The Estrogen Receptor and Its Role in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Biomarkers".

Deadline for manuscript submissions: 15 September 2024 | Viewed by 1433

Special Issue Editors


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Guest Editor
Massachusetts General Hospital, Department of Medicine, Division of Hematology and Oncology, Boston, MA, USA
Interests: breast cancer; cancer genetics; novel and targeted therapies for breast cancer treatment

E-Mail Website
Guest Editor
Department of Pharmacology & Toxicology and Pathology, Medical College of Wisconsin, Milwaukee, WI, USA
Interests: targeted therapies in breast cancer; anti-cancer therapeutics

Special Issue Information

Dear Colleagues,  

Estrogen-directed therapy has been the mainstay of treatment of both early-stage and metastatic breast cancer for decades. Recent genomic and molecular advances have provided new insights into the mechanisms of resistance to these commonly utilized drugs, and a variety of new agents and strategies are under active preclinical and clinical development. Expanding our understanding of the role the estrogen receptor plays in breast (and other) cancers, continuing to explore the biological basis of resistance to hormonal therapy, and developing new strategies for clinical deployment remain important priorities for the cancer research community.  

We are pleased to invite you to participate in this Special Issue, focused on the estrogen receptor and its role in cancer progression and drug resistance. This issue will be an opportunity to present articles both summarizing the tremendous progress in this area to date as well as presenting new and exciting advances in this field. We welcome articles for consideration related to basic science, translational research, and clinical studies in breast cancer (and other relevant tumor types). 

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: estrogen-related signaling in breast cancer (and other malignancies), novel insights into molecular and genomic mechanisms of resistance to hormonal therapy, new approaches to target antiestrogen resistance in breast cancer (and other malignancies) in the laboratory and clinic, and novel methodologies to image or track hormonal sensitivity.  

We look forward to receiving your contributions.

Dr. Seth A. Wander
Prof. Dr. Todd W. Miller
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • breast cancer
  • estrogen receptor
  • hormone signaling
  • therapy resistance
  • novel hormonal agents
  • antiestrogen therapy
  • selective estrogen receptor degraders
  • ESR1 mutation
  • genomic sequencing
  • precision oncology

Published Papers (1 paper)

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Research

16 pages, 2979 KiB  
Article
TRIM33 Is a Co-Regulator of Estrogen Receptor Alpha
by Bianca A. Romo, Barbara Karakyriakou, Lauren Cressey, Brooke L. Brauer, Huijuan Yang, Alexa Warren, Anneka L. Johnson, Arminja N. Kettenbach and Todd W. Miller
Cancers 2024, 16(5), 845; https://doi.org/10.3390/cancers16050845 - 20 Feb 2024
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Abstract
Estrogen receptor alpha (ER)-positive breast cancer is responsible for over 60% of breast cancer cases in the U.S. Among patients diagnosed with early-stage ER+ disease, 1/3 will experience recurrence despite treatment with adjuvant endocrine therapy. ER is a nuclear hormone receptor responsible for [...] Read more.
Estrogen receptor alpha (ER)-positive breast cancer is responsible for over 60% of breast cancer cases in the U.S. Among patients diagnosed with early-stage ER+ disease, 1/3 will experience recurrence despite treatment with adjuvant endocrine therapy. ER is a nuclear hormone receptor responsible for estrogen-driven tumor growth. ER transcriptional activity is modulated by interactions with coregulators. Dysregulation of the levels of these coregulators is involved in the development of endocrine resistance. To identify ER interactors that modulate transcriptional activity in breast cancer, we utilized biotin ligase proximity profiling of ER interactomes. Mass spectrometry analysis revealed tripartite motif containing 33 (TRIM33) as an estrogen-dependent interactor of ER. shRNA knockdown showed that TRIM33 promoted ER transcriptional activity and estrogen-induced cell growth. Despite its known role as an E3 ubiquitin ligase, TRIM33 increased the stability of endogenous ER in breast cancer cells. TRIM33 offers a novel target for inhibiting estrogen-induced cancer cell growth, particularly in cases of endocrine resistance driven by ER (ESR1) gene amplification or overexpression. Full article
(This article belongs to the Special Issue The Estrogen Receptor and Its Role in Cancer)
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