MED1 may explain the interaction between receptor tyrosine kinases and ERα66 in the complicated network of Tamoxifen resistance.

Abstract:

:According to the American Society of Clinical Oncology or ASCO's clinical practice guidelines, administration of Tamoxifen for hormone receptor positive patients improved outcomes. However, many studies have been conducted in this issue, with the rise of Tamoxifen resistance in recent decades. There are many alternative growth cascades that are activated in Tamoxifen resistant cells. The most common and well characterized components of such a resistant network are receptor tyrosine kinases, or RTKs, which can influence many other cellular processes. The interactions between estrogen dependent and independent pathways further complicate the networking. MED1, as a member of a mediator complex, which is activated by RTK growth pathways, plays role in co-activating ERα66 to transcribe genes and enhance cellular proliferation. Herein, we will discuss MED1, a novel biomarker which can explain how RTKs interact with ERα66 which results in Tamoxifen resistance.

journal_name

Eur J Pharmacol

authors

Mansouri S,Naghavi-Al-Hosseini F,Farahmand L,Majidzadeh-A K

doi

10.1016/j.ejphar.2017.03.026

subject

Has Abstract

pub_date

2017-06-05 00:00:00

pages

78-81

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(17)30196-6

journal_volume

804

pub_type

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