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Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment
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Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Oncology".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 24651

Special Issue Editor

Prof. Dr. Maja H. Oktay

E-Mail Website
Guest Editor
Department of Pathology, Department of Anatomy and Structural Biology, Albert Einstein College of Medicine/ Montefiore Medical Canter, Bronx, NY 10580, USA
Interests: tumor microenvironment; metastatic cancer cell dissemination; the effect of chemotherapy on tumor microenvironment; prognostic and predictive biomarkers of tumor dissemination

Special Issue Information

Dear Colleagues,

Extensive experimental evidence indicates that the tumor microenvironment (TME) regulates the phenotype of cancer cells. The TME particularly affects the induction of epithelial to mesenchymal transition (EMT) and activation of stem program, two processes critical for the acquisition of disseminating cancer cells. Moreover, there is a growing body of evidence indicating that therapies commonly used for treatment of cancer patients may modify TME and affect cancer progression. Since cancer cell dissemination causes 90% of cancer-related mortality, translation of this knowledge to the clinic could significantly impact our approach to the prognosis and treatment of cancer patients.

The aim of this Special Issue is to update current concepts regarding the effect of TME on cancer cell dissemination and the effect of various therapies currently used to treat cancer patients on TME and disease progression. In addition, this issue will provide a summary of current biomarkers and treatments that specifically target cancer cell dissemination. Therefore, we would like to invite original research, state-of-the-art reviews, and viewpoints. In particular, we encourage the submission of manuscripts covering important items regarding the effect of TME on disseminating cancer cell phenotype, the effect of current therapies on TME, and cancer cell dissemination, as well as the development of novel biomarkers and therapeutics targeting cancer cell dissemination.

We look forward to your submissions!

Prof. Dr. Maja H. Oktay
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. Journal of Clinical Medicine 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 2600 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

  • Tumor microenvironment
  • Disseminating cancer cell phenotype
  • Metastasis
  • Epithelial to mesenchymal transition
  • Stem program
  • Dissemination biomarkers
  • Therapies targeting cancer cell dissemination

Published Papers (6 papers)

