HR+, HER2- Advanced Breast Cancer and CDK4/6 Inhibitors: Mode of Action, Clinical Activity, and Safety Profiles.
Curr Cancer Drug Targets
; 17(7): 637-649, 2017.
Article
en En
| MEDLINE
| ID: mdl-28359238
ABSTRACT
BACKGROUND:
Cyclin-dependent kinase (CDK) 4/6 inhibitor-based therapies have shown great promise in improving clinical outcomes for patients with hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (HER2-) advanced breast cancer.OBJECTIVES:
1. Discuss the mode of action of the three CDK4/6 inhibitors in late clinical development palbociclib (PD-0332991; Pfizer), ribociclib (LEE011; Novartis), and abemaciclib (LY2835219; Lilly). 2. Describe the efficacy and safety data relating to their use in HR+, HER2- advanced breast cancer. 3. Discuss the key side effects associated with CDK4/6 inhibitors along with considerations for adverse event management and patient monitoring.METHOD:
Relevant information and data were assimilated from manuscripts, congress publications, and online sources.RESULTS:
CDK4/6 inhibitors have demonstrated improved progression-free survival in combination with endocrine therapy compared with endocrine therapy alone. The side-effect profile of each agent is described, along with implications for patient monitoring, and considerations for patient care providers and pharmacists.CONCLUSION:
Addition of a CDK4/6 inhibitor to endocrine therapy increases efficacy and delays disease progression. Insight into the unique side-effect profiles of this class of agents and effective patient monitoring will facilitate the successful use of CDK4/6 inhibitor-based therapies in the clinic.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias de la Mama
/
Inhibidores de Proteínas Quinasas
/
Quinasa 4 Dependiente de la Ciclina
/
Quinasa 6 Dependiente de la Ciclina
/
Antineoplásicos
Límite:
Female
/
Humans
Idioma:
En
Revista:
Curr Cancer Drug Targets
Asunto de la revista:
ANTINEOPLASICOS
/
NEOPLASIAS
Año:
2017
Tipo del documento:
Article