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Cancers
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Pathway in Breast Cancer
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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: closed (31 May 2024) | Viewed by 2989

Special Issue Editor

Dr. Julia Beretov

E-Mail Website
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 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
  • genetic alterations
  • signaling pathways
  • immune system interactions
  • targeted therapies
  • immunotherapies

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Published Papers (2 papers)

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Research

14 pages, 434 KiB  
Article
Somatic Mutations in KEAP1-NRF2 Complex in Breast Cancer
by Micaela Almeida, Catarina L. Ferreira, Rosa Maria Tomé, José Fonseca-Moutinho, António Polónia, Ana Cristina Ramalhinho and Luiza Breitenfeld
Cancers 2024, 16(13), 2411; https://doi.org/10.3390/cancers16132411 - 29 Jun 2024
Viewed by 1345
Abstract
Breast cancer remains the leading cause of cancer deaths for women. Long-term estrogen exposure is considered carcinogenic due to semiquinone production and to compromised detoxification. Metabolic regulator polymorphisms, such as KEAP1 (rs1048290) and NRF2 (rs35652124, rs6721961, rs6706649), can be valuable in understanding the [...] Read more.
Breast cancer remains the leading cause of cancer deaths for women. Long-term estrogen exposure is considered carcinogenic due to semiquinone production and to compromised detoxification. Metabolic regulator polymorphisms, such as KEAP1 (rs1048290) and NRF2 (rs35652124, rs6721961, rs6706649), can be valuable in understanding the individual cytoprotection profile. Thus, we aim to genotype these polymorphisms in blood, tumours and surrounding tissue, to identify somatic mutations and correlate it to prognoses. A total of 23 controls and 69 women with histological confirmed breast cancer were recruited, and DNA from blood/surrounding/tumour tissue was genotyped. Genotyping and clinicopathological data were correlated. We verified that rs35652124 presents different genotype distribution between the blood/surrounding tissue (p-value = 0.023) and tumour/surrounding tissues (p-value = 0.041). Apart from rs35652124 and considering the histological grade, the other four polymorphisms have different distributions among different tissues. There is a tendency towards the loss of heterozygosity in the surrounding tissue when compared to blood and tumour tissues, and higher genotype variability in histologic grade 2. These somatic mutations and different distribution patterns may indicate a heterogeneous and active microenvironment, influencing breast cancer outcome. Additionally, it would be pertinent to evaluate the predictive value of the histologic grade 2 considering somatic mutation profiles and distributions. Full article
(This article belongs to the Special Issue Pathway in Breast Cancer)
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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 2 | Viewed by 1280
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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