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Cancers
Special Issues
Targeted Therapies for Cancer Metastasis
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Targeted Therapies for Cancer Metastasis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 13512

Special Issue Editors

Prof. Dr. Katrien Remaut

E-Mail Website
Guest Editor
Lab General Biochemistry and Physical Pharmacy, Faculty of Pharmaceutical Sciences, Ghent University, Ottergemsesteenweg 460, 9000 Ghent, Belgium
Interests: peritoneal carcinomatosis; advanced microscopy methods; nucleic acid delivery; non-viral gene delivery; stability in biological fluids
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Wim P. Ceelen

E-Mail Website
Guest Editor
Department of GI Surgery and Cancer Research Institute Ghent (CRIG), Ghent University Hospital, 9000 Ghent, Belgium
Interests: colorectal cancer; peritoneal metastasis; intraperitoneal drug delivery; functional imaging in cancer; biophysics of tumor tissue; drug delivery modelling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleague,

Cancer, including breast cancer, skin cancer, lung cancer, colon cancer, and prostate cancer, still affects millions of people every year. Cancer treatment often includes non-specific interventions, such as surgery, chemotherapy, and/or radiation therapy. Targeted therapies, however, specifically interfere with the biology of the cancer cells, to prevent the growth and formation of metastasis. Biological therapies, such as immunotherapy, antibodies, gene therapy, and cell-based therapy, are rapidly progressing. Furthermore, smart delivery strategies, such as tumor-environment-responsive materials, controlled release formulations, or the application of local triggers (light, heat, ultrasound, etc.), can locally boost the therapeutic potential.

In this Special Issue, we will publish reviews and original research that provide new insights into targeted therapies for cancer metastasis. Moreover, insights into how locoregional treatment can advance therapeutic outcome are of interest, as well as novel insights into the delivery aspects of gene-targeted therapies.

Prof. Dr. Katrien Remaut
Prof. Dr. Wim P. Ceelen
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 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • nucleic acids in cancer treatment (siRNA, mRNA, pDNA, …)
  • antibodies in cancer treatment
  • immunotherapy
  • cancer vaccines
  • cancer gene therapy
  • cell based therapy
  • tumor environment responsive materials
  • controlled release formulations
  • locoregional triggered drug delivery
  • delivery barriers to targeted cancer therapies

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (5 papers)