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Review

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12 pages, 1105 KiB  
Review
Invasion and Metastasis as a Central Hallmark of Breast Cancer
by Trishna Saha, Jonathan Solomon, Abraham O. Samson and Hava Gil-Henn
J. Clin. Med. 2021, 10(16), 3498; https://doi.org/10.3390/jcm10163498 - 8 Aug 2021
Cited by 25 | Viewed by 5654
Abstract
Hanahan and Weinberg introduced the “hallmarks of cancer” and typified essential biological abilities acquired by human cancer. Since then, a growing understanding of hallmark principles associated with breast cancer has assisted knowledge-based therapeutics development; however, despite the rapidly increasing number of targeted therapeutics, [...] Read more.
Hanahan and Weinberg introduced the “hallmarks of cancer” and typified essential biological abilities acquired by human cancer. Since then, a growing understanding of hallmark principles associated with breast cancer has assisted knowledge-based therapeutics development; however, despite the rapidly increasing number of targeted therapeutics, enduring disease-free responses for most forms of breast cancer is rare. Invasion and metastasis are the most defining feature of breast cancer malignancy and the leading cause of patient mortality. Hence, we propose a modified hallmarks model adapted to breast cancer, in which invasion and metastasis are shifted to the center of attention, thereby emphasizing it as a potentially superior therapeutic target. Although the scientific community highly appreciates the importance of the invasion and metastasis hallmark, as can be demonstrated by the growing number of publications on breast cancer metastasis, very few clinical trials concentrate on testing anti-metastasis inhibitors and even fewer trials focus on inhibitors for breast cancer metastasis. Here, we discuss the obstacles of applying research on invasion and metastasis therapeutics into the clinic and present current developments that could provide a potential solution to this dilemma. Full article
(This article belongs to the Special Issue Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment)
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16 pages, 1696 KiB  
Review
ADAM 17 and Epithelial-to-Mesenchymal Transition: The Evolving Story and Its Link to Fibrosis and Cancer
by Margherita Sisto, Domenico Ribatti and Sabrina Lisi
J. Clin. Med. 2021, 10(15), 3373; https://doi.org/10.3390/jcm10153373 - 29 Jul 2021
Cited by 14 | Viewed by 3071
Abstract
For decades, metalloproteinase 17 (ADAM17) has been the goal of wide investigation. Since its discovery as the tumour necrosis factor-α convertase, it has been studied as the main drug target, especially in the context of inflammatory conditions and tumour. In fact, evidence is [...] Read more.
For decades, metalloproteinase 17 (ADAM17) has been the goal of wide investigation. Since its discovery as the tumour necrosis factor-α convertase, it has been studied as the main drug target, especially in the context of inflammatory conditions and tumour. In fact, evidence is mounting to support a key role of ADAM17 in the induction of the proliferation, migration and progression of tumour cells and the trigger of the pro-fibrotic process during chronic inflammatory conditions; this occurs, probably, through the activation of epithelial-to-mesenchymal transition (EMT). EMT is a central morphologic conversion that occurs in adults during wound healing, tumour progression and organ fibrosis. EMT is characterised by the disassembly of cell–cell contacts, remodelling of the actin cytoskeleton and separation of cells, and generates fibroblast-like cells that express mesenchymal markers and have migratory properties. This transition is characterised by loss of epithelial proteins such as E-cadherin and the acquisition of new mesenchymal markers, including vimentin and a-smooth muscle actin. The present review discusses the current understanding of molecular mechanisms involved in ADAM17-dependent EMT in order to individuate innovative therapeutic strategies using ADAM17-related pathways. Full article
(This article belongs to the Special Issue Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment)
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11 pages, 624 KiB  
Review
Prostate Cancer Dormancy and Reactivation in Bone Marrow
by Deepak K. Singh, Vaibhav G. Patel, William K. Oh and Julio A. Aguirre-Ghiso
J. Clin. Med. 2021, 10(12), 2648; https://doi.org/10.3390/jcm10122648 - 16 Jun 2021
Cited by 9 | Viewed by 4297
Abstract
Prostate cancer has a variable clinical course, ranging from curable local disease to lethal metastatic spread. Eradicating metastatic cells is a unique challenge that is rarely met with the available therapies. Thus, targeting prostate cancer cells in earlier disease states is a crucial [...] Read more.
Prostate cancer has a variable clinical course, ranging from curable local disease to lethal metastatic spread. Eradicating metastatic cells is a unique challenge that is rarely met with the available therapies. Thus, targeting prostate cancer cells in earlier disease states is a crucial window of opportunity. Interestingly, cancer cells migrate from their primary site during pre-cancerous and malignant phases to seed secondary organs. These cells, known as disseminated cancer cells (DCCs), may remain dormant for months or decades before activating to form metastases. Bone marrow, a dormancy-permissive site, is the major organ for housed DCCs and eventual metastases in prostate cancer. The dynamic interplay between DCCs and the primary tumor microenvironment (TME), as well as that between DCCs and the secondary organ niche, controls the conversion between states of dormancy and activation. Here, we discuss recent discoveries that have improved our understanding of dormancy signaling and the role of the TME in modulating the epigenetic reprogramming of DCCs. We offer potential strategies to target DCCs in prostate cancer. Full article
