbier: Institute of Biochemistry, University of Fribourg
S. Attoub: INSERM U482, Hôpital Saint-Antoine
R. Calvez: Institute of Biochemistry, University of Fribourg
M. Laffargue: Institute of Biochemistry, University of Fribourg
A. Jarry: INSERM U539, Hôtel-Dieu
M. Mareel: Laboratory of Experimental Cancerology, Ghent University
F. Altruda: Biologia e Biochimica, Università di Torino
C. Gespach: INSERM U482, Hôpital Saint-Antoine
D. Wu: University of Connecticut
B. Lu: Children's Hospital, Harvard Medical School
E. Hirsch: Biologia e Biochimica, Università di Torino
M. P. Wymann: Institute of Biochemistry, University of Fribourg

Nature, 2001, vol. 413, issue 6858, 796-796

Abstract: Abstract The catalytic γ-subunit of the enzyme phosphatidylinositol-3-OH kinase (PI(3)Kγ) relays signals from G- protein-coupled receptors at the cell membrane and mediates leukocyte responses to chemokines and chemoattractants1,2,3. Sasaki et al.4 report that mice that cannot produce PI(3)Kγ have a high incidence of colorectal carcinomas, causing weight loss and premature death. However, PI(3)Kγ-null mouse strains have been independently generated in three other laboratories; none of these mice developed tumours and their weight and lifespan were normal. This casts coubt on the idea that loss of functional PI(3)Kγ leads directly to transformation of colon epithelial cells and tumour progression.

Date: 2001
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DOI: 10.1038/35101660

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