Abstract
Aberrant growth factor receptor signaling can augment or suppress estrogen receptor (ER) function in hormone-dependent breast cancer cells and lead to escape from anti-estrogen therapy. Interruption of HER2/ER cross-talk with lapatinib can restore sensitivity to anti-estrogens and thus, should be investigated in combination with endocrine therapy in patients with ER+/HER2-negative breast cancers.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Antineoplastic Agents / therapeutic use*
-
Breast Neoplasms / drug therapy*
-
Breast Neoplasms / genetics
-
Breast Neoplasms / metabolism*
-
Clinical Trials as Topic
-
Drug Resistance, Neoplasm / physiology
-
Female
-
Humans
-
Lapatinib
-
Quinazolines / therapeutic use*
-
Receptor Cross-Talk / drug effects*
-
Receptor, ErbB-2 / metabolism*
-
Receptors, Estrogen / metabolism
Substances
-
Antineoplastic Agents
-
Quinazolines
-
Receptors, Estrogen
-
Lapatinib
-
Receptor, ErbB-2