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State-of-the-Art Molecular Oncology in Brazil, 3rd Edition
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State-of-the-Art Molecular Oncology in Brazil, 3rd Edition

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: 20 September 2025 | Viewed by 7469

Special Issue Editors

Dr. Tiago Rodrigues

E-Mail Website1 Website2
Guest Editor
Centro de Ciências Naturais e Humanas (CCNH), Universidade Federal do ABC (UFABC), Santo André 09210-580, Brazil
Interests: apoptosis; autophagy; calcium; cancer; chemotherapy; mitochondria; oxidative stress; drug development
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Roger Chammas

E-Mail Website
Guest Editor
Center for Translational Research in Oncology (LIM24), Department of Radiology and Oncology, Faculdade de Medicina da Universidade de São Paulo, São Paulo 01246-903, Brazil
Interests: carbohydrate-dependent cellular interactions; tumor microenvironment; chemo- and radiotherapy; extracellular vesicles; tumor-associated macrophages; novel therapeutic cargo to tumors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue follows the publication of the third edition on the topic “State-of-the-Art Molecular Oncology in Brazil”.

https://www.mdpi.com/journal/ijms/special_issues/Mol_Oncol_BR

https://www.mdpi.com/journal/ijms/special_issues/JKE9Y113YO

Cancer is a broad term to describe a large number of diseases characterized by the transformation of normal to abnormal tumor cells with uncontrolled proliferative capacity as a result of mutations, epigenetic alterations, exposure to toxicants and environmental conditions, as well as others. Tumor cells exhibit several molecular, morphological, and functional alterations, giving them proliferative advantages, the ability to escape from the immune system and cell death, and invasiveness capacity. In this regard, many studies focused on the molecular aspects of cancer have been conducted worldwide, aiming to improve our current understanding of tumor cell functioning, to describe molecular mechanisms of therapeutic options, and to discover novel targets and drugs for cancer treatment.

This Special Issue aims to highlight recent advances in cancer research in Brazil, focused on the molecular aspects of cancer. It includes studies conducted to unveil the molecular alterations exhibited by tumor cells, the proposal of novel targets for cancer therapy, and the mechanisms of action of drugs and drug candidates (including off-target effects and drug repurposing).

Thus, in order to provide a comprehensive view of recent advances in cancer research in Brazil, we invite researchers to submit original research papers and high-quality comprehensive reviews in the cancer research field to this Special Issue. Potential topics include but are not limited to the following:

  • Molecular aspects of tumorigenesis;
  • Mechanisms of evasion of cell death (apoptosis, necroptosis, autophagy, and others);
  • Ionic and metabolic alterations in cancer;
  • Molecular aspects of cancer therapy (mechanisms of drugs and drug candidates and new targets);
  • Drug resistance mechanisms in cancer therapy.

Dr. Tiago Rodrigues
Prof. Dr. Roger Chammas
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

  • apoptosis
  • autophagy
  • calcium
  • cancer
  • cell death
  • chemotherapy
  • metabolism
  • mitochondria
  • drug resistance
  • oxidative stress

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Published Papers (4 papers)

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Research

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23 pages, 6092 KiB  
Article
Exploiting Paradoxical Activation of Oncogenic MAPK Signaling by Targeting Mitochondria to Sensitize NRAS Mutant-Melanoma to Vemurafenib
by Laura Francisca Leite do Prado-Souza, Letícia Silva Ferraz, Tharcísio Citrangulo Tortelli, Jr., César Augusto João Ribeiro, Danilo Trabuco do Amaral, Denise Costa Arruda, Érica Aparecida de Oliveira, Roger Chammas, Silvya Stuchi Maria-Engler and Tiago Rodrigues
Int. J. Mol. Sci. 2025, 26(6), 2675; https://doi.org/10.3390/ijms26062675 - 16 Mar 2025
Cited by 1 | Viewed by 2708
Abstract
Vemurafenib is a BRAF (rapidly accelerated fibrosarcoma B-type)-targeted therapy used to treat patients with advanced, unresectable melanoma. It inhibits the MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) pathway and tumor proliferation in BRAFV600E-mutated melanoma cells. Resistance to vemurafenib has been reported [...] Read more.
Vemurafenib is a BRAF (rapidly accelerated fibrosarcoma B-type)-targeted therapy used to treat patients with advanced, unresectable melanoma. It inhibits the MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) pathway and tumor proliferation in BRAFV600E-mutated melanoma cells. Resistance to vemurafenib has been reported in melanoma patients due to secondary NRAS (neuroblastoma RAS viral oncogene homolog) mutations, which lead to paradoxical MAPK pathway activation and tumor proliferation. However, the impact of this paradoxical activation on mitochondrial dynamics and function in NRAS-mutated melanoma is unclear. Here, we investigated the effects of vemurafenib on NRASQ61R-mutated melanoma cells, focusing on mitochondrial dynamics and function. As expected, vemurafenib did not exhibit cytotoxicity in SK-MEL-147 NRASQ61R-mutated melanoma cells, even after 72 h of incubation. However, it significantly enhanced the MAPK/ERK signaling through paradoxical activation, accompanied by decreased expression of mitochondrial fusion proteins and activation of the fission protein DRP1 (dynamin-related protein 1), leading to small, rounded mitochondrial morphology. These observations were corroborated by transcriptome data obtained from NRAS-mutated melanoma patients, showing MFN1 (mitofusin 1) and OPA1 (optic atrophy 1) downregulation and DNM1L (DRP1 gene) upregulation. Interestingly, inhibition of mitochondrial fission with mdivi-1 or modulation of oxidative phosphorylation via respiratory chain inhibition or uncoupling significantly sensitized NRASQ61R-mutated melanoma cells to vemurafenib. Despite vemurafenib’s low cytotoxicity in NRAS-mutated melanoma, targeting mitochondrial dynamics and/or oxidative phosphorylation may offer a promising strategy for combined therapy. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Brazil, 3rd Edition)
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19 pages, 3881 KiB  
Article
DLK1 Is Associated with Stemness Phenotype in Medullary Thyroid Carcinoma Cell Lines
by Danilo Dias da Silva, Rodrigo Pinheiro Araldi, Mariana Rocha Belizario, Welbert Gomes Rocha, Rui Monteiro de Barros Maciel and Janete Maria Cerutti
Int. J. Mol. Sci. 2024, 25(22), 11924; https://doi.org/10.3390/ijms252211924 - 6 Nov 2024
Viewed by 1149
Abstract
Medullary thyroid carcinoma (MTC) is a rare and aggressive tumor, often requiring systemic treatment in advanced or metastatic stages, where drug resistance presents a significant challenge. Given the role of cancer stem cells (CSCs) in cancer recurrence and drug resistance, we aimed to [...] Read more.
Medullary thyroid carcinoma (MTC) is a rare and aggressive tumor, often requiring systemic treatment in advanced or metastatic stages, where drug resistance presents a significant challenge. Given the role of cancer stem cells (CSCs) in cancer recurrence and drug resistance, we aimed to identify CSC subpopulations within two MTC cell lines harboring pathogenic variants in the two most common MEN2-associated codons. We analyzed 15 stemness-associated markers, along with well-established thyroid stem cell markers (CD133, CD44, and ALDH1), a novel candidate (DLK1), and multidrug resistance proteins (MRP1 and MRP3). The ability to efflux the fluorescent dye Hoechst 3342 and form spheroids, representing CSC behavior, was also assessed. MZ-CRC-1 cells (p.M918T) displayed higher expressions of canonical markers, DLK1, and MRP proteins than TT cells (p.C634W). MZ-CRC-1 cells also formed more spheroids and showed less dye accumulation (p < 0.0001). Finally, we observed that DLK1+ cells (those expressing DLK1) in both cell lines exhibited significantly higher levels of stemness markers compared to DLK1− cells (those lacking DLK1 expression). These findings underscore DLK1’s role in enhancing the stemness phenotype, providing valuable insights into MTC progression and resistance and suggesting potential therapeutic implications. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Brazil, 3rd Edition)
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16 pages, 2129 KiB  
Article
Metabolomic Profiling of Breast Cancer Patients Undergoing Neoadjuvant Chemotherapy for Predicting Disease-Free and Overall Survival
by Maria Cecília Ramiro Talarico, Sophie Derchain, Lucas Ferreira da Silva, Maurício L. Sforça, Silvana A. Rocco, Marcella R. Cardoso and Luís Otávio Sarian
Int. J. Mol. Sci. 2024, 25(16), 8639; https://doi.org/10.3390/ijms25168639 - 8 Aug 2024
Cited by 2 | Viewed by 1594
Abstract
Breast cancer (BC) remains a significant global health concern, with neoadjuvant chemotherapy (NACT) offering preoperative benefits like tumor downstaging and treatment response assessment. However, identifying factors influencing post-NACT treatment response and survival outcomes is challenging. Metabolomic approaches offer promising insights into understanding these [...] Read more.
Breast cancer (BC) remains a significant global health concern, with neoadjuvant chemotherapy (NACT) offering preoperative benefits like tumor downstaging and treatment response assessment. However, identifying factors influencing post-NACT treatment response and survival outcomes is challenging. Metabolomic approaches offer promising insights into understanding these outcomes. This study analyzed the serum of 80 BC patients before and after NACT, followed for up to five years, correlating with disease-free survival (DFS) and overall survival (OS). Using untargeted nuclear magnetic resonance (NMR) spectroscopy and a novel statistical model that avoids collinearity issues, we identified metabolic changes associated with survival outcomes. Four metabolites (histidine, lactate, serine, and taurine) were significantly associated with DFS. We developed a metabolite-related survival score (MRSS) from these metabolites, stratifying patients into low- and high-risk relapse groups, independent of classical prognostic factors. High-risk patients had a hazard ratio (HR) for DFS of 3.42 (95% CI 1.51–7.74; p = 0.003) after adjustment for disease stage and age. A similar trend was observed for OS (HR of 3.34, 95% CI 1.64–6.80; p < 0.001). Multivariate Cox proportional hazards analysis confirmed the independent prognostic value of the MRSS. Our findings suggest the potential of metabolomic data, alongside traditional markers, in guiding personalized treatment decisions and risk stratification in BC patients undergoing NACT. This study provides a methodological framework for leveraging metabolomics in survival analyses. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Brazil, 3rd Edition)
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Review

