curcumin--a remarkable compound effective in ER- and ER+bc even w multidrugresistance

[Lani]

Now just to figure out what form, in what dosage, given at what frequency...(also her2+ bc not tested, just her2- bc results here):

Int J Mol Med. 2007 Sep;20(3):329-35.
The antitumor activities of curcumin and of its isoxazole analogue are not affected by multiple gene expression changes in an MDR model of the MCF-7 breast cancer cell line: Analysis of the possible molecular basis.

Poma P, Notarbartolo M, Labbozzetta M, Maurici A, Carina V, Alaimo A, Rizzi M, Simoni D, D'Alessandro N.
Department of Pharmacological Sciences, University of Palermo, 90127 Palermo, Italy.
We examined the effects of curcumin and of its isoxazole analogue MR 39 in the MCF-7 breast cancer cell line and in its multidrug-resistant (MDR) variant MCF-7R. In comparison with MCF-7, MCF-7R lacks estrogen receptor alpha (ERalpha) and overexpressess P-glycoprotein (P-gp), different IAPs (inhibitory of apoptosis proteins) and COX-2. Through analyses of the effects on cell proliferation, cycling and death, we have observed that the antitumor activity of curcumin and of the more potent (approximately two-fold) MR 39 is at least equal in the MDR cell line compared to the parental MCF-7. Similar results were observed also in an MDR variant of HL-60 leukemia. RT-PCR evaluations performed in MCF-7 and MCF-7R showed that curcumin or MR 39 produced early modifications in the amounts of relevant gene transcripts, which, however, were mostly diverse (i.e. represented by decreases in IAPs and COX-2 in MCF-7R versus reductions in Bcl-2 and Bcl-XL as well as increases in the Bcl-XS/Bcl-XL ratio in MCF-7) in the two cell lines. These results could not be explained by an involvement of NF-kappaB (p65 subunit) or STAT3, since the low nuclear levels of these transcription factors present in MCF-7 were only slightly, though significantly, elevated in MCF-7R; moreover, curcumin or MR 39 caused minor changes in NF-kappaB or STAT3 activation. Overall, these data underline that curcumin or MR 39 antitumor activities are not hampered by P-gp expression or lack of ERalpha in breast cancer cells. Remarkably, the agents appeared to modify their molecular effects according to the diverse gene expression patterns existing in the MDR and in the parental MCF-7. Clearly, the structure and properties of curcumin can form the basis for the development of antitumor compounds that are more effective against both chemosensitive and MDR cells. .
PMID: 17671737 [PubMed - in process]

[TSund]

Lani,

Let me know when you figure it out.

I've been itching to give Ruth curcumin, but must wait until after chemo. Is it safe during rads?

TRS

[Adriana Mangus]

Dear Lani: Thanks for your post.

Is there anything similar to curcumin for us Her2+???

Thanks.

[Lani]

only that the tests they did in this paper were on a her2- cell line
As different tumors have different pathways out of control (and as this can change in time and with treatment) it seemed positive that the multidrug resistance of this cell line did not affect the efficacy of curcumin against it.

Now to figure out how much, how often, etc. As no drug company money for it, it may not happen until a curcumin-like drug is developed and in trials...

[Donna]

Hi Lani,

I'm thinking it wouldn't hurt to take it - actually I have been supplementing with it for a month or so - not huge quantities, but I figure
it can't hurt and maybe it's helping. I get it from Puritan's Pride - 450 mg tumeric and 50mg tumeric extract. It's only one more pill among my many supplements.

Thanks for posting this,

Donna