Estrogen for the Treatment and Prevention of Breast Cancer

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 1682

Special Issue Editor

*
E-Mail Website
Guest Editor
Department of Breast Medical Oncology, MD Anderson Cancer Center, University of Texas, 1515 Holcombe Blvd., Unit 1354, Houston, TX 77030, USA
Interests: breast cancer; estrogen
* V. Craig Jordan, CMG, OBE, Ph.D, DSc, FMedSci

Special Issue Information

Dear Colleagues,

Estrogen exerts a significant influence on the development of breast cancer, primarily by binding to cellular estrogen receptors (ERs). Breast cancer can be categorized into two subtypes on the basis of the presence of ERs: ER-positive and ER-negative. In hormone receptor-positive (HR+) breast cancer, ERs serve as the principal transcription factors driving oncogenesis and play dual roles as both predictor and target of antiestrogen therapy response. Currently, available anti-estrogen therapies and HER-2 targeted therapies exhibit limited efficacy in the treatment of triple-negative breast cancer (TNBC). In the case of ERα-negative breast cancer, a combination of chemotherapy and molecular-targeted drugs is commonly employed, with potential effectiveness anticipated through immune checkpoint inhibitors. Additionally, hormone therapies may prove efficacious in instances where other hormone receptors such as androgen and glucocorticoid receptors are expressed in ERα-negative breast cancer. The involvement of germline BRCA1/2 mutations in both ER-negative and ER-positive breast cancer pathogenesis is well established; however, numerous unknown factors persist regarding the pathological characteristics, genetic background, and immunological features associated with ERα-negative breast cancer.

Prof. Dr. Virgil Craig Jordan
Guest Editor

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Keywords

  • estrogen
  • estrogen receptor alpha
  • ERα
  • breast cancer

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Published Papers (1 paper)

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Review

18 pages, 4158 KiB  
Review
DREAM On, DREAM Off: A Review of the Estrogen Paradox in Luminal A Breast Cancers
by Judith C. Hugh, Lacey S. J. Haddon and John Maringa Githaka
Biomedicines 2024, 12(6), 1300; https://doi.org/10.3390/biomedicines12061300 - 12 Jun 2024
Cited by 1 | Viewed by 1381
Abstract
It is generally assumed that all estrogen-receptor-positive (ER+) breast cancers proliferate in response to estrogen and, therefore, examples of the estrogen-induced regression of ER+ cancers are paradoxical. This review re-examines the estrogen regression paradox for the Luminal A subtype of ER+ breast cancers. [...] Read more.
It is generally assumed that all estrogen-receptor-positive (ER+) breast cancers proliferate in response to estrogen and, therefore, examples of the estrogen-induced regression of ER+ cancers are paradoxical. This review re-examines the estrogen regression paradox for the Luminal A subtype of ER+ breast cancers. The proliferative response to estrogen is shown to depend on the level of ER. Mechanistically, a window of opportunity study of pre-operative estradiol suggested that with higher levels of ER, estradiol could activate the DREAM-MMB (Dimerization partner, Retinoblastoma-like proteins, E2F4, and MuvB–MYB-MuvB) pathway to decrease proliferation. The response of breast epithelium and the incidence of breast cancers during hormonal variations that occur during the menstrual cycle and at the menopausal transition, respectively, suggest that a single hormone, either estrogen, progesterone or androgen, could activate the DREAM pathway, leading to reversible cell cycle arrest. Conversely, the presence of two hormones could switch the DREAM-MMB complex to a pro-proliferative pathway. Using publicly available data, we examine the gene expression changes after aromatase inhibitors and ICI 182,780 to provide support for the hypothesis. This review suggests that it might be possible to integrate all current hormonal therapies for Luminal A tumors within a single theoretical schema. Full article
(This article belongs to the Special Issue Estrogen for the Treatment and Prevention of Breast Cancer)
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