Pathway in Breast Cancer

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 950

Special Issue Editor


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Guest Editor
Cancer Care Centre, St George Hospital, Kogarah, NSW 2217, Australia
Interests: epithelial mesenchymal transition; cancer stem cell; triple-negative breast cancer

Special Issue Information

Dear Colleagues,

The Special Issue "Pathways in Breast Cancer" focuses on the complex molecular pathways involved in breast cancer development and progression. This collection of articles provides an overview of the current understanding of the diverse mechanisms underlying breast cancer, including genetic alterations, signaling pathways, and immune system interactions. It highlights recent advances in the diagnosis and treatment of breast cancer, such as targeted therapies and immunotherapies that specifically target these pathways. Additionally, the Special Issue emphasizes the importance of precision medicine and personalized therapy in breast cancer management, which involves tailoring treatment to each individual's unique genetic and molecular characteristics. Overall, this Special Issue sheds light on the intricacies of breast cancer pathogenesis and provides insights for further research and the development of effective therapies. We look forward to receiving your contributions.

Dr. Julia Beretov
Guest Editor

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.

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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
  • genetic alterations
  • signaling pathways
  • immune system interactions
  • targeted therapies
  • immunotherapies

Published Papers (1 paper)

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Research

19 pages, 7896 KiB  
Article
An Increase in HSF1 Expression Directs Human Mammary Epithelial Cells toward a Mesenchymal Phenotype
by Natalia Vydra, Agnieszka Toma-Jonik, Patryk Janus, Katarzyna Mrowiec, Tomasz Stokowy, Magdalena Głowala-Kosińska, Damian Robert Sojka, Magdalena Olbryt and Wiesława Widłak
Cancers 2023, 15(20), 4965; https://doi.org/10.3390/cancers15204965 - 12 Oct 2023
Cited by 1 | Viewed by 784
Abstract
HSF1 is a well-known heat shock protein expression regulator in response to stress. It also regulates processes important for growth, development or tumorigenesis. We studied the HSF1 influence on the phenotype of non-tumorigenic human mammary epithelial (MCF10A and MCF12A) and several triple-negative breast [...] Read more.
HSF1 is a well-known heat shock protein expression regulator in response to stress. It also regulates processes important for growth, development or tumorigenesis. We studied the HSF1 influence on the phenotype of non-tumorigenic human mammary epithelial (MCF10A and MCF12A) and several triple-negative breast cancer cell lines. MCF10A and MCF12A differ in terms of HSF1 levels, morphology, growth in Matrigel, expression of epithelial (CDH1) and mesenchymal (VIM) markers (MCF10A are epithelial cells; MCF12A resemble mesenchymal cells). HSF1 down-regulation led to a reduced proliferation rate and spheroid formation in Matrigel by MCF10A cells. However, it did not affect MCF12A proliferation but led to CDH1 up-regulation and the formation of better organized spheroids. HSF1 overexpression in MCF10A resulted in reduced CDH1 and increased VIM expression and the acquisition of elongated fibroblast-like morphology. The above-mentioned results suggest that elevated levels of HSF1 may direct mammary epithelial cells toward a mesenchymal phenotype, while a lowering of HSF1 could reverse the mesenchymal phenotype to an epithelial one. Therefore, HSF1 may be involved in the remodeling of mammary gland architecture over the female lifetime. Moreover, HSF1 levels positively correlated with the invasive phenotype of triple-negative breast cancer cells, and their growth was inhibited by the HSF1 inhibitor DTHIB. Full article
(This article belongs to the Special Issue Pathway in Breast Cancer)
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