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Research

Jump to: Review

17 pages, 5954 KiB  
Article
TCGAnalyzeR: An Online Pan-Cancer Tool for Integrative Visualization of Molecular and Clinical Data of Cancer Patients for Cohort and Associated Gene Discovery
by Talip Zengin, Başak Abak Masud and Tuğba Önal-Süzek
Cancers 2024, 16(2), 345; https://doi.org/10.3390/cancers16020345 - 13 Jan 2024
Viewed by 2335
Abstract
For humans, the parallel processing capability of visual recognition allows for faster comprehension of complex scenes and patterns. This is essential, especially for clinicians interpreting big data for whom the visualization tools play an even more vital role in transforming raw big data [...] Read more.
For humans, the parallel processing capability of visual recognition allows for faster comprehension of complex scenes and patterns. This is essential, especially for clinicians interpreting big data for whom the visualization tools play an even more vital role in transforming raw big data into clinical decision making by managing the inherent complexity and monitoring patterns interactively in real time. The Cancer Genome Atlas (TCGA) database’s size and data variety challenge the effective utilization of this valuable resource by clinicians and biologists. We re-analyzed the five molecular data types, i.e., mutation, transcriptome profile, copy number variation, miRNA, and methylation data, of ~11,000 cancer patients with all 33 cancer types and integrated the existing TCGA patient cohorts from the literature into a free and efficient web application: TCGAnalyzeR. TCGAnalyzeR provides an integrative visualization of pre-analyzed TCGA data with several novel modules: (i) simple nucleotide variations with driver prediction; (ii) recurrent copy number alterations; (iii) differential expression in tumor versus normal, with pathway and the survival analysis; (iv) TCGA clinical data including metastasis and survival analysis; (v) external subcohorts from the literature, curatedTCGAData, and BiocOncoTK R packages; (vi) internal patient clusters determined using an iClusterPlus R package or signature-based expression analysis of five molecular data types. TCGAnalyzeR integrated the multi-omics, pan-cancer TCGA with ~120 subcohorts from the literature along with clipboard panels, thus allowing users to create their own subcohorts, compare against existing external subcohorts (MSI, Immune, PAM50, Triple Negative, IDH1, miRNA, metastasis, etc.) along with our internal patient clusters, and visualize cohort-centric or gene-centric results interactively using TCGAnalyzeR. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer Metastasis)
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29 pages, 2563 KiB  
Article
Isogenic Cell Lines Derived from Specific Organ Metastases Exhibit Divergent Cytogenomic Aberrations
by Paul T. Winnard, Jr., Laura Morsberger, Raluca Yonescu, Liqun Jiang, Ying S. Zou and Venu Raman
Cancers 2023, 15(5), 1420; https://doi.org/10.3390/cancers15051420 - 23 Feb 2023
Cited by 1 | Viewed by 1981
Abstract
Aneuploidy, a deviation in chromosome numbers from the normal diploid set, is now recognized as a fundamental characteristic of all cancer types and is found in 70–90% of all solid tumors. The majority of aneuploidies are generated by chromosomal instability (CIN). CIN/aneuploidy is [...] Read more.
Aneuploidy, a deviation in chromosome numbers from the normal diploid set, is now recognized as a fundamental characteristic of all cancer types and is found in 70–90% of all solid tumors. The majority of aneuploidies are generated by chromosomal instability (CIN). CIN/aneuploidy is an independent prognostic marker of cancer survival and is a cause of drug resistance. Hence, ongoing research has been directed towards the development of therapeutics aimed at targeting CIN/aneuploidy. However, there are relatively limited reports on the evolution of CIN/aneuploidies within or across metastatic lesions. In this work, we built on our previous studies using a human xenograft model system of metastatic disease in mice that is based on isogenic cell lines derived from the primary tumor and specific metastatic organs (brain, liver, lung, and spine). As such, these studies were aimed at exploring distinctions and commonalities between the karyotypes; biological processes that have been implicated in CIN; single-nucleotide polymorphisms (SNPs); losses, gains, and amplifications of chromosomal regions; and gene mutation variants across these cell lines. Substantial amounts of inter- and intra-heterogeneity were found across karyotypes, along with distinctions between SNP frequencies across each chromosome of each metastatic cell line relative the primary tumor cell line. There were disconnects between chromosomal gains or amplifications and protein levels of the genes in those regions. However, commonalities across all cell lines provide opportunities to select biological processes as druggable targets that could have efficacy against the primary tumor, as well as metastases. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer Metastasis)
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Review

