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Molecular Research in Triple-Negative Breast Cancer
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Molecular Research in Triple-Negative Breast Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 September 2024 | Viewed by 8811

Special Issue Editor

Dr. Yong-Moon Lee

E-Mail Website
Guest Editor
College of Medicine, Dankook University, Cheonan 31116, Republic of Korea
Interests: triple negative breast cancer; molecular pathology; gene alteration; proteomics; deep neuarl network

Special Issue Information

Dear Colleagues,

Triple-negative breast cancer (TNBC) does not have receptors for estrogen, progesterone, or the HER2 protein, making it more aggressive and challenging to treat than other types of breast cancer. Moreover, TNBC has a higher rate of lymph node metastasis than other types of breast cancer, ranging from 30–50% in patients with early-stage cancer to 60–80% in patients with advanced-stage cancer. Therefore, by understanding lymph node metastasis and developing a unique prediction model of nodal metastasis in TNBC, combining molecular information with clinicopathological information will help patients make treatment decisions. The main purpose of this Special Issue is to provide an open-source sharing of significant works in the field of triple-negative breast cancer.

We invite authors to submit original research and review articles. Topics of this Special Issue include, but are not limited to:

  • Tumor microenvironment;
  • Molecular pathways of triple-negative breast cancer;
  • Lymph node metastasis;
  • Prediction model using deep learning;
  • Pathological and molecular diagnosis of triple-negative breast cancer;
  • Potential treatment of triple-negative breast cancer.

Dr. Yong-Moon Lee
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • triple negative breast cancer
  • lymph node metastasis
  • PMP22
  • prediction model using deep learning

Published Papers (7 papers)

