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Hurtado Group

Our group is interested in investigating the mechanisms of hormone resistance and breast cancer.

Breast cancer is the most common cancer in women of developed countries, and at least two thirds of breast tumors are positive for the expression of Estrogen Receptor alpha (ER). ER is a transcription factor that binds to estrogen and activates transcription in mammary cells. ER drives proliferation of this breast cancer type and current treatments pursuit targeting its activity.

Hormone resistance

Tamoxifen and Aromatase Inhibitors (AI) are the most used anti-estrogen drugs for adjuvant therapy in breast cancer patients, but patients frequently fail to respond to those treatments. To the present date, several works have described distinct factors that influence the function of ER and ultimately dictate the efficacy of the anti-estrogen therapies. The presence of these cooperative factors raises a new level of complexity for ER transcriptional regulation and endocrine response.

Our group is interested in investigating the mechanisms of hormone-resistance. In particular, the research of our group is structured in two comprehensive and often overlapping areas.

How anti-ER drugs performs

One area entails chemical systems approaches to: (1) functionally understand how anti-ER drugs perform their repressive effects and (2) identify novel mechanism by which hormone-resistant cells overcome ER inhibition.

Specifically, we are employing a combination of targeted proteomics, drug screenings, highthroutput sequencing of chromatin and sequencing of de novo transcripts (by means of GRO-seq) in the projects related with this part of my research.

How drugs influence tumor growth

The second area involves in vivo approaches from patient derived xenographs of breast cancer tumors. With this research we aim to test how drugs identified in our drug screening influence the tumor growth of breast cancer tumors. Moreover, we will validate which compounds might be used as alternative therapies for patients with poor response to current anti-ER therapies using hormone-resistant breast cancer in vivo models.

Published Dec. 6, 2016 2:27 PM - Last modified Dec. 28, 2016 2:17 PM