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Cancers
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Advances in Tumor Angiogenesis
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Advances in Tumor Angiogenesis

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (20 November 2022) | Viewed by 14780

Special Issue Editor

Dr. Francesca Margheri

E-Mail Website
Guest Editor
Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Florence, 50134 Firenze, Italy
Interests: fibrinolytic system (uPA/uPAR system); tumour invasion and metastasis; angiogenesis; tumour extracellular vesicles; tumour microenvironment; melanoma cells; endothelial cells; cancer immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Angiogenesis is the process of formation of new blood vessels orchestrated by proangiogenic and antiangiogenic factors during development, reproduction, and repair. Of utmost importance is pathological angiogenesis, especially in the context of neoplastic disease. Tumor cells rapidly proliferate and need a continuous supply of oxygen and nutrients and thereby have a steady requirement for infiltrating blood vessels. Angiogenesis is one of the hallmarks of cancer. Targeting the angiogenic process is regarded as a logical approach to the treatment of various malignancies, and, as such, various antiangiogenic treatment agents have been developed and tested in clinical trials. Here, we focus on new anti-angiogenic strategies and on vessel remodeling in response to evidence demonstrating that vessel normalization and tumor oxygenation are intertwined and crucial for combination therapies. In particular, the aim of this Special Issue is to identify new therapeutic options in order to inhibit tumor vascularization or to improve vessel normalization in tumors.

Dr. Francesca Margheri
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. 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

  • tumor
  • angiogenesis
  • new anti-angiogenic strategies
  • vessel remodeling

Published Papers (6 papers)

