A model of estrogen-related gene expression reveals non-linear effects in transcriptional response to tamoxifen.

ABSTRACT:

Background

Estrogen receptors alpha (ER) are implicated in many types of female cancers, and are the common target for anti-cancer therapy using selective estrogen receptor modulators (SERMs, such as tamoxifen). However, cell-type specific and patient-to-patient variability in response to SERMs (from suppression to stimulation of cancer growth), as well as frequent emergence of drug resistance, represents a serious problem. The molecular processes behind mixed effects of SERMs remain poorly understood, and this strongly motivates application of systems approaches. In this work, we aimed to establish a mathematical model of ER-dependent gene expression to explore potential mechanisms underlying the variable actions of SERMs.

Results

We developed an equilibrium model of ER bin

SUBMITTER: Lebedeva G 

PROVIDER: S-EPMC3573949 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature