HER2 Support Group Forums - View Single Post - The traditional diet of Greece and cancer.

R.B. · 08-03-2008, 02:41 PM

Complicated but interesting.

Prostaglandins and leukotrienes are products of Omega Six.

It is an interesting suggestion that CLA may inhibit the downstream products of Omega 6. But as ever it is easier to cut down on excess Omega Six and balance with 3s, so avoiding excess Omega 6 products in the first place.

RB

Proliferative responses of normal human mammary and MCF-7 breast cancer cells to linoleic acid, conjugated linoleic acid and eicosanoid synthesis inhibitors in culture

Anticancer Research (Greece) , 1997, 17/1 A (197-203)

Potential mechanisms for the stimulation or inhibition of cell growth by linoleic acid (LA) and conjugated linoleic acid (CLA) were investigated by using eicosanoid linoleic acid (CLA) were investigated by using eicosanoid synthesis inhibitors. Normal human mammary epithelial cells (HMEC) and MCF-7 breast cancer cells were incubated in serum-free medium supplemented with LA or CLA and cyclooxygenase (indomethacin; INDO) or lipoxygenase (nordihydroguaiaretic acid; NDGA) inhibitors. Linoleic acid stimulated the growth and (3H)thymidine incorporation of normal HMEC and MCF-7 cancer cells, while CLA was inhibitory. Supplementation with LA increased intracellular lipid peroxide concentrations in normal HMEC and MCF-7 cancer cells, whereas CLA did not affect lipid peroxide formation. Normal HMEC and MCF-7 cells supplemented with LA and INDO or NDGA resulted in growth inhibition. The treatment of normal HMEC with CLA and INDO or NDGA, and MCF-7 cells with CLA and INDO stimulated cell growth. However, the addition of CLA and NDGA to MCF-7 cells resulted in synergistic growth suppression suggesting that CLA effects were mediated through lipoxygenase inhibition. Although NDGA was more inhibitory of cell growth in the presence of LA or CLA than INDO, growth was associate with both prostaglandin and leukotriene production. Additional studies are warranted to elucidate the mechanism(s)

whereby LA or CLA affect breast cell growth.

08-03-2008, 02:41 PM	#255
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	Complicated but interesting. Prostaglandins and leukotrienes are products of Omega Six. It is an interesting suggestion that CLA may inhibit the downstream products of Omega 6. But as ever it is easier to cut down on excess Omega Six and balance with 3s, so avoiding excess Omega 6 products in the first place. RB Proliferative responses of normal human mammary and MCF-7 breast cancer cells to linoleic acid, conjugated linoleic acid and eicosanoid synthesis inhibitors in culture Anticancer Research (Greece) , 1997, 17/1 A (197-203) Potential mechanisms for the stimulation or inhibition of cell growth by linoleic acid (LA) and conjugated linoleic acid (CLA) were investigated by using eicosanoid linoleic acid (CLA) were investigated by using eicosanoid synthesis inhibitors. Normal human mammary epithelial cells (HMEC) and MCF-7 breast cancer cells were incubated in serum-free medium supplemented with LA or CLA and cyclooxygenase (indomethacin; INDO) or lipoxygenase (nordihydroguaiaretic acid; NDGA) inhibitors. Linoleic acid stimulated the growth and (3H)thymidine incorporation of normal HMEC and MCF-7 cancer cells, while CLA was inhibitory. Supplementation with LA increased intracellular lipid peroxide concentrations in normal HMEC and MCF-7 cancer cells, whereas CLA did not affect lipid peroxide formation. Normal HMEC and MCF-7 cells supplemented with LA and INDO or NDGA resulted in growth inhibition. The treatment of normal HMEC with CLA and INDO or NDGA, and MCF-7 cells with CLA and INDO stimulated cell growth. However, the addition of CLA and NDGA to MCF-7 cells resulted in synergistic growth suppression suggesting that CLA effects were mediated through lipoxygenase inhibition. Although NDGA was more inhibitory of cell growth in the presence of LA or CLA than INDO, growth was associate with both prostaglandin and leukotriene production. Additional studies are warranted to elucidate the mechanism(s) whereby LA or CLA affect breast cell growth.