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Research

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17 pages, 3434 KiB  
Article
Prognostic Markers in Tyrosine Kinases Specific to Basal-like 2 Subtype of Triple-Negative Breast Cancer
by Praopim Limsakul, Pongsakorn Choochuen, Thawirasm Jungrungrueang and Krit Charupanit
Int. J. Mol. Sci. 2024, 25(3), 1405; https://doi.org/10.3390/ijms25031405 - 24 Jan 2024
Cited by 1 | Viewed by 1402
Abstract
Triple-negative breast cancer (TNBC), a heterogeneous and therapeutically challenging subtype, comprises over 50% of patients categorized into basal-like 1 (BL1) and basal-like 2 (BL2) intrinsic molecular subtypes. Despite their shared basal-like classification, BL2 is associated with a poor response to neoadjuvant chemotherapy and [...] Read more.
Triple-negative breast cancer (TNBC), a heterogeneous and therapeutically challenging subtype, comprises over 50% of patients categorized into basal-like 1 (BL1) and basal-like 2 (BL2) intrinsic molecular subtypes. Despite their shared basal-like classification, BL2 is associated with a poor response to neoadjuvant chemotherapy and reduced relapse-free survival compared to BL1. Here, the study focused on identifying subtype-specific markers for BL2 through transcriptomic analysis of TNBC patients using RNA-seq and clinical integration. Six receptor tyrosine kinase (TK) genes, including EGFR, EPHA4, EPHB2, PDGFRA, PDGFRB, and ROR1, were identified as potential differentiators for BL2. Correlations between TK mRNA expression and TNBC prognosis, particularly EGFR, PDGFRA, and PDGFRB, revealed potential synergistic interactions in pathways related to cell survival and proliferation. Our findings also suggest promising dual markers for predicting disease prognosis. Furthermore, RT-qPCR validation demonstrated that identified BL2-specific TKs were expressed at a higher level in BL2 than in BL1 cell lines, providing insights into unique characteristics. This study advances the understanding of TNBC heterogeneity within the basal-like subtypes, which could lead to novel clinical treatment approaches and the development of targeted therapies. Full article
(This article belongs to the Special Issue Molecular Research in Triple-Negative Breast Cancer)
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17 pages, 7111 KiB  
Article
miR-877-5p as a Potential Link between Triple-Negative Breast Cancer Development and Metabolic Syndrome
by Juana Moro, Agustina Grinpelc, Paula Lucía Farré, Rocío Belén Duca, Ezequiel Lacunza, Karen Daniela Graña, Georgina Daniela Scalise, Guillermo Nicolás Dalton, Cintia Massillo, Flavia Piccioni, Federico Dimase, Emilio Batagelj, Adriana De Siervi and Paola De Luca
Int. J. Mol. Sci. 2023, 24(23), 16758; https://doi.org/10.3390/ijms242316758 - 25 Nov 2023
Cited by 1 | Viewed by 1412
Abstract
Metabolic syndrome (MS) is a risk factor for breast cancer (BC) that increases its aggressiveness and metastasis. The prevalence of MS is higher in triple-negative breast cancer (TNBC), which is the molecular subtype with the worst prognosis. The molecular mechanisms underlying this association [...] Read more.
Metabolic syndrome (MS) is a risk factor for breast cancer (BC) that increases its aggressiveness and metastasis. The prevalence of MS is higher in triple-negative breast cancer (TNBC), which is the molecular subtype with the worst prognosis. The molecular mechanisms underlying this association have not been fully elucidated. MiRNAs are small, non-coding RNAs that regulate gene expression. Aberrant expression of miRNAs in both tissues and fluids are linked to several pathologies. The aim of this work was to identify circulating miRNAs in patients with alterations associated with MS (AAMS) that also impact on BC. Using microarray technology, we detected 23 miRNAs altered in the plasma of women with AAMS that modulate processes linked to cancer. We found that let-7b-5p and miR-28-3p were decreased in plasma from patients with AAMS and also in BC tumors, while miR-877-5p was increased. Interestingly, miR-877-5p expression was associated with lower patient survival, and its expression was higher in PAM50 basal-like BC tumors compared to the other molecular subtypes. Analyses from public databases revealed that miR-877-5p was also increased in plasma from BC patients compared to plasma from healthy donors. We identified IGF2 and TIMP3 as validated target genes of miR-877-5p whose expression was decreased in BC tissue and moreover, was negatively correlated with the levels of this miRNA in the tumors. Finally, a miRNA inhibitor against miR-877-5p diminished viability and tumor growth of the TNBC model 4T1. These results reveal that miR-877-5p inhibition could be a therapeutic option for the treatment of TNBC. Further studies are needed to investigate the role of this miRNA in TNBC progression. Full article
(This article belongs to the Special Issue Molecular Research in Triple-Negative Breast Cancer)
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14 pages, 2009 KiB  
Article
Kinesin Family Member C1 (KIFC1/HSET) Underlies Aggressive Disease in Androgen Receptor-Low and Basal-Like Triple-Negative Breast Cancers
by Nikita Jinna, Yate-Ching Yuan and Padmashree Rida
Int. J. Mol. Sci. 2023, 24(22), 16072; https://doi.org/10.3390/ijms242216072 - 08 Nov 2023
Viewed by 751
Abstract
Quadruple-negative breast cancer (QNBC) lacks traditional actionable targets, including androgen receptor (AR). QNBC disproportionately afflicts and impacts patients of African genetic ancestry. Kinesin family member C1 (KIFC1/HSET), a centrosome clustering protein that prevents cancer cells from undergoing centrosome-amplification-induced apoptosis, has been reported to [...] Read more.
Quadruple-negative breast cancer (QNBC) lacks traditional actionable targets, including androgen receptor (AR). QNBC disproportionately afflicts and impacts patients of African genetic ancestry. Kinesin family member C1 (KIFC1/HSET), a centrosome clustering protein that prevents cancer cells from undergoing centrosome-amplification-induced apoptosis, has been reported to be upregulated in TNBCs and African-American (AA) TNBCs. Herein, we analyzed KIFC1 RNA levels and their associations with clinical features and outcomes among AR-low and AR-high TNBC tumors in three distinct publicly available gene expression datasets and in the breast cancer gene expression database (bc-GenExMiner). KIFC1 levels were significantly higher in AR-low and basal-like TNBCs than in AR-high and non-basal-like TNBCs, irrespective of the stage, grade, tumor size, and lymph node status. KIFC1 levels were also upregulated in AR-low tumors relative to AR-high tumors among Black and premenopausal women with TNBC. High KIFC1 levels conferred significantly shorter overall survival, disease-free survival, and distant metastasis-free survival among AR-low and basal-like TNBC patients in Kaplan–Meier analyses. In conclusion, KIFC1 levels may be upregulated in AR-low tumors and, specifically, in those of African descent, wherein it may promote poor outcomes. KIFC1 may be an actionable cancer-cell-specific target for the AR-low TNBC subpopulation and could aid in alleviating racial disparities in TNBC outcomes. Full article
(This article belongs to the Special Issue Molecular Research in Triple-Negative Breast Cancer)
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18 pages, 1110 KiB  
Article
Untargeted LC-MS/MS Metabolomics Study of HO-AAVPA and VPA on Breast Cancer Cell Lines
by Alan Rubén Estrada-Pérez, Juan Benjamín García-Vázquez, Humberto L. Mendoza-Figueroa, Martha Cecilia Rosales-Hernández, Cynthia Fernández-Pomares and José Correa-Basurto
Int. J. Mol. Sci. 2023, 24(19), 14543; https://doi.org/10.3390/ijms241914543 - 26 Sep 2023
Viewed by 1012
Abstract
Breast cancer (BC) is one of the biggest health problems worldwide, characterized by intricate metabolic and biochemical complexities stemming from pronounced variations across dysregulated molecular pathways. If BC is not diagnosed early, complications may lead to death. Thus, the pursuit of novel therapeutic [...] Read more.
Breast cancer (BC) is one of the biggest health problems worldwide, characterized by intricate metabolic and biochemical complexities stemming from pronounced variations across dysregulated molecular pathways. If BC is not diagnosed early, complications may lead to death. Thus, the pursuit of novel therapeutic avenues persists, notably focusing on epigenetic pathways such as histone deacetylases (HDACs). The compound N-(2-hydroxyphenyl)-2-propylpentanamide (HO-AAVPA), a derivative of valproic acid (VPA), has emerged as a promising candidate warranting pre-clinical investigation. HO-AAVPA is an HDAC inhibitor with antiproliferative effects on BC, but its molecular mechanism has yet to be deciphered. Furthermore, in the present study, we determined the metabolomic effects of HO-AAVPA and VPA on cells of luminal breast cancer (MCF-7) and triple-negative breast cancer (MDA-MB-231) subtypes. The LC-MS untargeted metabolomic study allowed for the simultaneous measurement of multiple metabolites and pathways, identifying that both compounds affect glycerophospholipid and sphingolipid metabolism in the MCF-7 and MDA-MB-231 cell lines, suggesting that other biological targets were different from HDACs. In addition, there are different dysregulate metabolites, possibly due to the physicochemical differences between HO-AAVPA and VPA. Full article
(This article belongs to the Special Issue Molecular Research in Triple-Negative Breast Cancer)
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Review

