[Becky]

Another way to look at it is at this very basic level (and this is VERY basic). When a cell divides, it reproduces its strands of DNA and then half goes to one cells and the other half goes to the other cell. Now, let’s say that half doesn’t go to one cell but one cell gets an extra strand (3 copies of a strand) – that means that the other cell only got one copy of that strand. Now, those 2 cells might be cancer precursors. Now those cells divide and since they are not “right” they may also not split up the strands of DNA evenly so now you have 2 differing lines of cells that are making mistakes (the line that has “more” and the line that has “less”). One line may preferentially take over because it is ER+ (in a younger premenopausal woman with plenty of estrogen). If the same thing happened in a perimenopausal woman, perhaps she would also have ER+ disease but it would only be 40% instead of 90% ER+ . The basic chemistry of the woman may come into play to predict the line that actually becomes the cancer or one or more of the lines may end up mutating so badly that they are not viable at all.<O</O
One must also consider that in all this, you may have a very dominant line and a very repressed line. Chemo or other treatments might knock out the dominant line and then the repressed line may rear its ugly head (might be a reason why cancer “changes” and becomes ER+ when it was once ER- etc). Just some food for thought on this interesting research work done in this study.

Also, not to be forgotten is that what kind of cell in the duct or lobe can predict pathology (inside lining of the duct, more internal or the outside cells (ie: basal cells aka triple negative cancers)<O</O