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Biomolecules
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Molecular Targets for Breast Cancer Therapy, 2nd Edition
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Molecular Targets for Breast Cancer Therapy, 2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 1044

Special Issue Editor

Dr. Hamidreza Montazeri Aliabadi

E-Mail Website
Guest Editor
Department of Biomedical and Pharmaceutical Sciences, Chapman University School of Pharmacy, Harry and Diane Rinker Health Science Campus, Irvine, CA 92618, USA
Interests: pharmaceutics; targeted delivery; RNA interference; cancer biology; signaling pathways
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following a very successful first edition, we are pleased to announce the launch of the second edition of this Special Issue, entitled “Molecular Targets for Breast Cancer Therapy, 2nd Edition”.

After the cytotoxic chemotherapy era, marked by severe toxicities and multi-drug resistance, “molecularly targeted drugs” have brought new hope in the battle against cancer. However, despite the occasional introduction of new drugs, resistance seems to be inevitable. A sub-population of the tumor cells often fails to respond favorably to the initial treatment (likely due to tumor cell heterogeneity causing intrinsic resistance). This “Darwinian clone selection” is documented in different types of cancer in response to a variety of molecularly targeted drugs. On the other hand, initially responsive cells become resistant shortly after repeated doses (acquired resistance), which, in addition to point mutations, could be due to the plasticity of cancer cells that have access to a variety of signaling pathways that can compensate for the targeted protein. Therefore, the identification of new targets is crucial to overcoming these obstacles. This Special Issue focuses on breast cancer and sheds light on the most recent efforts in the identification of novel molecular targets or the newly discovered crosstalk among the established signaling pathways. Our goal is to create a platform to present information about the molecular mechanism(s) involved in proliferation, survival, and/or resistance in breast cancer cells that can lead to new treatment strategies.

Dr. Hamidreza Montazeri Aliabadi
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.

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. Biomolecules is an international peer-reviewed open access monthly 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 2700 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
  • molecular targets
  • signaling pathways
  • proliferation
  • survival
  • resistance
  • crosstalk

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Published Papers (1 paper)

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Research

18 pages, 3873 KiB  
Article
The Immunohistochemical Prognostic Value of Nuclear and Cytoplasmic Silent Information Regulator 1 Protein Expression in Saudi Patients with Breast Cancer
by Bayan Alharbi, Alia Aldahlawi, Mourad Assidi, Fatemah Basingab, Kawther Zaher, Jehan Alrahimi, Sara Mokhtar, Jaudah Al-Maghrabi, Abdelbaset Buhmeida and Kaltoom Al-Sakkaf
Biomolecules 2025, 15(1), 50; https://doi.org/10.3390/biom15010050 - 2 Jan 2025
Viewed by 672
Abstract
Background: The mammalian NAD-dependent deacetylase sirtuin-1 family (named also silent information regulator or SIRT family, where NAD stands for “nicotinamide adenine dinucleotide” (NAD)) appears to have a dual role in several human cancers by modulating cell proliferation and death. This study examines how [...] Read more.
Background: The mammalian NAD-dependent deacetylase sirtuin-1 family (named also silent information regulator or SIRT family, where NAD stands for “nicotinamide adenine dinucleotide” (NAD)) appears to have a dual role in several human cancers by modulating cell proliferation and death. This study examines how SIRT1 protein levels correlate with clinicopathological characteristics and survival outcomes in patients with breast cancer. Methods: A total of 407 BC formalin-fixed paraffin-embedded (FFPE) samples were collected from King Abdulaziz University Hospital, Saudi Arabia. SIRT1 was stained on tissue microarray slides using automated immunohistochemistry. Results: All BC subtypes expressed more nuclear SIRT1 proteins than their cytoplasm counterparts. In luminal A, luminal B, and TNBC, nuclear and cytoplasmic SIRT1 were highly associated (p < 0.001). Kaplan–Meier analysis showed reduced disease-specific survival (DSS) in H2BC with high SIRT1 nuclear expression (p = 0.001, log-rank). Moreover, the cytoplasmic expression of SIRT1 in HER2-positive BC was associated with a larger tumor size (p = 0.036) and lymph node metastasis (p = 0.045). Nuclear SIRT1 expression was also positively associated with lymph node metastasis (LNM) (p = 0.048). As low-grade tumors had a higher frequency of SIRT1 protein expression than other groups, SIRT1 expression was associated with a favorable prognosis in patients with luminal A BC (p < 0.001). Conclusions: SIRT1 expression seems to be involved in different molecular pathways either suppressing or promoting tumor growth depending on the subtype of BC. These molecular functions require further investigations and validation on larger BC cohorts. Full article
(This article belongs to the Special Issue Molecular Targets for Breast Cancer Therapy, 2nd Edition)
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