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

R.B. · 03-06-2008, 11:03 AM

Intriguing !

" Considerable evidence suggests strongly that the n-3 polyunsaturated fatty acid (PUFA) content of adipose breast tissue is inversely associated with an increased risk of breast cancer."

More questions than answers but these two trials do underline fats play important roles in breast function, which given breasts function is to supply nutrients including fats, is unsurprising.

Long chain Omega 3s DHA and EPA may be fundamental to function breasts in pregnancy, and may have a part in explaining lower rates in women that have been pregnant based on trials in mice.

Also FAS an enzyme critical to making fats from scratch is often hyperactive and over expressed in some aggressive breast cancers, and may be driven in the line of cells examined by HER2. Why does the breast switch on its fat making enzymes in cancer and what has it got do do with HER2? Omega 3s may turn down FAS.

http://www.ncbi.nlm.nih.gov/pubmed/1...ractPlusDrugs1

"Activity and expression of fatty acid synthase (FAS), a critical enzyme in the de novo biosynthesis of fatty acids in mammals, is exquisitely sensitive to nutritional regulation of lipogenesis in liver or adipose tissue. Surprisingly, a number of studies have demonstrated hyperactivity and overexpression of FAS (oncogenic antigen-519) in a biologically aggressive subset of human breast carcinomas,"......"FAS overexpression in SK-Br3 breast cancer cells is driven by increases in HER-2/neu signaling,"......"GLA- and/or omega-3 PUFA-induced repression of tumor-associated FAS may represent a novel mechanism of PUFA-induced cytotoxicity clinically useful against breast carcinomas carrying overexpression of FAS enzyme;"

BUT if you don't eat it you don't have it as the body cannot make Omega 3s from other fats. The body just is not able to make Omega 3s. It can convert the mother fat found in vegetable sources to the long chain fats if the pathways are not blocked.

This trial below is essentially saying that if you could make your own Omega 3 your breasts would want to make more of it in pregnancy because that is what genetically altered mice that can make Omega 3s do.

And that Omega 3s have a big part to play in changing the status of fat producing cells in the breast.

The mouse referred to is a genetically altered mouse with genes from a worm that allows the mouse to convert Omega six to omega three (which we cannot do) and from vague memory even make its own Omega six which we also cannot do.

Activation of Stat5 and induction of a pregnancy-like mammary gland differentiation by eicosapentaenoic and docosapentaenoic omega-3 fatty acids.
Liu YE, Pu W, Wang J, Kang JX, Shi YE.

Feinstein Institute for Medical Research, Department of Radiation Oncology, Long Island Jewish Medical Center, The Albert Einstein College of Medicine, New Hyde Park, NY 11040, USA.

The protective effect of early pregnancy against breast cancer can be attributed to the transition from undifferentiated cells in the nulliparous to the differentiated mature cells during pregnancy. Considerable evidence suggests strongly that the n-3 polyunsaturated fatty acid (PUFA) content of adipose breast tissue is inversely associated with an increased risk of breast cancer. Here, we report that there was a decrease in the n-6/n-3 PUFA ratio and a significant increase in concentration of n-3 PUFA docosapentaenoic acid and eicosapentaenoic acid in the pregnant gland. The functional role of n-3 PUFAs on differentiation was supported by the studies in the fat-1 transgenic mouse, which converts endogenous n-6 to n-3 PUFAs. Alternation of the n-6/n-3 ratio in favor of n-3 PUFA, and particularly docosapentaenoic acid, in the mammary gland of fat-1 mouse resulted in development of lobulo-alveolar-like structure and milk protein beta-casein expression, mimicking the differentiated state of the pregnant gland. Docosapentaenoic acid and eicosapentaenoic acid activated the Jak2/Stat5 signaling pathway and induced a functional differentiation with production of beta-casein. Expression of brain type fatty acid binding protein brain type fatty acid binding protein in virgin transgenic mice also resulted in a reduced ratio of n-6/n-3 PUFA, a robust increase in docosapentaenoic acid accumulation, and mammary differentiation. These data indicate a role of mammary derived growth inhibitor related gene for preferential accumulation of n-3 docosapentaenoic acid and eicosapentaenoic acid in the differentiated gland during pregnancy. Thus, alternation of n-6/n-3 fatty acid compositional ratio in favor of n-3 PUFA, and particularly docosapentaenoic acid and eicosapentaenoic acid, is one of the underlying mechanisms of pregnancy-induced mammary differentiation.