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Research

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14 pages, 4913 KiB  
Article
The Mutually Mediated Chloride Intracellular Channel Protein 1 (CLIC1) Relationship between Malignant Cells and Tumor Blood Vessel Endothelium Exhibits a Significant Impact on Tumor Angiogenesis, Progression, and Metastasis in Clear Cell Renal Cell Carcinoma (ccRCC)
by Adela Maria Ferician, Ovidiu Catalin Ferician, Alexandru Nesiu, Andrei Alexandru Cosma, Borislav Dusan Caplar, Eugen Melnic and Anca Maria Cimpean
Cancers 2022, 14(23), 5981; https://doi.org/10.3390/cancers14235981 - 3 Dec 2022
Cited by 3 | Viewed by 1190
Abstract
Background: Overexpression of chloride intracellular channel protein 1 (CLIC1) in tumor cells has been confirmed, but it has received less attention in the tumor blood vessel endothelium. Aim: The assessment of CLIC1 expression in ccRCC tumor blood vessels and its relationship with TNM [...] Read more.
Background: Overexpression of chloride intracellular channel protein 1 (CLIC1) in tumor cells has been confirmed, but it has received less attention in the tumor blood vessel endothelium. Aim: The assessment of CLIC1 expression in ccRCC tumor blood vessels and its relationship with TNM parameters and tumor cell CLIC1 expression. Methods: CLIC1 immunostaining in ccRCC was evaluated in 50 cases in both malignant cells and tumor blood vessels (CLIC1 microvessel density-CLIC1-MVD) and was correlated with TNM staging parameters. Results: CLIC1-MVD was observed in approximately 65% of cases, and CLIC1 co-localization in both tumor and endothelial cells was observed in 59% of cases. ccRCC was classified into four groups (Classes 0–3) based on the percentage of positive tumor cells, with each group including sub-groups defined by CLIC1 expression in the endothelium. Class 3 (60–100% positive tumor cells) had the highest CLIC1-MVD, with an impact on T and M parameters (p value = 0.007 for T, and p value = 0.006 for M). For cases with CLIC1 intracellular translocation, there was a strong correlation between CLIC1-MVD and M (p value < 0.001). Conclusions: Co-expression of ccRCC tumor and endothelial cells promotes tumor progression and metastasis and should be investigated further as a potential therapeutic target for ccRCC and other human malignancies. Full article
(This article belongs to the Special Issue Advances in Tumor Angiogenesis)
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18 pages, 5293 KiB  
Article
Anti-PTK7 Monoclonal Antibodies Inhibit Angiogenesis by Suppressing PTK7 Function
by Si Won Oh, Won-Sik Shin and Seung-Taek Lee
Cancers 2022, 14(18), 4463; https://doi.org/10.3390/cancers14184463 - 14 Sep 2022
Cited by 8 | Viewed by 1984
Abstract
PTK7, a catalytically defective receptor protein tyrosine kinase, promotes angiogenesis by activating KDR through direct interaction and induction of KDR oligomerization. This study developed anti-PTK7 monoclonal antibodies (mAbs) to regulate angiogenesis by inhibiting PTK7 function. The effect of anti-PTK7 mAbs on vascular endothelial [...] Read more.
PTK7, a catalytically defective receptor protein tyrosine kinase, promotes angiogenesis by activating KDR through direct interaction and induction of KDR oligomerization. This study developed anti-PTK7 monoclonal antibodies (mAbs) to regulate angiogenesis by inhibiting PTK7 function. The effect of anti-PTK7 mAbs on vascular endothelial growth factor (VEGF)-induced angiogenic phenotypes in human umbilical vascular endothelial cells (HUVECs) was examined. Analysis of mAb binding with PTK7 deletion mutants revealed that mAb-43 and mAb-52 recognize immunoglobulin (Ig) domain 2 of PTK7, whereas mAb-32 and mAb-50 recognize Ig domains 6–7. Anti-PTK7 mAbs inhibited VEGF-induced adhesion and wound healing in HUVECs. mAb-32, mAb-43, and mAb-52 dose-dependently mitigated VEGF-induced migration and invasion in HUVECs without exerting cytotoxic effects. Additionally, mAb-32, mAb-43, and mAb-52 inhibited capillary-like tube formation in HUVECs, and mAb-32 and mAb-43 suppressed angiogenesis ex vivo (aortic ring assay) and in vivo (Matrigel plug assay). Furthermore, mAb-32 and mAb-43 downregulated VEGF-induced KDR activation and downstream signaling and inhibited PTK7–KDR interaction in PTK7-overexpressing and KDR-overexpressing HEK293 cells. Thus, anti-PTK7 mAbs inhibit angiogenic phenotypes by blocking PTK7–KDR interaction. These findings indicate that anti-PTK7 mAbs that neutralize PTK7 function can alleviate impaired angiogenesis-associated pathological conditions, such as cancer metastasis. Full article
(This article belongs to the Special Issue Advances in Tumor Angiogenesis)
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16 pages, 3896 KiB  
Article
Periostin Exon-21 Antibody Neutralization of Triple-Negative Breast Cancer Cell-Derived Periostin Regulates Tumor-Associated Macrophage Polarization and Angiogenesis
by Tatsuya Fujikawa, Fumihiro Sanada, Yoshiaki Taniyama, Kana Shibata, Naruto Katsuragi, Nobutaka Koibuchi, Kaori Akazawa, Yuko Kanemoto, Hidehito Kuroyanagi, Kenzo Shimazu, Hiromi Rakugi and Ryuichi Morishita
Cancers 2021, 13(20), 5072; https://doi.org/10.3390/cancers13205072 - 11 Oct 2021
Cited by 4 | Viewed by 2830
Abstract
Periostin (Pn) is involved in multiple processes of cancer progression. Previously, we reported that Pn expression is correlated with mesenchymal tumor markers and poor prognosis in triple-negative breast cancer (TNBC). In the TNBC xenograft model, chemotherapy increased expression of a Pn alternative splicing [...] Read more.
Periostin (Pn) is involved in multiple processes of cancer progression. Previously, we reported that Pn expression is correlated with mesenchymal tumor markers and poor prognosis in triple-negative breast cancer (TNBC). In the TNBC xenograft model, chemotherapy increased expression of a Pn alternative splicing variant (ASV) with exon 21, and administration of the neutralizing antibody against Pn with exon 21 (Pn-21 Ab) overcame chemoresistance with a reduction in the mesenchymal cancer cell fraction. In the present study, the role of Pn ASV with exon 21 in TNBC progression has been addressed. We first established a stable cell line carrying a fluorescence-based splicing reporter. Pn-positive TNBC has higher expression of genes related to tumor-associated macrophage (TAM) recruitment and ECM-receptor interaction than Pn-negative cells. In a xenograft model, only Pn-positive cells initiated tumor formation, and the Pn-21 Ab suppressed tumor cell growth, accompanied by decreased M2 TAM polarization and the number of tumor vessels. These data suggest that cancer cell-derived Pn ASV educates TAMs and regulates angiogenesis, which in turn establishes a microenvironmental niche that is supportive of TNBC. Full article
(This article belongs to the Special Issue Advances in Tumor Angiogenesis)
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Review

