Taka
Sat, May-24-08, 06:15
Guess what they fed the experimental animals - CORN OIL ...
Cancer Res. 2008 Apr 15;68(8):3066-73.
Effect of low-fat diet on development of prostate cancer and
Akt phosphorylation in the Hi-Myc transgenic mouse model.
Kobayashi N, Barnard RJ, Said J, Hong-Gonzalez J, Corman DM,
Ku M, Doan NB, Gui D, Elashoff D, Cohen P, Aronson WJ.
Department of Urology, School of Medicine, University of
California, Los Angeles, CA 90095-1738, USA.
This study evaluated the effect of dietary fat on prostate
cancer development by using the Hi-Myc mouse transgenic
prostate cancer model. Hi-Myc mice develop murine prostatic
intraepithelial neoplasia (mPIN) as early as 2 to 4 weeks and
invasive adenocarcinoma between 6 and 9 months due to the
overexpression of human c-Myc in the mouse prostate.
Three-week-old male Hi-Myc mice were placed on high-fat (HF;
42% Kcal) or low-fat (LF; 12% Kcal) diets, and equal caloric
intake was maintained until euthanasia at 7 months. The number
of mice that developed invasive adenocarcinoma at 7 months was
27% less in the LF diet group (12/28) compared with the HF
diet group (23/33, P < 0.05). Epithelial cells in mPIN lesions
in the LF group had a significantly lower proliferative index
compared with epithelial cells in the HF group (21.7% versus
28.9%, P < 0.05). During the mPIN phase of carcinogenesis (4
months), the LF group had higher serum insulin-like growth
factor (IGF) binding protein-1 levels (21.0 +/- 8.9 ng/mL
versus 3.2 +/- 0.8 ng/mL, P < 0.05) relative to the HF group.
Akt (Ser(473)) phosphorylation, Akt kinase activity, and
phosphorylation of downstream targets of Akt in prostates were
significantly reduced in the LF diet group compared with the
HF group. We conclude that dietary fat reduction delays
transition from mPIN to invasive cancer in this Myc-driven
transgenic mouse model, possibly through suppression of the
IGF-Akt pathway and decreased proliferation of mPIN epithelial
cells. PMID: 18413778
Taka
Cancer Res. 2008 Apr 15;68(8):3066-73.
Effect of low-fat diet on development of prostate cancer and
Akt phosphorylation in the Hi-Myc transgenic mouse model.
Kobayashi N, Barnard RJ, Said J, Hong-Gonzalez J, Corman DM,
Ku M, Doan NB, Gui D, Elashoff D, Cohen P, Aronson WJ.
Department of Urology, School of Medicine, University of
California, Los Angeles, CA 90095-1738, USA.
This study evaluated the effect of dietary fat on prostate
cancer development by using the Hi-Myc mouse transgenic
prostate cancer model. Hi-Myc mice develop murine prostatic
intraepithelial neoplasia (mPIN) as early as 2 to 4 weeks and
invasive adenocarcinoma between 6 and 9 months due to the
overexpression of human c-Myc in the mouse prostate.
Three-week-old male Hi-Myc mice were placed on high-fat (HF;
42% Kcal) or low-fat (LF; 12% Kcal) diets, and equal caloric
intake was maintained until euthanasia at 7 months. The number
of mice that developed invasive adenocarcinoma at 7 months was
27% less in the LF diet group (12/28) compared with the HF
diet group (23/33, P < 0.05). Epithelial cells in mPIN lesions
in the LF group had a significantly lower proliferative index
compared with epithelial cells in the HF group (21.7% versus
28.9%, P < 0.05). During the mPIN phase of carcinogenesis (4
months), the LF group had higher serum insulin-like growth
factor (IGF) binding protein-1 levels (21.0 +/- 8.9 ng/mL
versus 3.2 +/- 0.8 ng/mL, P < 0.05) relative to the HF group.
Akt (Ser(473)) phosphorylation, Akt kinase activity, and
phosphorylation of downstream targets of Akt in prostates were
significantly reduced in the LF diet group compared with the
HF group. We conclude that dietary fat reduction delays
transition from mPIN to invasive cancer in this Myc-driven
transgenic mouse model, possibly through suppression of the
IGF-Akt pathway and decreased proliferation of mPIN epithelial
cells. PMID: 18413778
Taka