Signaling Pathways of Breast Cancer

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

Deadline for manuscript submissions: 30 August 2024 | Viewed by 3018

Special Issue Editors


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Guest Editor
Translational Oncobiology Lab., Instituto de Medicina Molecular – João Lobo Antunes, Faculdade de Medicina de Lisboa, Lisbon, Portugal
Interests: breast cancer; bone metastases; drug resistance; RANKL-RANK pathway

E-Mail Website
Guest Editor
Translational Oncobiology Lab., Instituto de Medicina Molecular – João Lobo Antunes, Faculdade de Medicina de Lisboa, Lisbon, Portugal
Interests: breast cancer; drug resistance; PLC family

Special Issue Information

Dear Colleagues,

Breast cancer is the most common malignancy worldwide. Its heterogeneous etiology, histology and molecular profile are translated into distinct intrinsic sub-types, associated with different types of biology and prognoses.

Major breakthroughs in breast cancer treatment were fueled by targeted therapies, with the most striking being the endocrine and anti-HER2 therapies and, more recently, the CDK4/6 inhibitors. However, intrinsic and acquired resistance are almost inevitable.

By increasing our knowledge about the signaling pathways involved in major breast cancer hallmarks, about their crosstalk and target ability, and about their role in response to standard of care or new therapies, we may envisage an improvement in the prognosis of breast cancer patients.

This Special Issue of Cancers intends to gather new breakthrough research, focusing on the multiple aspects and relevance of signaling pathways in breast cancer.

Prof. Dr. Sandra Casimiro
Dr. Marta Martins
Guest Editors

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.

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
  • signal transduction
  • targeted therapies
  • resistance to therapy
  • novel molecular mechanisms

Published Papers (2 papers)

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Review

21 pages, 941 KiB  
Review
NORAD-Regulated Signaling Pathways in Breast Cancer Progression
by Ana Maria Capela, Carlota Tavares-Marcos, Hugo F. Estima-Arede, Sandrina Nóbrega-Pereira and Bruno Bernardes de Jesus
Cancers 2024, 16(3), 636; https://doi.org/10.3390/cancers16030636 - 01 Feb 2024
Viewed by 955
Abstract
Long non-coding RNA activated by DNA damage (NORAD) has recently been associated with pathologic mechanisms underlying cancer progression. Due to NORAD’s extended range of interacting partners, there has been contradictory data on its oncogenic or tumor suppressor roles in BC. [...] Read more.
Long non-coding RNA activated by DNA damage (NORAD) has recently been associated with pathologic mechanisms underlying cancer progression. Due to NORAD’s extended range of interacting partners, there has been contradictory data on its oncogenic or tumor suppressor roles in BC. This review will summarize the function of NORAD in different BC subtypes and how NORAD impacts crucial signaling pathways in this pathology. Through the preferential binding to pumilio (PUM) proteins PUM1 and PUM2, NORAD has been shown to be involved in the control of cell cycle, angiogenesis, mitosis, DNA replication and transcription and protein translation. More recently, NORAD has been associated with PUM-independent roles, accomplished by interacting with other ncRNAs, mRNAs and proteins. The intricate network of NORAD-mediated signaling pathways may provide insights into the potential design of novel unexplored strategies to overcome chemotherapy resistance in BC treatment. Full article
(This article belongs to the Special Issue Signaling Pathways of Breast Cancer)
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36 pages, 1227 KiB  
Review
The Evolving Pathways of the Efficacy of and Resistance to CDK4/6 Inhibitors in Breast Cancer
by Inês Gomes, Catarina Abreu, Luis Costa and Sandra Casimiro
Cancers 2023, 15(19), 4835; https://doi.org/10.3390/cancers15194835 - 02 Oct 2023
Cited by 2 | Viewed by 1810
Abstract
The approval of cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6i) in combination with endocrine therapy (ET) has remarkably improved the survival outcomes of patients with advanced hormone receptor-positive (HR+) breast cancer (BC), becoming the new standard of care treatment in these patients. Despite [...] Read more.
The approval of cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6i) in combination with endocrine therapy (ET) has remarkably improved the survival outcomes of patients with advanced hormone receptor-positive (HR+) breast cancer (BC), becoming the new standard of care treatment in these patients. Despite the efficacy of this therapeutic combination, intrinsic and acquired resistance inevitably occurs and represents a major clinical challenge. Several mechanisms associated with resistance to CDK4/6i have been identified, including both cell cycle-related and cell cycle-nonspecific mechanisms. This review discusses new insights underlying the mechanisms of action of CDK4/6i, which are more far-reaching than initially thought, and the currently available evidence of the mechanisms of resistance to CDK4/6i in BC. Finally, it highlights possible treatment strategies to improve CDK4/6i efficacy, summarizing the most relevant clinical data on novel combination therapies involving CDK4/6i. Full article
(This article belongs to the Special Issue Signaling Pathways of Breast Cancer)
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