Lobular carcinoma in situ (LCIS) is considered to be
a risk factor for the development of invasive breast
carcinoma, but it may also be a non-obligate precursor
to invasive lobular carcinoma (ILC). Many LCIS lesions
do not progress to ILC, and the molecular changes
that are necessary for progression from LCIS to ILC
are poorly understood. Disruption in the E-cadherin
complex is the hallmark of lobular lesions, but other
signaling molecules, such as PIK3CA and c-src, are
consistently altered in LCIS. This review focuses on
the molecular drivers of lobular carcinoma, a more
complete understanding of which may give perspective
on which LCIS lesions progress, and which will not, thus
having immense clinical implications.