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26 pages, 1854 KiB  
Review
Breast Tumor Metastasis and Its Microenvironment: It Takes Both Seed and Soil to Grow a Tumor and Target It for Treatment
by Shirin Bonni, David N. Brindley, M. Dean Chamberlain, Nima Daneshvar-Baghbadorani, Andrew Freywald, Denise G. Hemmings, Sabine Hombach-Klonisch, Thomas Klonisch, Afshin Raouf, Carrie Simone Shemanko, Diana Topolnitska, Kaitlyn Visser, Franco J. Vizeacoumar, Edwin Wang and Spencer B. Gibson
Cancers 2024, 16(5), 911; https://doi.org/10.3390/cancers16050911 - 23 Feb 2024
Cited by 1 | Viewed by 2681
Abstract
Metastasis remains a major challenge in treating breast cancer. Breast tumors metastasize to organ-specific locations such as the brain, lungs, and bone, but why some organs are favored over others remains unclear. Breast tumors also show heterogeneity, plasticity, and distinct microenvironments. This contributes [...] Read more.
Metastasis remains a major challenge in treating breast cancer. Breast tumors metastasize to organ-specific locations such as the brain, lungs, and bone, but why some organs are favored over others remains unclear. Breast tumors also show heterogeneity, plasticity, and distinct microenvironments. This contributes to treatment failure and relapse. The interaction of breast cancer cells with their metastatic microenvironment has led to the concept that primary breast cancer cells act as seeds, whereas the metastatic tissue microenvironment (TME) is the soil. Improving our understanding of this interaction could lead to better treatment strategies for metastatic breast cancer. Targeted treatments for different subtypes of breast cancers have improved overall patient survival, even with metastasis. However, these targeted treatments are based upon the biology of the primary tumor and often these patients’ relapse, after therapy, with metastatic tumors. The advent of immunotherapy allowed the immune system to target metastatic tumors. Unfortunately, immunotherapy has not been as effective in metastatic breast cancer relative to other cancers with metastases, such as melanoma. This review will describe the heterogeneic nature of breast cancer cells and their microenvironments. The distinct properties of metastatic breast cancer cells and their microenvironments that allow interactions, especially in bone and brain metastasis, will also be described. Finally, we will review immunotherapy approaches to treat metastatic breast tumors and discuss future therapeutic approaches to improve treatments for metastatic breast cancer. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer Metastasis)
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21 pages, 1816 KiB  
Review
Lipocalin-2: A Nurturer of Tumor Progression and a Novel Candidate for Targeted Cancer Therapy
by Maida Živalj, Jo A. Van Ginderachter and Benoit Stijlemans
Cancers 2023, 15(21), 5159; https://doi.org/10.3390/cancers15215159 - 26 Oct 2023
Cited by 6 | Viewed by 2538
Abstract
Within the tumor microenvironment (TME) exists a complex signaling network between cancer cells and stromal cells, which determines the fate of tumor progression. Hence, interfering with this signaling network forms the basis for cancer therapy. Yet, many types of cancer, in particular, solid [...] Read more.
Within the tumor microenvironment (TME) exists a complex signaling network between cancer cells and stromal cells, which determines the fate of tumor progression. Hence, interfering with this signaling network forms the basis for cancer therapy. Yet, many types of cancer, in particular, solid tumors, are refractory to the currently used treatments, so there is an urgent need for novel molecular targets that could improve current anti-cancer therapeutic strategies. Lipocalin-2 (Lcn-2), a secreted siderophore-binding glycoprotein that regulates iron homeostasis, is highly upregulated in various cancer types. Due to its pleiotropic role in the crosstalk between cancer cells and stromal cells, favoring tumor progression, it could be considered as a novel biomarker for prognostic and therapeutic purposes. However, the exact signaling route by which Lcn-2 promotes tumorigenesis remains unknown, and Lcn-2-targeting moieties are largely uninvestigated. This review will (i) provide an overview on the role of Lcn-2 in orchestrating the TME at the level of iron homeostasis, macrophage polarization, extracellular matrix remodeling, and cell migration and survival, and (ii) discuss the potential of Lcn-2 as a promising novel drug target that should be pursued in future translational research. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer Metastasis)
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29 pages, 1724 KiB  
Review
Targeting KRAS in Pancreatic Ductal Adenocarcinoma: The Long Road to Cure
by Victor Hugo Fonseca de Jesus, Maria Cecília Mathias-Machado, João Paulo Fogacci de Farias, Marcelo Porfirio Sunagua Aruquipa, Alexandre A. Jácome and Renata D’Alpino Peixoto
Cancers 2023, 15(20), 5015; https://doi.org/10.3390/cancers15205015 - 17 Oct 2023
Cited by 12 | Viewed by 3232
Abstract
Pancreatic ductal adenocarcinoma (PDAC) remains an important cause of cancer-related mortality, and it is expected to play an even bigger part in cancer burden in the years to come. Despite concerted efforts from scientists and physicians, patients have experienced little improvement in survival [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) remains an important cause of cancer-related mortality, and it is expected to play an even bigger part in cancer burden in the years to come. Despite concerted efforts from scientists and physicians, patients have experienced little improvement in survival over the past decades, possibly because of the non-specific nature of the tested treatment modalities. Recently, the discovery of potentially targetable molecular alterations has paved the way for the personalized treatment of PDAC. Indeed, the central piece in the molecular framework of PDAC is starting to be unveiled. KRAS mutations are seen in 90% of PDACs, and multiple studies have demonstrated their pivotal role in pancreatic carcinogenesis. Recent investigations have shed light on the differences in prognosis as well as therapeutic implications of the different KRAS mutations and disentangled the relationship between KRAS and effectors of downstream and parallel signaling pathways. Additionally, the recognition of other mechanisms involving KRAS-mediated pathogenesis, such as KRAS dosing and allelic imbalance, has contributed to broadening the current knowledge regarding this molecular alteration. Finally, KRAS G12C inhibitors have been recently tested in patients with pancreatic cancer with relative success, and inhibitors of KRAS harboring other mutations are under clinical development. These drugs currently represent a true hope for a meaningful leap forward in this dreadful disease. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer Metastasis)
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