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State-of-the-Art Molecular Oncology in Chile
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State-of-the-Art Molecular Oncology in Chile

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 January 2024) | Viewed by 12506

Special Issue Editors

Prof. Dr. Juan Carlos Roa

E-Mail Website
Guest Editor
Millennium Institute on Immunology and Immunotherapy, Department of Pathology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago 8380000, Chile
Interests: gallbladder cancer; biomarkers; biobank; liquid biopsy
Prof. Dr. Carmen Aurora Romero

E-Mail Website
Guest Editor
Departamento de Obstetricia y Ginecología, Facultad de Medicina, Hospital Clínico Universidad de Chile, Universidad de Chile, Santiago 8380453, Chile
Interests: ovarian cancer; neurotrophins; angiogenesis; microRNAs for cancer treatment; ovarian cancer pathogenesis; neuroendocrine regulation of ovary
Special Issues, Collections and Topics in MDPI journals
Dr. Hector R. Contreras

E-Mail Website
Guest Editor
Laboratory of Cellular and Molecular Oncology, Department of Basic and Clinical Oncology, Faculty of Medicine, University de Chile, Santiago 8380453, Chile
Interests: epithelial–mesenchymal transition; cancer stem cell; prostate cancer; colon cancer; breast cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The aim of this Special Issue is to present the latest advances in cancer research in Chile from the point of view of different research studies in molecular oncology.

With the situation of the SARS-CoV-2 (COVID-19) pandemic, cancer patients have delayed their diagnoses and treatments; as such, the main cause of death in the near future will be cancer, not only in Chile but also in many other countries.

The assessment of basic and clinical studies of different types of cancer is fundamental to the search for better biomarkers that can be applied in the prevention and early detection of cancer. Moreover, the finding of genetic markers will allow typing and/or classifying tumors in target tissues from a therapeutic point of view. In addition, it is relevant to gain knowledge on the participation of different oncoproteins in cancer progression. Therefore, the search for new therapies complementary to the current ones is of great importance, since cancers eventually end up becoming resistant to those therapies in most cases.

Additionally, molecular biology has been a fundamental tool to successfully overcome these challenges and achieve the proposed objectives. In fact, in recent years, a relevant course of study involves finding new molecules, such as oncoproteins and noncoding RNAs, that are both involved in cancer progression and can be utilized in potential adjuvant therapies.

In this regard, there is currently great interest in the importance of exosomes in some processes of cancer, such as metastasis, and the role of exosomes with specific cargo that may potentially be used in therapy. In addition, the development of nanoparticle systems with different molecules as cargo for use in possible new therapies will be of importance.

The aim of this Special Issue is to provide a comprehensive view of recent advances in cancer research in Chile. We invite you to submit research and review papers that will consolidate our understanding in this area. Potential topics include but are not limited to the following:

  1. Process involved in EMT in different type of cancer
  2. Oncoproteins involved in different process in cancer
  3. Role of exosomes in cancer    
  4. Role of noncoding RNAs in cancer
  5. Use of nanosystems as adjuvant or complementary therapies in cancer
  6. Use of bioinformatics in cancer with a strong emphasis on molecular biology and molecular medicine
  7. Tumoral microenvironment
  8. Carcinogenesis in prevalent cancers in the Chilean population

Prof. Dr. Juan Carlos Roa
Prof. Dr. Carmen Aurora Romero
Dr. Hector R. Contreras
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. 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

  • molecular oncology
  • prognostics
  • progression
  • metastasis
  • cancer therapy

Published Papers (6 papers)