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15 pages, 912 KiB  
Review
Squalamines in Blockade of Tumor-Associated Angiogenesis and Cancer Progression
by Colin Sterling, Jr., Diana Márquez-Garbán, Jaydutt V. Vadgama and Richard J. Pietras
Cancers 2022, 14(20), 5154; https://doi.org/10.3390/cancers14205154 - 21 Oct 2022
Cited by 1 | Viewed by 1721
Abstract
Mechanisms of action of squalamine in human vascular endothelial cells indicate that this compound attaches to cell membranes, potentially interacting with calmodulin, Na+/H+ exchanger isoform NHE3 and other signaling pathways involved in the angiogenic process. Thus, squalamine elicits blockade of [...] Read more.
Mechanisms of action of squalamine in human vascular endothelial cells indicate that this compound attaches to cell membranes, potentially interacting with calmodulin, Na+/H+ exchanger isoform NHE3 and other signaling pathways involved in the angiogenic process. Thus, squalamine elicits blockade of VEGF-induced endothelial tube-like formation in vitro. Further, squalamine reduces growth of several preclinical models of human cancers in vivo and acts to stop metastatic tumor spread, actions due largely to blockade of angiogenesis induced by the tumor and tumor microenvironment. Squalamine in Phase I/II trials, alone or combined with standard care, shows promising antitumor activity with limited side-effects in patients with advanced solid cancers. Increased attention on squalamine regulation of signaling pathways with or without combination treatments in solid malignancies deserves further study. Full article
(This article belongs to the Special Issue Advances in Tumor Angiogenesis)
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21 pages, 1737 KiB  
Review
The Role of Periostin in Angiogenesis and Lymphangiogenesis in Tumors
by Adrian Wasik, Katarzyna Ratajczak-Wielgomas, Arkadiusz Badzinski, Piotr Dziegiel and Marzenna Podhorska-Okolow
Cancers 2022, 14(17), 4225; https://doi.org/10.3390/cancers14174225 - 30 Aug 2022
Cited by 8 | Viewed by 3191
Abstract
Periostin (POSTN) is a protein that is part of the extracellular matrix (ECM) and which significantly affects the control of intracellular signaling pathways (PI3K-AKT, FAK) through binding integrin receptors (αvβ3, αvβ5, α6β4). In addition, increased POSTN expression enhances the expression of VEGF family [...] Read more.
Periostin (POSTN) is a protein that is part of the extracellular matrix (ECM) and which significantly affects the control of intracellular signaling pathways (PI3K-AKT, FAK) through binding integrin receptors (αvβ3, αvβ5, α6β4). In addition, increased POSTN expression enhances the expression of VEGF family growth factors and promotes Erk phosphorylation. As a result, this glycoprotein controls the Erk/VEGF pathway. Therefore, it plays a crucial role in the formation of new blood and lymphatic vessels, which may be significant in the process of metastasis. Moreover, POSTN is involved in the proliferation, progression, migration and epithelial-mesenchymal transition (EMT) of tumor cells. Its increased expression has been detected in many cancers, including breast cancer, ovarian cancer, non-small cell lung carcinoma and glioblastoma. Many studies have shown that this protein may be an independent prognostic and predictive factor in many cancers, which may influence the choice of optimal therapy. Full article
(This article belongs to the Special Issue Advances in Tumor Angiogenesis)
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21 pages, 1456 KiB  
Review
Propensity for Early Metastatic Spread in Breast Cancer: Role of Tumor Vascularization Features and Tumor Immune Infiltrate
by Mario Rosario D’Andrea, Vittore Cereda, Luigi Coppola, Guido Giordano, Andrea Remo and Elena De Santis
Cancers 2021, 13(23), 5917; https://doi.org/10.3390/cancers13235917 - 25 Nov 2021
Cited by 6 | Viewed by 2903
Abstract
Breast cancer is a complex and highly heterogeneous disease consisting of various subtypes. It is classified into human epidermal growth receptor 2 (HER-2)-enriched, luminal A, luminal B and basal-like/triple negative (TNBC) breast cancer, based on histological and molecular features. At present, clinical decision-making [...] Read more.
Breast cancer is a complex and highly heterogeneous disease consisting of various subtypes. It is classified into human epidermal growth receptor 2 (HER-2)-enriched, luminal A, luminal B and basal-like/triple negative (TNBC) breast cancer, based on histological and molecular features. At present, clinical decision-making in breast cancer is focused only on the assessment of tumor cells; nevertheless, it has been recognized that the tumor microenvironment (TME) plays a critical biologic role in breast cancer. This is constituted by a large group of immune and non-immune cells, but also by non-cellular components, such as several cytokines. TME is deeply involved in angiogenesis, immune-evasion strategies, and propensity for early metastatic spread, impacting on prognosis and prediction of response to specific treatments. In this review, we focused our attention on the early morphological changes of tumor microenvironment (tumor vasculature features, presence of immune and non-immune cells infiltrating the stroma, levels of cytokines) during breast cancer development. At the same time, we correlate these characteristics with early metastatic propensity (defined as synchronous metastasis or early recurrence) with particular attention to breast cancer subtypes. Full article
(This article belongs to the Special Issue Advances in Tumor Angiogenesis)
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