(This article belongs to the Special Issue Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment)
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20 pages, 1124 KiB  
Review
Epithelial-to-Mesenchymal Transition in the Light of Plasticity and Hybrid E/M States
by Laura Bornes, Guillaume Belthier and Jacco van Rheenen
J. Clin. Med. 2021, 10(11), 2403; https://doi.org/10.3390/jcm10112403 - 29 May 2021
Cited by 28 | Viewed by 4533
Abstract
Epithelial-to-mesenchymal transition (EMT) is a cellular program which leads to cells losing epithelial features, including cell polarity, cell–cell adhesion and attachment to the basement membrane, while gaining mesenchymal characteristics, such as invasive properties and stemness. This program is involved in embryogenesis, wound healing [...] Read more.
Epithelial-to-mesenchymal transition (EMT) is a cellular program which leads to cells losing epithelial features, including cell polarity, cell–cell adhesion and attachment to the basement membrane, while gaining mesenchymal characteristics, such as invasive properties and stemness. This program is involved in embryogenesis, wound healing and cancer progression. Over the years, the role of EMT in cancer progression has been heavily debated, and the requirement of this process in metastasis even has been disputed. In this review, we discuss previous discrepancies in the light of recent findings on EMT, plasticity and hybrid E/M states. Moreover, we highlight various tumor microenvironmental cues and cell intrinsic signaling pathways that induce and sustain EMT programs, plasticity and hybrid E/M states. Lastly, we discuss how recent findings on plasticity, especially on those that enable cells to switch between hybrid E/M states, have changed our understanding on the role of EMT in cancer metastasis, stemness and therapy resistance. Full article
(This article belongs to the Special Issue Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment)
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23 pages, 1947 KiB  
Review
The Dichotomous Role of Bone Marrow Derived Cells in the Chemotherapy-Treated Tumor Microenvironment
by Avital Vorontsova, Tal Kan, Ziv Raviv and Yuval Shaked
J. Clin. Med. 2020, 9(12), 3912; https://doi.org/10.3390/jcm9123912 - 2 Dec 2020
Cited by 6 | Viewed by 2648
Abstract
Bone marrow derived cells (BMDCs) play a wide variety of pro- and anti-tumorigenic roles in the tumor microenvironment (TME) and in the metastatic process. In response to chemotherapy, the anti-tumorigenic function of BMDCs can be enhanced due to chemotherapy-induced immunogenic cell death. However, [...] Read more.
Bone marrow derived cells (BMDCs) play a wide variety of pro- and anti-tumorigenic roles in the tumor microenvironment (TME) and in the metastatic process. In response to chemotherapy, the anti-tumorigenic function of BMDCs can be enhanced due to chemotherapy-induced immunogenic cell death. However, in recent years, a growing body of evidence suggests that chemotherapy or other anti-cancer drugs can also facilitate a pro-tumorigenic function in BMDCs. This includes elevated angiogenesis, tumor cell proliferation and pro-tumorigenic immune modulation, ultimately contributing to therapy resistance. Such effects do not only contribute to the re-growth of primary tumors but can also support metastasis. Thus, the delicate balance of BMDC activities in the TME is violated following tumor perturbation, further requiring a better understanding of the complex crosstalk between tumor cells and BMDCs. In this review, we discuss the different types of BMDCs that reside in the TME and their activities in tumors following chemotherapy, with a major focus on their pro-tumorigenic role. We also cover aspects of rationally designed combination treatments that target or manipulate specific BMDC types to improve therapy outcomes. Full article
(This article belongs to the Special Issue Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment)
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9 pages, 985 KiB  
Brief Report
Breast Cancer Cell Re-Dissemination from Lung Metastases—A Mechanism for Enhancing Metastatic Burden
by Lucia Borriello, John Condeelis, David Entenberg and Maja H. Oktay
J. Clin. Med. 2021, 10(11), 2340; https://doi.org/10.3390/jcm10112340 - 27 May 2021
Cited by 12 | Viewed by 3658
Abstract
Although metastatic disease is the primary cause of mortality in cancer patients, the mechanisms leading to overwhelming metastatic burden are still incompletely understood. Metastases are the endpoint of a series of multi-step events involving cancer cell intravasation, dissemination to distant organs, and outgrowth [...] Read more.
Although metastatic disease is the primary cause of mortality in cancer patients, the mechanisms leading to overwhelming metastatic burden are still incompletely understood. Metastases are the endpoint of a series of multi-step events involving cancer cell intravasation, dissemination to distant organs, and outgrowth to metastatic colonies. Here we show, for the first-time, that breast cancer cells do not solely disseminate to distant organs from primary tumors and metastatic nodules in the lymph nodes, but also do so from lung metastases. Thus, our findings indicate that metastatic dissemination could continue even after the removal of the primary tumor. Provided that the re-disseminated cancer cells initiate growth upon arrival to distant sites, cancer cell re-dissemination from metastatic foci could be one of the crucial mechanisms leading to overt metastases and patient demise. Therefore, the development of new therapeutic strategies to block cancer cell re-dissemination would be crucial to improving survival of patients with metastatic disease. Full article
(This article belongs to the Special Issue Cutting-Edge Topics in Cancer Cell Dissemination and Tumor Microenvironment)
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