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Research

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10 pages, 1305 KiB  
Article
Association of FANCM Mutations with Familial and Early-Onset Breast Cancer Risk in a South American Population
by Sebastian Morales-Pison, Sarai Morales-González, Ricardo Fernandez-Ramires, Julio C. Tapia, Edio Maldonado, Gloria M. Calaf and Lilian Jara
Int. J. Mol. Sci. 2023, 24(4), 4041; https://doi.org/10.3390/ijms24044041 - 17 Feb 2023
Viewed by 1687
Abstract
Breast cancer (BC) is the most common cancer among women worldwide. BRCA1/2 are responsible for 16–20% of the risk for hereditary BC. Other susceptibility genes have been identified; Fanconi Anemia Complementation Group M (FANCM) being one of these. Two variants in [...] Read more.
Breast cancer (BC) is the most common cancer among women worldwide. BRCA1/2 are responsible for 16–20% of the risk for hereditary BC. Other susceptibility genes have been identified; Fanconi Anemia Complementation Group M (FANCM) being one of these. Two variants in FANCM, rs144567652 and rs147021911, are associated with BC risk. These variants have been described in Finland, Italy, France, Spain, Germany, Australia, the United States, Sweden, Finnish, and the Netherlands, but not in the South American populations. Our study evaluated the association of the SNPs rs144567652 and rs147021911 with BC risk in non-carriers of BRCA1/2 mutations from a South American population. The SNPs were genotyped in 492 BRCA1/2-negative BC cases and 673 controls. Our data do not support an association between FANCM rs147021911 and rs144567652 SNPs and BC risk. Nevertheless, two BC cases, one with a family history of BC and the other with sporadic early-onset BC, were C/T heterozygotes for rs144567652. In conclusion, this is the first study related contribution of FANCM mutations and BC risk in a South American population. Nevertheless, more studies are necessary to evaluate if rs144567652 could be responsible for familial BC in BRCA1/2-negatives and for early-onset non-familial BC in Chilean BC cases. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Chile)
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21 pages, 9905 KiB  
Article
Dosimetry Effects Due to the Presence of Fe Nanoparticles for Potential Combination of Hyperthermic Cancer Treatment with MRI-Based Image-Guided Radiotherapy
by Amiel Gayol, Francisco Malano, Clara Ribo Montenovo, Pedro Pérez and Mauro Valente
Int. J. Mol. Sci. 2023, 24(1), 514; https://doi.org/10.3390/ijms24010514 - 28 Dec 2022
Cited by 4 | Viewed by 1611
Abstract
Nanoparticles have proven to be biocompatible and suitable for many biomedical applications. Currently, hyperthermia cancer treatments based on Fe nanoparticle infusion excited by alternating magnetic fields are commonly used. In addition to this, MRI-based image-guided radiotherapy represents, nowadays, one of the most promising [...] Read more.
Nanoparticles have proven to be biocompatible and suitable for many biomedical applications. Currently, hyperthermia cancer treatments based on Fe nanoparticle infusion excited by alternating magnetic fields are commonly used. In addition to this, MRI-based image-guided radiotherapy represents, nowadays, one of the most promising accurate radiotherapy modalities. Hence, assessing the feasibility of combining both techniques requires preliminary characterization of the corresponding dosimetry effects. The present work reports on a theoretical and numerical simulation feasibility study aimed at pointing out preliminary dosimetry issues. Spatial dose distributions incorporating magnetic