03-06-2008, 11:03 AM	#207
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	The protective effect of early pregnancy against breast cancer and DHA EPA etc Intriguing ! " Considerable evidence suggests strongly that the n-3 polyunsaturated fatty acid (PUFA) content of adipose breast tissue is inversely associated with an increased risk of breast cancer." More questions than answers but these two trials do underline fats play important roles in breast function, which given breasts function is to supply nutrients including fats, is unsurprising. Long chain Omega 3s DHA and EPA may be fundamental to function breasts in pregnancy, and may have a part in explaining lower rates in women that have been pregnant based on trials in mice. Also FAS an enzyme critical to making fats from scratch is often hyperactive and over expressed in some aggressive breast cancers, and may be driven in the line of cells examined by HER2. Why does the breast switch on its fat making enzymes in cancer and what has it got do do with HER2? Omega 3s may turn down FAS. http://www.ncbi.nlm.nih.gov/pubmed/1...ractPlusDrugs1 "Activity and expression of fatty acid synthase (FAS), a critical enzyme in the de novo biosynthesis of fatty acids in mammals, is exquisitely sensitive to nutritional regulation of lipogenesis in liver or adipose tissue. Surprisingly, a number of studies have demonstrated hyperactivity and overexpression of FAS (oncogenic antigen-519) in a biologically aggressive subset of human breast carcinomas,"......"FAS overexpression in SK-Br3 breast cancer cells is driven by increases in HER-2/neu signaling,"......"GLA- and/or omega-3 PUFA-induced repression of tumor-associated FAS may represent a novel mechanism of PUFA-induced cytotoxicity clinically useful against breast carcinomas carrying overexpression of FAS enzyme;" BUT if you don't eat it you don't have it as the body cannot make Omega 3s from other fats. The body just is not able to make Omega 3s. It can convert the mother fat found in vegetable sources to the long chain fats if the pathways are not blocked. This trial below is essentially saying that if you could make your own Omega 3 your breasts would want to make more of it in pregnancy because that is what genetically altered mice that can make Omega 3s do. And that Omega 3s have a big part to play in changing the status of fat producing cells in the breast. The mouse referred to is a genetically altered mouse with genes from a worm that allows the mouse to convert Omega six to omega three (which we cannot do) and from vague memory even make its own Omega six which we also cannot do. Activation of Stat5 and induction of a pregnancy-like mammary gland differentiation by eicosapentaenoic and docosapentaenoic omega-3 fatty acids. Liu YE, Pu W, Wang J, Kang JX, Shi YE. Feinstein Institute for Medical Research, Department of Radiation Oncology, Long Island Jewish Medical Center, The Albert Einstein College of Medicine, New Hyde Park, NY 11040, USA. The protective effect of early pregnancy against breast cancer can be attributed to the transition from undifferentiated cells in the nulliparous to the differentiated mature cells during pregnancy. Considerable evidence suggests strongly that the n-3 polyunsaturated fatty acid (PUFA) content of adipose breast tissue is inversely associated with an increased risk of breast cancer. Here, we report that there was a decrease in the n-6/n-3 PUFA ratio and a significant increase in concentration of n-3 PUFA docosapentaenoic acid and eicosapentaenoic acid in the pregnant gland. The functional role of n-3 PUFAs on differentiation was supported by the studies in the fat-1 transgenic mouse, which converts endogenous n-6 to n-3 PUFAs. Alternation of the n-6/n-3 ratio in favor of n-3 PUFA, and particularly docosapentaenoic acid, in the mammary gland of fat-1 mouse resulted in development of lobulo-alveolar-like structure and milk protein beta-casein expression, mimicking the differentiated state of the pregnant gland. Docosapentaenoic acid and eicosapentaenoic acid activated the Jak2/Stat5 signaling pathway and induced a functional differentiation with production of beta-casein. Expression of brain type fatty acid binding protein brain type fatty acid binding protein in virgin transgenic mice also resulted in a reduced ratio of n-6/n-3 PUFA, a robust increase in docosapentaenoic acid accumulation, and mammary differentiation. These data indicate a role of mammary derived growth inhibitor related gene for preferential accumulation of n-3 docosapentaenoic acid and eicosapentaenoic acid in the differentiated gland during pregnancy. Thus, alternation of n-6/n-3 fatty acid compositional ratio in favor of n-3 PUFA, and particularly docosapentaenoic acid and eicosapentaenoic acid, is one of the underlying mechanisms of pregnancy-induced mammary differentiation.