HER2 Support Group Forums - View Single Post - open access editorial in JCO accompanies article which MAY show equivalence of

Lani · 01-23-2011, 11:28 AM

In fact I just read an article about treating er-pr- patients with a combination of an HDAC inhibitor and an AI. The HDAC inhibitor takes the epigenetic markers off the part of the chromosome that hides the gene, in this case the ER gene, so that it can be read and the ER protein produced. In this way, ER- bc cells are made ER+ so the AI can work. There are some her2- patients that herceptin works on and they are still trying to figure out why--probably because they have some her2+ clones.

I guess the question is what the cell is which makes the tumor grow.ie the stem cell or an early progenitor cell and what its characteristics are. The other cells, which make up ~85-97% of the bulk of the tumor can be gotten rid of but are not the ones that make it come back.

So the AI may work on part of the tumor with ER+ clones but will it work on the "real culprits" which cause recurrence and metastasis.

We are learning more and studying DTC (bone marrow) and CTCs may help
researchers understand more.

01-23-2011, 11:28 AM	#11
Lani Senior Member Join Date: Mar 2006 Posts: 4,783	Re: open access editorial in JCO accompanies article which MAY show equivalence of In fact I just read an article about treating er-pr- patients with a combination of an HDAC inhibitor and an AI. The HDAC inhibitor takes the epigenetic markers off the part of the chromosome that hides the gene, in this case the ER gene, so that it can be read and the ER protein produced. In this way, ER- bc cells are made ER+ so the AI can work. There are some her2- patients that herceptin works on and they are still trying to figure out why--probably because they have some her2+ clones. I guess the question is what the cell is which makes the tumor grow.ie the stem cell or an early progenitor cell and what its characteristics are. The other cells, which make up ~85-97% of the bulk of the tumor can be gotten rid of but are not the ones that make it come back. So the AI may work on part of the tumor with ER+ clones but will it work on the "real culprits" which cause recurrence and metastasis. We are learning more and studying DTC (bone marrow) and CTCs may help researchers understand more.