nanoparticles in MRI-based image-guided radiotherapy have been obtained by Monte Carlo simulation approaches accounting for all relevant radiation interaction properties as well as charged particles coupling with strong external magnetic fields, which are representative of typical MRI-LINAC devices. Two main effects have been evidenced: local dose enhancement (up to 60% at local level) within the infused volume, and non-negligible changes in the dose distribution at the interfaces between different tissues, developing to over 70% for low-density anatomical cavities. Moreover, cellular uptakes up to 10% have been modeled by means of considering different Fe nanoparticle concentrations. A theoretical temperature-dependent model for the thermal enhancement ratio (TER) has been used to account for radiosensitization due to hyperthermia. The outcomes demonstrated the reliability of the Monte Carlo approach in accounting for strong magnetic fields and mass distributions from patient-specific anatomy CT scans to assess dose distributions in MRI-based image-guided radiotherapy combined with magnetic nanoparticles, while the hyperthermic radiosensitization provides further and synergic contributions. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Chile)
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13 pages, 1621 KiB  
Article
Differentially Expressed Genes and Signaling Pathways Potentially Involved in Primary Resistance to Chemo-Immunotherapy in Advanced-Stage Gastric Cancer Patients
by Mauricio P. Pinto, Matías Muñoz-Medel, Ignacio N. Retamal, MariaLoreto Bravo, Verónica Latapiat, Miguel Córdova-Delgado, Charlotte N. Hill, M. Fernanda Fernández, Carolina Sánchez, Mauricio A. Sáez, Alberto J. M. Martin, Sebastián Morales-Pison, Ricardo Fernandez-Ramires, Benjamín García-Bloj, Gareth I. Owen and Marcelo Garrido
Int. J. Mol. Sci. 2023, 24(1), 1; https://doi.org/10.3390/ijms24010001 - 20 Dec 2022
Cited by 4 | Viewed by 2522
Abstract
Recently, the combination of chemotherapy plus nivolumab (chemo-immunotherapy) has become the standard of care for advanced-stage gastric cancer (GC) patients. However, despite its efficacy, up to 40% of patients do not respond to these treatments. Our study sought to identify variations in gene [...] Read more.
Recently, the combination of chemotherapy plus nivolumab (chemo-immunotherapy) has become the standard of care for advanced-stage gastric cancer (GC) patients. However, despite its efficacy, up to 40% of patients do not respond to these treatments. Our study sought to identify variations in gene expression associated with primary resistance to chemo-immunotherapy. Diagnostic endoscopic biopsies were retrospectively obtained from advanced GC patients previously categorized as responders (R) or non-responders (NR). Thirty-four tumor biopsies (R: n = 16, NR: n = 18) were analyzed by 3′ massive analysis of cDNA ends (3′MACE). We found >30 differentially expressed genes between R and NRs. Subsequent pathway enrichment analyses demonstrated that angiogenesis and the Wnt-β-catenin signaling pathway were enriched in NRs. Concomitantly, we performed next generation sequencing (NGS) analyses in a subset of four NR patients that confirmed alterations in genes that belonged to the Wnt/β-catenin and the phosphoinositide 3-kinase (PI3K) pathways. We speculate that angiogenesis, the Wnt, and the PI3K pathways might offer actionable targets. We also discuss therapeutic alternatives for chemo-immunotherapy-resistant advanced-stage GC patients. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Chile)
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Review

