Crazy ?

[RhondaH]

I may be WAY off base with this, but with the new information showing that diet helps reduce the risk of BC recurrence in ER/PR- and the "theory" that IGF-1 Receptor could be the reason for this, is there or have there been any clinical trials using diabetic drugs? Thank you. Take care and God bless.

Rhonda

[Lani]

and also Rhonda, there is one antidiabetic agent felt to be helpful in breast cancer (again not her2 specifically) --there may be a trial but I doubt it would include her2s who have had herceptin (that confuses things too much in looking at which agent is working)

Cancer Res. 2007 Jan 1;67(1):391-7.
Down-regulation of type I insulin-like growth factor receptor increases sensitivity of breast cancer cells to insulin.

Zhang H,
Pelzer AM,
Kiang DT,
Yee D.
University of Minnesota Cancer Center, 420 Delaware Street Southeast, Minneapolis, MN 55455, USA
The type I insulin-like growth factor receptor (IGF1R) and insulin receptor (IR) are structurally and functionally related heterotetrameric receptors. Activation of IGF1R has been shown to regulate breast cancer cell biology, and it has become an attractive therapeutic target. Most strategies have focused on targeting IGF1R alone without affecting IR levels given the known physiologic functions of IR. Human breast cancer cell lines and tissues revealed mRNA expression of both IGF1R and IR. Because alphabeta chains of IGF1R and IR form hybrid receptors, we hypothesized that agents solely targeting IGF1R may affect tumor biology mediated by IGF1R/IR hybrids and IR. We used small interfering RNA (siRNA) technology to specifically down-regulate IGF1R by 60% to 80% in the MDA-435/LCC6 cell line, which was sufficient to diminish activation of IGF1R by IGF-I. IGF1R down-regulation by siRNA did not affect IR levels but, interestingly, sensitized cells to insulin activation of downstream signaling pathways in several breast cancer cell lines. IGF1R siRNA treatment diminished hybrid receptor formation, suggesting that specific down-regulation of IGF1R resulted in enhanced holo-IR formation. In addition, IGF1R down-regulation increased insulin binding consistent with the formation of an increased number of holo-IR on the cell surface. Accordingly, insulin-stimulated glucose uptake was enhanced on IGF1R down-regulation. In conclusion, our data suggest that specific siRNA targeting of IGF1R alone in breast cancer increases insulin sensitivity. Because IR also activates signaling pathways similar to IGF1R in breast cancer cells, agents targeting both receptors may be necessary to disrupt the malignant phenotype regulated by this growth factor system.
PMID: 17210722 [PubMed - in process]

[RhondaH]

Sorry, I should have prefased my ? that this was not "specifically Her2" related. I'm weakly HER2 (3.16), so in some ways I consider myself triple neg. Thank you for the info...just my mind working (scary thought:). Take care and God bless.

Rhonda