Ok, so I'm studying for the boards now as well, and this whole progesterone thing is driving me nuts. But let me summarize what I did come up with.
1st point- There are certain types of BreastCA that are estrogen receptor positive and then there are those that are progesterone receptor positive. They can both be positive at the same time, negative at the same time, and/or one can be positive while the other is negative.
2nd Point- Estrogen is mainly involved in breast tissue proliferation/"hyperplasia," while progesterone is mainly involved in breast tissue "differentiation."
3rd Point- When on combined oral contraceptives treatment (estrogen and progestin) women are at higher risk for developing breast cancer than women on estrogen therapy alone.
Ok.. So as I understand it, but keep in mind that I'm still a bit confused, is that progesterone (given exogenously via OCP) actually increases your risk of developing breast cancer. I'm not entirely sure how this happens yet, especially since progesterone is a cell "differentiator" not proliferator. Maybe its acting on the progesterone receptor + types of BreastCA?...
So here's the big question then. How does nulliparity increase your risk of Breast cancer? So most of you are right in that in pregnancy, your progesterone levels are very high. Progesterone (endogenous) in pregnancy is causing an increased breast tissue differentiation in preparation for lactation. Because there are more breast cells differentiated, there are less stem cells that are available for neoplastic division. (so endo progesterone lower risk of BreastCA, while progestin OCP increases the risk?)
Listen up to this point though. So many of you, might be confusing nulliparity and its association with ENDOMETRIAL cancer. So here, the pathophys is different. In nulliparity, you do have less estrogen levels than pregnant women, but the key difference here is that you also have less progesterone. So the problem with nulliparity is that you do not have the PROTECTIVE effect of progesterone on endometrial cells.
Summary:
Nulliparity in BreastCA- less progesterone for tissue differentiation.
Nulliparity in EndometrialCA- less progesterone to counteract estrogen's negative role on endo hyperplasia
OCP with added Progestin- increased risk of BreastCA (don't quite understand why)
I used a combo of Robbins and uptodate to find most of this stuff. I'm giving this answer not as a final statement on the subject, but more as a summary as how I understand what is going on. Please feel free to comment and edit any areas that might be wrong.