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14 pages, 1622 KiB  
Review
NSD3 in Cancer: Unraveling Methyltransferase-Dependent and Isoform-Specific Functions
by Yanara Nuñez, Sebastian Vera, Victor Baeza and Valentina Gonzalez-Pecchi
Int. J. Mol. Sci. 2024, 25(2), 944; https://doi.org/10.3390/ijms25020944 - 12 Jan 2024
Viewed by 1120
Abstract
NSD3 (nuclear receptor-binding SET domain protein 3) is a member of the NSD histone methyltransferase family of proteins. In recent years, it has been identified as a potential oncogene in certain types of cancer. The NSD3 gene encodes three isoforms, the long version [...] Read more.
NSD3 (nuclear receptor-binding SET domain protein 3) is a member of the NSD histone methyltransferase family of proteins. In recent years, it has been identified as a potential oncogene in certain types of cancer. The NSD3 gene encodes three isoforms, the long version (NSD3L), a short version (NSD3S) and the WHISTLE isoforms. Importantly, the NSD3S isoform corresponds to the N-terminal region of the full-length protein, lacking the methyltransferase domain. The chromosomal location of NSD3 is frequently amplified across cancer types, such as breast, lung, and colon, among others. Recently, this amplification has been correlated to a chromothripsis event, that could explain the different NSD3 alterations found in cancer. The fusion proteins containing NSD3 have also been reported in leukemia (NSD3-NUP98), and in NUT (nuclear protein of the testis) midline carcinoma (NSD3-NUT). Its role as an oncogene has been described by modulating different cancer pathways through its methyltransferase activity, or the short isoform of the protein, through protein interactions. Specifically, in this review we will focus on the functions that have been characterized as methyltransferase dependent, and those that have been correlated with the expression of the NSD3S isoform. There is evidence that both the NSD3L and NSD3S isoforms are relevant for cancer progression, establishing NSD3 as a therapeutic target. However, further functional studies are needed to differentiate NSD3 oncogenic activity as dependent or independent of the catalytic domain of the protein, as well as the contribution of each isoform and its clinical significance in cancer progression. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Chile)
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13 pages, 908 KiB  
Review
Cancer Stemness/Epithelial–Mesenchymal Transition Axis Influences Metastasis and Castration Resistance in Prostate Cancer: Potential Therapeutic Target
by Enrique A. Castellón, Sebastián Indo and Héctor R. Contreras
Int. J. Mol. Sci. 2022, 23(23), 14917; https://doi.org/10.3390/ijms232314917 - 29 Nov 2022
Cited by 11 | Viewed by 1836
Abstract
Prostate cancer (PCa) is a leading cause of cancer death in men, worldwide. Mortality is highly related to metastasis and hormone resistance, but the molecular underlying mechanisms are poorly understood. We have studied the presence and role of cancer stem cells (CSCs) and [...] Read more.
Prostate cancer (PCa) is a leading cause of cancer death in men, worldwide. Mortality is highly related to metastasis and hormone resistance, but the molecular underlying mechanisms are poorly understood. We have studied the presence and role of cancer stem cells (CSCs) and the Epithelial–Mesenchymal transition (EMT) in PCa, using both in vitro and in vivo models, thereby providing evidence that the stemness–mesenchymal axis seems to be a critical process related to relapse, metastasis and resistance. These are complex and related processes that involve a cooperative action of different cancer cell subpopulations, in which CSCs and mesenchymal cancer cells (MCCs) would be responsible for invading, colonizing pre-metastatic niches, initiating metastasis and an evading treatments response. Manipulating the stemness–EMT axis genes on the androgen receptor (AR) may shed some light on the effect of this axis on metastasis and castration resistance in PCa. It is suggested that the EMT gene SNAI2/Slug up regulates the stemness gene Sox2, and vice versa, inducing AR expression, promoting metastasis and castration resistance. This approach will provide new sight about the role of the stemness–mesenchymal axis in the metastasis and resistance mechanisms in PCa and their potential control, contributing to develop new therapeutic strategies for patients with metastatic and castration-resistant PCa. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Chile)
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16 pages, 1106 KiB  
Review
MET Signaling Pathways, Resistance Mechanisms, and Opportunities for Target Therapies
by Solange Rivas, Arnaldo Marín, Suraj Samtani, Evelin González-Feliú and Ricardo Armisén
Int. J. Mol. Sci. 2022, 23(22), 13898; https://doi.org/10.3390/ijms232213898 - 11 Nov 2022
Cited by 10 | Viewed by 2837
Abstract
The MET gene, known as MET proto-oncogene receptor tyrosine kinase, was first identified to induce tumor cell migration, invasion, and proliferation/survival through canonical RAS-CDC42-PAK-Rho kinase, RAS-MAPK, PI3K-AKT-mTOR, and β-catenin signaling pathways, and its driver mutations, such as MET gene amplification (METamp) [...] Read more.
The MET gene, known as MET proto-oncogene receptor tyrosine kinase, was first identified to induce tumor cell migration, invasion, and proliferation/survival through canonical RAS-CDC42-PAK-Rho kinase, RAS-MAPK, PI3K-AKT-mTOR, and β-catenin signaling pathways, and its driver mutations, such as MET gene amplification (METamp) and the exon 14 skipping alterations (METex14), activate cell transformation, cancer progression, and worse patient prognosis, principally in lung cancer through the overactivation of their own oncogenic and MET parallel signaling pathways. Because of this, MET driver alterations have become of interest in lung adenocarcinomas since the FDA approval of target therapies for METamp and METex14 in 2020. However, after using MET target therapies, tumor cells develop adaptative changes, favoring tumor resistance to drugs, the main current challenge to precision medicine. Here, we review a link between the resistance mechanism and MET signaling pathways, which is not only limited to MET. The resistance impacts MET parallel tyrosine kinase receptors and signals shared hubs. Therefore, this information could be relevant in the patient’s mutational profile evaluation before the first target therapy prescription and follow-up to reduce the risk of drug resistance. However, to develop a resistance mechanism to a MET inhibitor, patients must have access to the drugs. For instance, none of the FDA approved MET inhibitors are registered as such in Chile and other developing countries. Constant cross-feeding between basic and clinical research will thus be required to meet future challenges imposed by the acquired resistance to targeted therapies. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Chile)
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