scholarly journals Endocrine Resistance in Breast Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-27 ◽  
Author(s):  
J. M. Dixon
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Disease Resistance ◽  
Estrogen Receptor Alpha ◽  
Endocrine Resistance ◽  
Breast Cancers ◽  
Resistance To Therapy ◽  
Receptor Alpha ◽  
Number Of Patients

Around 70% of all breast cancers are estrogen receptor alpha positive and hence their development is highly dependent on estradiol. While the invention of endocrine therapies has revolusioned the treatment of the disease, resistance to therapy eventually occurs in a large number of patients. This paper seeks to illustrate and discuss the complexity and heterogeneity of the mechanisms which underlie resistance and the approaches proposed to combat them. It will also focus on the use and development of methods for predicting which patients are likely to develop resistance.

scholarly journals RASSF1A-Mediated Suppression of Estrogen Receptor Alpha (ERα)-Driven Breast Cancer Cell Growth Depends on the Hippo-Kinases LATS1 and 2

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2868
Author(s):  
Sven Roßwag ◽  
Jonathan P. Sleeman ◽  
Sonja Thaler
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Tumor Suppressor ◽  
Estrogen Receptor Alpha ◽  
Molecular Mechanisms ◽  
Hippo Pathway ◽  
Hippo Signaling ◽  
Breast Cancers ◽  
Receptor Alpha ◽  
And Function

Around 70% of breast cancers express the estrogen receptor alpha (ERα). This receptor is of central importance for breast cancer development and estrogen-dependent tumor growth. However, the molecular mechanisms that are responsible for the control of ERα expression and function in the context of breast carcinogenesis are complex and not fully understood. In previous work, we have demonstrated that the tumor suppressor RASSF1A suppresses estrogen-dependent growth of breast cancer cells through a complex network that keeps ERα expression and function under control. We observed that RASSF1A mediates the suppression of ERα expression through modulation of the Hippo effector Yes-associated protein 1 (YAP1) activity. Here we report that RASSF1A-mediated alteration of YAP1 depends on the Hippo-kinases LATS1 and LATS2. Based on these results, we conclude that inactivation of RASSF1A causes changes in the function of the Hippo signaling pathway and altered activation of YAP1, and as a consequence, increased expression and function of ERα. Thus, the inactivation of RASSF1A might constitute a fundamental event that supports the initiation of ERα-dependent breast cancer. Furthermore, our results support the notion that the Hippo pathway is important for the suppression of luminal breast cancers, and that the tumor-suppressor function of RASSF1A depends on LATS1 and LATS2.

scholarly journals Intratumoural inflammation and endocrine resistance in breast cancer

2014 ◽  
Vol 22 (1) ◽  
pp. R51-R67 ◽  
Author(s):  
Jill I Murray ◽  
Nathan R West ◽  
Leigh C Murphy ◽  
Peter H Watson
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Endocrine Therapy ◽  
Therapeutic Target ◽  
Estrogen Receptor Alpha ◽  
Endocrine Resistance ◽  
Receptor Alpha ◽  
The Relationship

It is becoming clear that inflammation-associated mechanisms can affect progression of breast cancer and modulate responses to treatment. Estrogen receptor alpha (ERα (ESR1)) is the principal biomarker and therapeutic target for endocrine therapies in breast cancer. Over 70% of patients are ESR1-positive at diagnosis and are candidates for endocrine therapy. However, ESR1-positive tumours can become resistant to endocrine therapy. Multiple mechanisms of endocrine resistance have been proposed, including suppression of ESR1. This review discusses the relationship between intratumoural inflammation and endocrine resistance with a particular focus on inflammation-mediated suppression of ESR1.

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