c-Myc - pivotal role - Another one for the EPA DHA possible risk reduction list.

[R.B.]

Another one for the EPA DHA possible risk reduction list.

This would also appear to link to pregnancy.

Telomerase are bits that protect genes from change, and connect to ageing, so damage to telomerase could equate in some circumstances to genetic damage etc. http://en.wikipedia.org/wiki/Telomerase

EPA and DHA may down regulate c-Myc which has a "pivotal role" in BC.

Something else I found a while ago and have just refound, and better realised its significance. I can see the wood even if the trees are a blur.


RB



Dual mechanisms for telomerase inhibition in DLD-1 human colorectal adenocarcinoma cells by polyunsaturated fatty acids

Takahiro Eitsuka A1, Kiyotaka Nakagawa A1, Teruo Miyazawa A1

http://iospress.metapress.com/app/ho...lts,1:103144,1

Abstract:

Polyunsaturated fatty acids (PUFAs) have been reported to have antitumor activity. In this study, we have tested whether telomerase might be a target for the antitumor effect of fatty acids using DLD-1 colorectal adenocarcinoma cells. In a cell-free approach, fatty acids were added directly to cell lysates, and we confirmed that increasing fatty acid unsaturation correlates with increased inhibition of telomerase activity. Using a cell culture approach, DLD-1 cells were cultured with fatty acids. In a time and dose dependent manner, EPA and DHA suppressed cellular telomerase activity and the mRNAs encoding hTERT (human telomerase reverse transcriptase) and c-myc. Based on these observations, we suggest that PUFAs inhibit telomerase activity through dual mechanisms: direct inhibition of enzymatic activity and down regulation of hTERT, one of the telomerase components.





Knockdown of c-Myc expression by RNAi inhibits MCF-7 breast tumor cells growth in vitro and in vivo
http://www.pubmedcentral.gov/article...medid=15743499


Abstracts

"Breast cancer is the leading cause of cancer death in women worldwide. Elevated expression of c-Myc is a frequent genetic abnormality seen in this malignancy.............c-Myc has a pivotal function in the development of breast cancer. Our data show that decreasing the c-Myc protein level in MCF-7 cells by RNAi could significantly inhibit tumor growth both in vitro and in vivo, and imply the therapeutic potential of RNAi on the treatment of breast cancer by targeting overexpression oncogenes such as c-myc, and c-myc might be a potential therapeutic target for human breast cancer. …………

c-Myc is believed to participate in most aspects of cellular function, including replication, growth, metabolism, differentiation, and apoptosis [2]…

[Hopeful]

In the last issue of Breast Cancer Update http://www.breastcancerupdate.com/bcu2007/3/default.asp at page 35, Dr. Paik explains why Her2+ patients that have cMYC amplification have an exceptionally good response to Herceptin.

Hopeful

[RobinP]

RB, where is your resource that pregnancy has a deleterious effect on the beneficial oils, DHA and EPA? Thanks.

[R.B.]

Please can you clarify your question. I am sorry I was not clearer.

I was trying to reflect that trials are showing a suggestion of communality between mechanisms employed by the body to make babies and tumours.

If you were asking about the effect of pregnancy on DHA:

Re pregnancy and omega threes and sixes - a subject on its own - but in essence babies need large amounts of DHA to make brains eyes etc. Babies are "Parasitic", in that they take preference over the mother. They will even strip mothers brain of essential fats inc DHA if they have to. So for women who have had one or more pregnancies and a diet lacking in long chain omega threes/ and or mother omega three / and or inability to make long chain fats ..........they may have much lower levels than normal of DHA.

Some small trials link lower levels of DHA with higher BC risk


RB