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27.03.2018

Animal study: SAM-e inhibits breast cancer

Supplements with S-adenosylmethionine [usually abbreviated to SAM-e] may prevent breast cancer or, if that disease is already present, inhibit the spread of the cancer over the body. This is evident from an animal study that researchers at McGill University in Canada published in Oncotarget.

SAM-e
SAM-e is a substance that the body produces in relatively large quantities. SAM-e is a methyl donor, and delivers methyl groups. These are necessary for the functioning of the DNA. If the cell does not need genes, it silences them by sticking a methyl group to it.

Study
The researchers implanted MDA-MB-231 breast cancer cells in lab mice. MDA-MB-231 is an aggressive breast cancer cell line that is not sensitive to estradiol.

Three days after the implantation, the researchers started giving the mice SAM-e every day via the oral route. The human equivalent of the dose given that one group was given was about 200-300 milligrams of SAM-e per day, the other group received twice as much. A control group received no active substances.

Ten weeks after they had inserted the breast cancer cells, the researchers sacrificed the mice, and studied them.

Results
The high dose of SAM-e prevented tumors from forming in some mice. Both the high and low dose SAM-e reduced the growth of the tumors, and the number of metastases.

In the tumors of the lab mice, SAM-e inhibited a number of genes that are involved in, among other things, the spread of the cancer cells.

When the researchers looked at the functioning of these genes in women with breast cancer, they saw that the chance of metastasis was smaller for women whose genes were less active [A] than for women whose genes were fully active [B].

Conclusion
"To our knowledge, this is the first direct evidence for the potential therapeutic effect of S-adenosyl methionine in a well recognized model of breast cancer", the researchers write. "Results from these studies provide compelling evidence to evaluate the therapeutic as well as a chemopreventive potential of epigenetic-based agents such as S-adenosyl methionine alone and in the combination setting for patients with several common cancers including breast cancer.

Careful...
The tenor of this piece is not that cancer survivors people should start taking SAM-e. Yes, in many cancer cell types fewer genes are methylated than in healthy cells. If you have such a type of cancer, supplementation with SAM-e might be an option. But in other cancer cell types important genes are more often methylated than in healthy cells. And if you have such a type of cancer, you might not want to use supplements like SAM-e.

"A major concern with the use of hypermethylating agents is the possible silencing of tumor suppressor genes through hypermethylation of promoter and other regulatory regions", the researchers acknowledge. "Such methylation could override the beneficial effect of S-adenosyl methionine."

"When we checked the expression of some of recognized tumor-suppressor genes in MDA-MB-231 tumors, there was no significant difference between control and SAM-treated groups. This also complements our previous genome-wide analyses in prostate cancer and osteosarcoma cell lines where the methylation effect of SAM was limited to cancer promoting genes for yet unknown reasons." [Br J Pharmacol. 2015 Jun;172(11):2769-81.] [Cancer Med. 2015 May;4(5):732-44.]

"More interestingly, database search using the panel of seven genes (MUC1, PLAU, FABP7, SPARC, HAS2, HAS3, SOX4) downregulated by SAM revealed that these genes are highly expressed in basal B-type breast cancer cell lines and higher expression of these genes significantly decreases the probability of distant metastasis-free survival in breast cancer patients." [Breast Cancer Res Treat. 2010 Oct;123(3):725-31.]

Source:
Oncotarget. 2017 Dec 26;9(4):5169-83.

More:
SAM-e as effective as anti-inflammatories for joint pain 08.10.2009
SAM-e causes rise in testosterone 04.05.2009

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