Relationship b/w gene # 666, BCL-2, and breast cancer?
I have been seeking spiritual answers in my life lately.
Last night, I had a dream about two mothers. I don't think the details are important, just that it was vivid and interesting enough for me to get up and google. So...
I woke up and googled "two mothers".
I came to an article about mice and monkeys having been created without a father, with two mothers. (http://www.livescience.com/health/etc/090827-monkeys-born-two-mothers.html and http://www.genomenewsnetwork.org/articles/2004/04/23/fatherless.php)
I read something somewhere in my reading about genes in those articles about gene markers. Googled "gene 666" and came across the page: http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=666
Then did some more googling and found out that "strategies designed to block Bcl-2 might prove useful in sensitizing tumor cells to chemotherapy-induced apoptosis from the page: http://www.springerlink.com/content/m8w5651m16322upn/
So, what I would be interested to know is, since I am not a scientist, what is the relationship between gene number 666, BCL-2, and breast cancer? I don't think I would have been led here if there wasn't a link. Would somebody in the scientific community possibly please, please, be able to look into this, read related papers, or ask one of your peers? (I don't understand all of the science-garble I read in these articles). Is this relationship something that has been known and/or applied for some time?
I am particularly concerned about John Edwards' wife, who says God isn't going to cure her. If my dream led to the unearthing or awareness of something that may help scientists to help her, then God is trying to cure her.
Just a long shot... but wanted to throw this out there just in case it would help.
Thanks.
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Vitamin D appears to depress aromatase inhibitor by acting through cytochrome P 450. This evidence along with pre-clinical and clinical studies, justify the inclusion of vitamin D in future clinical trials related to breast cancer in order to determine its efficacy as a part of the breast cancer therapeutic armament.
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Apparently gene 666 is in the bcl-2 family of genes. Bcl-2 was the first gene identified in this family, and is an 'oncogene' -- a gene that, when overactive, promotes (or even causes) cancer. The original bcl-2 was so named because it was the 2nd gene identified as relevant to b-cell lymphoma (B-cells are lymphocytes; a b-cell lymphoma is a blood cancer of these immune-system cells).
Apparently, however, the bcl-family is quite diverse. Some genes in the bcl family promote apotosis (programmed cell death, which would make them more like tumor repressor genes, so it is quite complicated. I don't know which type 666 is -- didn't look that far.
However, to answer your question: yes, scientists are aware of the connection between bcl-2 family genes and breast cancer. In fact, bcl-2 activity is considered a strong prognostic marker for bc progression - if i remember correctly, it is part of the omcotype screen.
The other thing to remember is this: it's a long way from recognizing a connection to using the information in treatment. So far, despite all the accumulating information about breast cancer-associated genes, the best that's been doable is to develop prognostic markers - like BRCA 1 1nd 2, or the oncotype-DX test. All anyone can do is say -- you have over-activity (or underactivity) in such and such a gene (or genes) -- they can't turn them on or off, which is what would be needed to alter the course of the tumor.
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Abstract The biological role of vitamin D outside of calcium homeostasis is still under evaluation. The ability of vitamin D to inhibit cell proliferation and induce differentiation makes it a potential modifier of neoplastic transformation. Vitamin D affects the cell cycle, apoptosis, hormone receptors, angiogenesis, and hypoxia, all of which are related to the breast cancer growth, progression and metastasis. A large percentage of the industrial-world population is deficient in vitamin D. Epidemiological evidence suggests that vitamin D deficiency increases the risk of breast cancer. Vitamin D may have synergistic, additive, or antagonistic effects when combined with other therapeutic agents against breast cancer. Vitamin D appears to depress aromatase inhibitor by acting through cytochrome P 450. This evidence along with pre-clinical and clinical studies, justify the inclusion of vitamin D in future clinical trials related to breast cancer in order to determine its efficacy as a part of the breast cancer therapeutic armament.
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Hi Moore --
That's an interesting abstract -- where is it from? I'd like to see the article! (When i click on your link, i get a dating site).
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