Role of biologic therapy and chemotherapy in hormone receptor- and HER2-positive breast cancer.
BACKGROUND
To review the efficacy of chemotherapy and human epidermal growth factor receptor 2 (HER2)-targeted therapy when used in addition to hormonal therapy for the optimal management of estrogen receptor-positive (ER+)/human epidermal growth factor receptor 2-positive (HER2+) breast cancer.


METHODS
Literature published from January 2003 to March 2008 was reviewed to assess the use of chemotherapy and biologic therapy in addition to hormonal agents.


RESULTS
Aromatase inhibitors (AIs) demonstrated greater effectiveness in the adjuvant setting than tamoxifen for the management of ER+ and HER2+ breast cancer. Evidence of cross talk between HER2- and ER-signaling pathways suggests that combined treatment with HER2 blockade and hormonal therapy may offer clinical advantages beyond those provided by hormonal therapy alone in ER+/HER2+ disease. Combined therapy with trastuzumab plus an aromatase AI significantly improves progression-free survival, response rates, and clinical benefits when compared with AI monotherapy in postmenopausal women. Several large studies demonstrated that trastuzumab significantly improves disease-free and overall survival when given in combination with, or following, chemotherapy, regardless of hormone receptor status.


CONCLUSIONS
HER2-targeted therapy maybe combined with AIs for the treatment of ER+/HER2+ metastatic breast cancer in postmenopausal women. HER2-targeted therapy in combination with AIs for treatment of ER+/HER2+ early breast cancer needs to be prospectively evaluated.
Buzdar
A U
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Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. abuzdar@mdanderson.org
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001691:Biological Therapy; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism*; D019008:Drug Resistance, Neoplasm; D005260:Female; D006801:Humans; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000096:biosynthesis; D011960:Receptors, Estrogen / Q000096:biosynthesis; D011980:Receptors, Progesterone / Q000096:biosynthesis; D015398:Signal Transduction
D000970:Antineoplastic Agents; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone