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Editorial Board Members’ Collection Series: Cancer Metastasis

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 December 2024 | Viewed by 4702

Special Issue Editors


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Guest Editor
Cell-Cell Communication & Inflammation Unit, Centre for Molecular Biology “Severo Ochoa” (CSIC-UAM), 28049 Madrid, Spain
Interests: cell-cell communication; adhesion molecules; integrins; extracellular vesicles; tumor development and progression
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Special Issue Information

Dear Colleagues,

We are delighted to announce a call for submissions to a Special Issue of the International Journal of Molecular Sciences on the broad topic of cancer metastasis.

Cancer metastasis is defined as the spread of neoplastic cells from a primary site (primary tumor) to distant or secondary sites within the body, where cancer cells establish and form new tumors. Metastasis is a hallmark of cancer and is the primary cause of cancer morbidity and mortality. Neoplastic cells acquire metastatic capacity through the metastatic cascade, a multi-step process generally comprising proliferation, angiogenesis and local invasion at the primary tumor, access to a transport route (hematogenous, lymphatic, transcoelomic), extravasation and colonization of distant organs.

This Special Issue of IJMS welcomes both original research and review articles related to any of the following aspects of cancer metastasis:

  • Cancer metastasis routes;
  • Molecular mechanisms of cancer metastasis;
  • Genetic and epigenetic determinants of cancer metastasis;
  • Cell communication in cancer metastasis mediated by extracellular vesicles;
  • Mechanisms of chemoresistance in cancer metastasis;
  • Angiogenesis and cancer metastasis;
  • Immune evasion and suppression in cancer metastasis;
  • Liquid biopsy and molecular biomarkers for the early detection of cancer metastases;
  • Circulating tumor cells in cancer metastasis;
  • Pre-metastatic niche formation and development.

All submitted articles will undergo a peer review.

Dr. Carlos Cabañas
Prof. Dr. Sung-Hoon Kim
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

  • biomarkers
  • liquid biopsy
  • premetastatic niche
  • angiogenesis
  • immune evasion and suppression
  • genetic and epigenetic determinants
  • chemoresistance
  • extracellular vesicles

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Published Papers (3 papers)

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Review

14 pages, 1384 KiB  
Review
Leader Cells: Invade and Evade—The Frontline of Cancer Progression
by Brittany R. Doran, Laura R. Moffitt, Amy L. Wilson, Andrew N. Stephens and Maree Bilandzic
Int. J. Mol. Sci. 2024, 25(19), 10554; https://doi.org/10.3390/ijms251910554 - 30 Sep 2024
Viewed by 731
Abstract
Metastasis is the leading cause of cancer-related mortality; however, a complete understanding of the molecular programs driving the metastatic cascade is lacking. Metastasis is dependent on collective invasion—a developmental process exploited by many epithelial cancers to establish secondary tumours and promote widespread disease. [...] Read more.
Metastasis is the leading cause of cancer-related mortality; however, a complete understanding of the molecular programs driving the metastatic cascade is lacking. Metastasis is dependent on collective invasion—a developmental process exploited by many epithelial cancers to establish secondary tumours and promote widespread disease. The key drivers of collective invasion are “Leader Cells”, a functionally distinct subpopulation of cells that direct migration, cellular contractility, and lead trailing or follower cells. While a significant body of research has focused on leader cell biology in the traditional context of collective invasion, the influence of metastasis-promoting leader cells is an emerging area of study. This review provides insights into the expanded role of leader cells, detailing emerging evidence on the hybrid epithelial–mesenchymal transition (EMT) state and the phenotypical plasticity exhibited by leader cells. Additionally, we explore the role of leader cells in chemotherapeutic resistance and immune evasion, highlighting their potential as effective and diverse targets for novel cancer therapies. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Cancer Metastasis)
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12 pages, 242 KiB  
Review
Targeted Therapies for EGFR Exon 20 Insertion Mutation in Non-Small-Cell Lung Cancer
by Donghyun Seo and Jun Hyeok Lim
Int. J. Mol. Sci. 2024, 25(11), 5917; https://doi.org/10.3390/ijms25115917 - 29 May 2024
Viewed by 2009
Abstract
Non-small-cell lung cancer (NSCLC) frequently harbors mutations in the epidermal growth factor receptor (EGFR), with exon 20 insertions comprising 1–10% of these mutations. EGFR exon 20 insertions are less responsive to conventional tyrosine kinase inhibitors (TKIs), leading to the development of targeted agents. [...] Read more.
Non-small-cell lung cancer (NSCLC) frequently harbors mutations in the epidermal growth factor receptor (EGFR), with exon 20 insertions comprising 1–10% of these mutations. EGFR exon 20 insertions are less responsive to conventional tyrosine kinase inhibitors (TKIs), leading to the development of targeted agents. This review explores key therapeutic agents, such as Amivantamab, Mobocertinib, Poziotinib, Zipalertinib, and Sunvozertinib, which have shown promise in treating NSCLC with EGFR exon 20 insertions. Amivantamab, a bispecific antibody-targeting EGFR and c-MET, demonstrates significant efficacy, particularly when combined with chemotherapy. Mobocertinib, a TKI, selectively targets EGFR exon 20 mutations but faces limitations in efficacy. Poziotinib, another oral TKI, shows mixed results due to mutation-specific responses. Zipalertinib and Sunvozertinib have emerged as potent TKIs with promising clinical data. Despite these advances, challenges in overcoming resistance mutations and improving central nervous system penetration remain. Future research should focus on optimizing first-line combination therapies and enhancing diagnostic strategies for comprehensive mutation profiling. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Cancer Metastasis)
21 pages, 6301 KiB  
Review
Molecular Determinants Involved in the Docking and Uptake of Tumor-Derived Extracellular Vesicles: Implications in Cancer
by Irene Clares-Pedrero, Almudena Rocha-Mulero, Miguel Palma-Cobo, Beatriz Cardeñes, María Yáñez-Mó and Carlos Cabañas
Int. J. Mol. Sci. 2024, 25(6), 3449; https://doi.org/10.3390/ijms25063449 - 19 Mar 2024
Cited by 1 | Viewed by 1513
Abstract
Extracellular vesicles produced by tumor cells (TEVs) influence all stages of cancer development and spread, including tumorigenesis, cancer progression, and metastasis. TEVs can trigger profound phenotypic and functional changes in target cells through three main general mechanisms: (i) docking of TEVs on target [...] Read more.
Extracellular vesicles produced by tumor cells (TEVs) influence all stages of cancer development and spread, including tumorigenesis, cancer progression, and metastasis. TEVs can trigger profound phenotypic and functional changes in target cells through three main general mechanisms: (i) docking of TEVs on target cells and triggering of intra-cellular signaling; (ii) fusion of TEVs and target cell membranes with release of TEVs molecular cargo in the cytoplasm of recipient cell; and (iii) uptake of TEVs by recipient cells. Though the overall tumor-promoting effects of TEVs as well as the general mechanisms involved in TEVs interactions with, and uptake by, recipient cells are relatively well established, current knowledge about the molecular determinants that mediate the docking and uptake of tumor-derived EVs by specific target cells is still rather deficient. These molecular determinants dictate the cell and organ tropism of TEVs and ultimately control the specificity of TEVs-promoted metastases. Here, we will review current knowledge on selected specific molecules that mediate the tropism of TEVs towards specific target cells and organs, including the integrins, ICAM-1 Inter-Cellular Adhesion Molecule), ALCAM (Activated Leukocyte Cell Adhesion Molecule), CD44, the metalloproteinases ADAM17 (A Disintegrin And Metalloproteinase member 17) and ADAM10 (A Disintegrin And Metalloproteinase member 10), and the tetraspanin CD9. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Cancer Metastasis)
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