Tamoxifen resistance: Emerging molecular targets

Milena Rondón-Lagos, Victoria E. Villegas, Nelson Rangel, Magda Carolina Sánchez, Peter G. Zaphiropoulos

Resultado de la investigación: Contribución a RevistaRevisión Literaria

30 Citas (Scopus)

Resumen

© 2016 by the authors; licensee MDPI, Basel, Switzerland.17β-Estradiol (E2) plays a pivotal role in the development and progression of breast cancer. As a result, blockade of the E2 signal through either tamoxifen (TAM) or aromatase inhibitors is an important therapeutic strategy to treat or prevent estrogen receptor (ER) positive breast cancer. However, resistance to TAM is the major obstacle in endocrine therapy. This resistance occurs either de novo or is acquired after an initial beneficial response. The underlying mechanisms for TAM resistance are probably multifactorial and remain largely unknown. Considering that breast cancer is a very heterogeneous disease and patients respond differently to treatment, the molecular analysis of TAM’s biological activity could provide the necessary framework to understand the complex effects of this drug in target cells. Moreover, this could explain, at least in part, the development of resistance and indicate an optimal therapeutic option. This review highlights the implications of TAM in breast cancer as well as the role of receptors/signal pathways recently suggested to be involved in the development of TAM resistance. G protein—coupled estrogen receptor, Androgen Receptor and Hedgehog signaling pathways are emerging as novel therapeutic targets and prognostic indicators for breast cancer, based on their ability to mediate estrogenic signaling in ERα-positive or-negative breast cancer.
Idioma originalEnglish (US)
PublicaciónInternational Journal of Molecular Sciences
DOI
EstadoPublished - ago 19 2016

Huella dactilar

Tamoxifen
breast
emerging
cancer
Breast Neoplasms
Bioactivity
estrogens
Proteins
Estrogen Receptors
Therapeutics
Aromatase Inhibitors
Androgen Receptors
G-Protein-Coupled Receptors
activity (biology)
GTP-Binding Proteins
progressions
inhibitors
Estrogens
Estradiol
therapy

Citar esto

Rondón-Lagos, Milena ; Villegas, Victoria E. ; Rangel, Nelson ; Sánchez, Magda Carolina ; Zaphiropoulos, Peter G. / Tamoxifen resistance: Emerging molecular targets. En: International Journal of Molecular Sciences. 2016.
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Tamoxifen resistance: Emerging molecular targets. / Rondón-Lagos, Milena; Villegas, Victoria E.; Rangel, Nelson; Sánchez, Magda Carolina; Zaphiropoulos, Peter G.

En: International Journal of Molecular Sciences, 19.08.2016.

Resultado de la investigación: Contribución a RevistaRevisión Literaria

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AB - © 2016 by the authors; licensee MDPI, Basel, Switzerland.17β-Estradiol (E2) plays a pivotal role in the development and progression of breast cancer. As a result, blockade of the E2 signal through either tamoxifen (TAM) or aromatase inhibitors is an important therapeutic strategy to treat or prevent estrogen receptor (ER) positive breast cancer. However, resistance to TAM is the major obstacle in endocrine therapy. This resistance occurs either de novo or is acquired after an initial beneficial response. The underlying mechanisms for TAM resistance are probably multifactorial and remain largely unknown. Considering that breast cancer is a very heterogeneous disease and patients respond differently to treatment, the molecular analysis of TAM’s biological activity could provide the necessary framework to understand the complex effects of this drug in target cells. Moreover, this could explain, at least in part, the development of resistance and indicate an optimal therapeutic option. This review highlights the implications of TAM in breast cancer as well as the role of receptors/signal pathways recently suggested to be involved in the development of TAM resistance. G protein—coupled estrogen receptor, Androgen Receptor and Hedgehog signaling pathways are emerging as novel therapeutic targets and prognostic indicators for breast cancer, based on their ability to mediate estrogenic signaling in ERα-positive or-negative breast cancer.

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