title: Current approaches to the management of Her2-negative metastatic breast cancer.
abstract: While metastatic breast cancer (MBC) remains incurable, a vast array of active therapeutic agents has provided the opportunity for long-term disease control while maintaining quality of life and physical function. Optimal management of MBC balances a multitude of factors, including a woman's performance status, social support, symptoms, disease burden, prior therapies, and surrogates for tumor biology. Choosing the most appropriate initial therapy and subsequent sequence of treatments demands flexibility as goals and patient preferences may change. Knowledge of the estrogen receptor (ER), progesterone receptor (PR), and Her2 receptor status of the metastatic tumor has become critical to determining the optimal treatment strategy in the metastatic setting as targeted therapeutic approaches are developed. Patients with ER+ or PR+ breast cancer or both have a wide array of hormonal therapy options that can forestall the use of cytotoxic therapies, although rapidly progressive phenotypes and the emergence of resistance may ultimately lead to the need for chemotherapy in this setting. So-called 'triple-negative' breast cancer - lacking ER, PR, and Her2 overexpression - remains a major challenge. These tumors have an aggressive phenotype, and clear targets for therapy have not yet been established. Chemotherapy remains the mainstay of treatment in this group, but biologically based clinical trials of new agents are critical to developing a more effective set of therapies for this patient population.
authors.affiliation: Rena Rowan Breast Center, Abramson Cancer Center, University of Pennsylvania, Perelman Center for Advanced Medicine, West Pavilion, 3rd Floor, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
authors.forename: Keerthi
authors.initials: K
authors.lastname: Gogineni
authors.forename: Angela
authors.initials: A
authors.lastname: DeMichele
mesh_terms: D000964:Antimetabolites, Antineoplastic / Q000627:therapeutic use; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use; D047072:Aromatase Inhibitors / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology*; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D004317:Doxorubicin / Q000627:therapeutic use; D004958:Estradiol / Q000031:analogs & derivatives / Q000627:therapeutic use; D005260:Female; D000077267:Fulvestrant; D006801:Humans; D008535:Megestrol / Q000627:therapeutic use; D010053:Ovary / Q000187:drug effects; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors; D013629:Tamoxifen / Q000627:therapeutic use; D000093542:Gemcitabine
chemical_list: D000964:Antimetabolites, Antineoplastic; D018931:Antineoplastic Agents, Hormonal; D047072:Aromatase Inhibitors; D003841:Deoxycytidine; D004317:Doxorubicin; D004958:Estradiol; D000077267:Fulvestrant; D008535:Megestrol; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D058570:TOR Serine-Threonine Kinases; D013629:Tamoxifen; D000093542:Gemcitabine; C546842:MTOR protein, human; C508053:ERBB2 protein, human