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.
Lobular carcinoma in situ (LCIS) is considered to bea risk factor for the development of invasive breastcarcinoma, but it may also be a non-obligate precursorto invasive lobular carcinoma (ILC). Many LCIS lesionsdo not progress to ILC, and the molecular changesthat are necessary for progression from LCIS to ILCare poorly understood. Disruption in the E-cadherincomplex is the hallmark of lobular lesions, but othersignaling molecules, such as PIK3CA and c-src, areconsistently altered in LCIS. This review focuses onthe molecular drivers of lobular carcinoma, a morecomplete understanding of which may give perspectiveon which LCIS lesions progress, and which will not, thushaving immense clinical implications.
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