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18 pages, 4207 KiB  
Review
The Therapeutic Potential of Physical Exercise in Cancer: The Role of Chemokines
by Glenda B. B. Buzaglo, Guilherme D. Telles, Rafaela B. Araújo, Gilmar D. S. Junior, Olivia M. Ruberti, Marina L. V. Ferreira, Sophie F. M. Derchain, Felipe C. Vechin and Miguel S. Conceição
Int. J. Mol. Sci. 2024, 25(24), 13740; https://doi.org/10.3390/ijms252413740 - 23 Dec 2024
Cited by 1 | Viewed by 1448
Abstract
The global increase in cancer cases and mortality has been associated with inflammatory processes, in which chemokines play crucial roles. These molecules, a subfamily of cytokines, are essential for the migration, adhesion, interaction, and positioning of immune cells throughout the body. Chemokines primarily [...] Read more.
The global increase in cancer cases and mortality has been associated with inflammatory processes, in which chemokines play crucial roles. These molecules, a subfamily of cytokines, are essential for the migration, adhesion, interaction, and positioning of immune cells throughout the body. Chemokines primarily originate in response to pathogenic stimuli and inflammatory cytokines. They are expressed by lymphocytes in the bloodstream and are divided into four classes (CC, CXC, XC, and CX3C), playing multifaceted roles in the tumor environment (TME). In the TME, chemokines regulate immune behavior by recruiting cells such as tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), which promote tumor survival. Additionally, they directly influence tumor behavior, promoting pathological angiogenesis, invasion, and metastasis. On the other hand, chemokines can also induce antitumor responses by mobilizing CD8+ T cells and natural killer (NK) cells to the tumor, reducing pro-inflammatory chemokines and enhancing essential antitumor responses. Given the complex interaction between chemokines, the immune system, angiogenic factors, and metastasis, it becomes evident how important it is to target these pathways in therapeutic interventions to counteract cancer progression. In this context, physical exercise emerges as a promising strategy due to its role modulating the expression of anti-inflammatory chemokines and enhancing the antitumor response. Aerobic and resistance exercises have been associated with a beneficial inflammatory profile in cancer, increased infiltration of CD8+ T cells in the TME, and improvement of intratumoral vasculature. This creates an environment less favorable to tumor growth and supports the circulation of antitumor immune cells and chemokines. Therefore, understanding the impact of exercise on the expression of chemokines can provide valuable insights for therapeutic interventions in cancer treatment and prevention. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Brazil, 3rd Edition)
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