And Researchers have done the work

And as we have suggested, down the belly of the beast, the dance was uncovered...and for triple negative breast cancer, we now know that the main event is the surge in prolactin which is aimed at stimulating breast development but secondarily promote Casein genes.  And we have described Casein genes as they  lead to random phosphorylation of other genes.
One model shows Casein phosphorylation of CHEK1 which in turn phosphorylates CDC25 inhibiting it for removing the Phosphate brought by wee1 to stop Mitosis promotion.   Putting this as a control of mitosis (but not hyperplasia) in the breast.

Explaining how my achondroplastic woman developed breast cancer became a little easier since Achondroplasia is 99 percent due to FGFR gene abnormalities, and that FGFR interacts with FGF1 which in turn interacts directly with the Casein Kinase 2, and within the presence of BRCA1, Achondroplasia will lead to cdc25 within million seconds!

It is nice to note that Achondroplasia is the thing about not only disturbance of connective tissue through the FGFR3 but also associated calcium distribution (as it occurs on mammogram for breast cancer diagnosis), may be through activity of the SYT-1, or is it S100A.
Note the action of FGF1 on CSNKs!