Oestrogen receptor positive breast cancer and its embedded mechanism: breast cancer resistance to conventional drugs and related therapies, a review

Sep 21, 2026

Uploaded by Liam

Oestrogen receptor positive breast cancer is driven by long-term oestrogen exposure and is increasingly prevalent worldwide, with incidence figures highlighted by the Global Cancer Observatory. The review focuses on why conventional therapies fail, emphasizing drug resistance shaped by genetic differences, epigenetic remodeling, and miRNA alterations. It links resistance in breast cancer cell lines to changes such as mutational events, histone acetylation, and CTCF hypermethylation, and outlines conventional and novel counter-strategies.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages17

Reading Time43 min

AccessFree to download

Introduction

Oestrogen receptor positive breast cancer incidence and risk factors

Molecular classification by ER status and subtypes

Mechanisms of drug resistance and therapeutic targets

Therapeutic approaches to overcome resistance

Selective oestrogen receptor modulators and degraders

Novel combination therapies and emerging inhibitors

Cite this article: Yadav M, Vaishkiar I, Sharma A, Shukla A, Mohan A, Girdhar M, Kumar A, Malik T, Mohan A. 2024 Oestrogen receptor positive breast cancer and its embedded mechanism: breast cancer resistance to conventional drugs and related therapies, a review. Open Biol. 14: 230272. [https://doi.org/10.1098/rsob.230272](https://doi.org/10.1098/rsob.230272) [Received: 10 August 2023](Received: 10 August 2023) [Accepted: 14 March 2024](Accepted: 14 March 2024) Subject Areas: cellular biology, developmental biology, genomics Keywords: breast cancer, drug-resistance, therapeutic approaches, miRNA alteration, epigenetic alterations, novel target Authors for correspondence: Tabarak Malik e-mails: [tabarak.malik@ju.edu.et](tabarak.malik@ju.edu.et); [malikitrc@gmail.com](malikitrc@gmail.com) Anand Mohan e-mail: [anandmohan77@gmail.com](anandmohan77@gmail.com) Oestrogen receptor positive breast cancer and its embedded mechanism: breast cancer resistance to conventional drugs and related therapies, a review Manu Yadav1, Ishita Vaishkiar2, Ananya Sharma3, Akanksha Shukla4, Aradhana Mohan6, Madhuri Girdhar5, Anil Kumar7, Tabarak Malik8 and Anand Mohan4 1Division of Genetics, ICAR-Indian Agricultural Research Institute, Pusa, New Delhi, India 2Amity Institute of Biotechnology (AIB) University, Amity University Noida, Noida, India 3Department: Botany and Microbiology, Hemwati Nandan Bahuguna Garhwal University, Srinagar, India 4School of Bioengineering and Biosciences, and 5Division of Research and Development, Lovely Professional University, Phagwara, Punjab, India 6Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA 7Gene Regulation Laboratory, National Institute of Immunology, New Delhi, India 8Department of Biomedical Sciences, Institute of Health, Jimma University, Jimma, Oromia 378, Ethiopia AK, 0000-0002-8785-6033; TM, 0000-0002-8332-7927; AM, 0000-0002-8314-0425 Traditional medication and alternative therapies have long been used to treat breast cancer. One of the main problems with current treatments is that there is an increase in drug resistance in the cancer cells owing to genetic differences such as mutational changes, epigenetic changes and miRNA (microRNA) alterations such as miR-1246, miR-298, miR-27band miR-33a, along with epigenetic modifications, such as Histone3 acetylation and CCCTC-Binding Factor (CTCF) hypermethylation for drug resistance in breast cancer cell lines. Certain forms of conventional drug resistance have been linked to genetic changes in genes such as ABCB1, AKT, S100A8/A9, TAGLN2 and NPM. This review aims to explore the current approaches to counter breast cancer, the action mechanism, along with novel therapeutic methods endowing potential drug resistance. The investigation of novel therapeutic approaches shedslight on the phenomenon of drug resistance including genetic variations that impact distinct forms of oestrogen receptor (ER) cancer, genetic changes, epigenetics-reported resistance and their identification in patients. Long-term effective therapy for breast cancer includes selective oestrogen receptor modulators, selective oestrogen receptor degraders and genetic variations, such as mutations in nuclear genes, epigenetic modificationsand miRNA alterations in target proteins. Novel research addressing combinational therapies including maytansine, photodynamic therapy, guajadiol, talazoparib, COX2 inhibitors and miRNA 1246 inhibitors have been developed to improve patient survival rates. 1. Introduction Cancer incidence has increased over the past years. According to the Global Cancer Observatory (GCO), in 2020, overall 19.3 million cases of cancer were reported worldwide, which was an approximately 6.1% increase in the total cancer cases in comparison to 2018 data. It is evident in the 2020 report of GCO, where breast cancer (BC) incidences show a significant percentage of 11.7, the highest among all cancers (figure 1) . Th

FAQs

What main problem does the review identify in current breast cancer treatments?

A key problem is the development of drug resistance in cancer cells driven by genetic differences, epigenetic changes, and miRNA alterations.

Which biological mechanisms are highlighted as contributors to drug resistance in ER+ breast cancer?

The review highlights mutational changes and resistance-associated genes, along with epigenetic modifications like histone acetylation and CTCF hypermethylation, plus miRNA alterations such as miR-1246 and miR-298.

What therapeutic directions does the review discuss to counter drug resistance?

It discusses approaches including selective oestrogen receptor modulators, selective oestrogen receptor degraders, and novel combination therapies such as maytansine, photodynamic therapy, talazoparib, COX2 inhibitors, and miRNA 1246 inhibitors.

Sep 21, 2026

Uploaded by Liam