Open Research Newcastle
Browse

The potential role of miRNAs in therapy of breast and ovarian cancers associated with BRCA1 mutation

Download (346.21 kB)
journal contribution
posted on 2025-05-11, 13:21 authored by Agnieszka Strumidło, Sylwia Skiba, Rodney ScottRodney Scott, Jan Lubiński
Germline variants within BRCA1 or BRCA2 genes account for approximately 25% of familial aggregations of breast-ovarian cancers. Low or no expression of BRCA1 in breast and ovarian cancers is associated with a good clinical response to treatment with platinum therapies and PARP1 inhibitors. Recent studies demonstrated that microRNAs - small non-coding RNAs, involved in the control of gene expression, can decrease BRCA1 expression by targeting the 3'UTR region of the gene. This article reviews reported relationships between various miRNAs, such as miRNA-9, miRNA-146a, miRNA-182 miRNA-218, miRNA-638 and the response to cytostatic drugs, mainly to platins and PARP1 inhbitors, for the treatment of breast and ovarian cancer associated with BRCA1 mutations.

History

Journal title

Hereditary Cancer in Clinical Practice

Volume

15

Article number

15

Publisher

BioMed Central

Language

  • en, English

College/Research Centre

Faculty of Health and Medicine

School

School of Biomedical Sciences and Pharmacy

Rights statement

© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Usage metrics

    Publications

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC