It is widely believed that breast cancer dissemination involves
a succession of clinical and pathological stages starting with carcinoma in situ, progressing into invasive
lesion and culminating in metastatic disease. Such changes have frequently been attributed to the
sequential acquisition of various alterations in a single cell followed by clonal selection and expansion,
thus leading to intra-tumor diversity. According to this multi-step view, extensive genotype and phenotype
(marker expression, grade) shift may occur in a same tumor during progression; this may lead to the
coexistence of molecularly and/or pathologically different areas in a same lesion. An increasing number
of data of various natures appear now to challenge this conception: only a few distinct "portraits",
with relations to estrogen receptor (ER)-status and grade, may be found among tumors. Moreover, although
undergoing increasing genetic alteration, most individual lesions largely maintain their phenotype when
they evolve from in situ to the metastatic state. While many of the data presented here are related to
ductal tumors, lobular cancer is also discussed. Moreover, a discussion on breast tumor stem cells is
incorporated.