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13 pages, 3537 KiB  
Review
Local Production of Acute Phase Proteins: A Defense Reaction of Cancer Cells to Injury with Focus on Fibrinogen
by Péter Hamar
Int. J. Mol. Sci. 2024, 25(6), 3435; https://doi.org/10.3390/ijms25063435 - 19 Mar 2024
Viewed by 640
Abstract
This review is intended to demonstrate that the local production of acute phase proteins (termed local acute phase response (lAPR)) and especially fibrin/fibrinogen (FN) is a defense mechanism of cancer cells to therapy, and inhibition of the lAPR can augment the effectiveness of [...] Read more.
This review is intended to demonstrate that the local production of acute phase proteins (termed local acute phase response (lAPR)) and especially fibrin/fibrinogen (FN) is a defense mechanism of cancer cells to therapy, and inhibition of the lAPR can augment the effectiveness of cancer therapy. Previously we detected a lAPR accompanying tumor cell death during the treatment of triple-negative breast cancer (TNBC) with modulated electro-hyperthermia (mEHT) in mice. We observed a similar lAPR in in hypoxic mouse kidneys. In both models, production of FN chains was predominant among the locally produced acute phase proteins. The production and extracellular release of FN into the tumor microenvironment is a known method of self-defense in tumor cells. We propose that the lAPR is a new, novel cellular defense mechanism like the heat shock response (HSR). In this review, we demonstrate a potential synergism between FN inhibition and mEHT in cancer treatment, suggesting that the effectiveness of mEHT and chemotherapy can be enhanced by inhibiting the HSR and/or the lAPR. Non-anticoagulant inhibition of FN offers potential new therapeutic options for cancer treatment. Full article
(This article belongs to the Special Issue Molecular Research in Triple-Negative Breast Cancer)
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20 pages, 730 KiB  
Review
Advances in the Management of Early-Stage Triple-Negative Breast Cancer
by Prarthna V. Bhardwaj, Yue Wang, Elizabeth Brunk, Philip M. Spanheimer and Yara G. Abdou
Int. J. Mol. Sci. 2023, 24(15), 12478; https://doi.org/10.3390/ijms241512478 - 05 Aug 2023
Viewed by 1673
Abstract
Triple-negative breast cancer (TNBC) is a subtype of breast cancer with both inter- and intratumor heterogeneity, thought to result in a more aggressive course and worse outcomes. Neoadjuvant therapy (NAT) has become the preferred treatment modality of early-stage TNBC as it allows for [...] Read more.
Triple-negative breast cancer (TNBC) is a subtype of breast cancer with both inter- and intratumor heterogeneity, thought to result in a more aggressive course and worse outcomes. Neoadjuvant therapy (NAT) has become the preferred treatment modality of early-stage TNBC as it allows for the downstaging of tumors in the breast and axilla, monitoring early treatment response, and most importantly, provides important prognostic information that is essential to determining post-surgical therapies to improve outcomes. It focuses on combinations of systemic drugs to optimize pathologic complete response (pCR). Excellent response to NAT has allowed surgical de-escalation in ideal candidates. Further, treatment algorithms guide the systemic management of patients based on their pCR status following surgery. The expanding knowledge of molecular pathways, genomic sequencing, and the immunological profile of TNBC has led to the use of immune checkpoint inhibitors and targeted agents, including PARP inhibitors, further revolutionizing the therapeutic landscape of this clinical entity. However, subgroups most likely to benefit from these novel approaches in TNBC remain elusive and are being extensively studied. In this review, we describe current practices and promising therapeutic options on the horizon for TNBC, surgical advances, and future trends in molecular determinants of response to therapy in early-stage TNBC. Full article
(This article belongs to the Special Issue Molecular Research in Triple-Negative Breast Cancer)
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Other

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10 pages, 1602 KiB  
Brief Report
Matrix Metalloproteinase-9 Expression Is Associated with the Absence of Response to Neoadjuvant Chemotherapy in Triple-Negative Breast Cancer Patients
by Marylène Lejeune, Laia Reverté, Noèlia Gallardo, Esther Sauras, Ramon Bosch, Daniel Mata, Albert Roso, Anna Petit, Vicente Peg, Francisco Riu, Joan García-Fontgivell, Fernanda Relea, Begoña Vieites, Luis de la Cruz-Merino, Meritxell Arenas, Valeri Rodriguez, Juana Galera, Anna Korzynska, Benoît Plancoulaine, Tomás Álvaro and Carlos Lópezadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2023, 24(14), 11297; https://doi.org/10.3390/ijms241411297 - 11 Jul 2023
Viewed by 1229
Abstract
Triple-negative breast cancer (TNBC) is particularly challenging due to the weak or absent response to therapeutics and its poor prognosis. The effectiveness of neoadjuvant chemotherapy (NAC) response is strongly influenced by changes in elements of the tumor microenvironment (TME). This work aimed to [...] Read more.
Triple-negative breast cancer (TNBC) is particularly challenging due to the weak or absent response to therapeutics and its poor prognosis. The effectiveness of neoadjuvant chemotherapy (NAC) response is strongly influenced by changes in elements of the tumor microenvironment (TME). This work aimed to characterize the residual TME composition in 96 TNBC patients using immunohistochemistry and in situ hybridization techniques and evaluate its prognostic implications for partial responders vs. non-responders. Compared with non-responders, partial responders containing higher levels of CD83+ mature dendritic cells, FOXP3+ regulatory T cells, and IL-15 expression but lower CD138+ cell concentration exhibited better OS and RFS. However, along with tumor diameter and positive nodal status at diagnosis, matrix metalloproteinase-9 (MMP-9) expression in the residual TME was identified as an independent factor associated with the impaired response to NAC. This study yields new insights into the key components of the residual tumor bed, such as MMP-9, which is strictly associated with the lack of a pathological response to NAC. This knowledge might help early identification of TNBC patients less likely to respond to NAC and allow the establishment of new therapeutic targets. Full article
(This article belongs to the Special Issue Molecular Research in Triple-Negative Breast Cancer)
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