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New Emerging Connections in Tumor Angiogenesis, Lymphangiogenesis and Their Therapeutic...
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New Emerging Connections in Tumor Angiogenesis, Lymphangiogenesis and Their Therapeutic Relevance

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

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 12084

Special Issue Editors

Prof. Dr. Curzio R. Rüegg

E-Mail Website
Guest Editor
Faculty of Science and Medicine, University of Fribourg, Fribourg, Switzerland
Interests: breast cancer metastasis; biomarkers; therapy; translational studies
Special Issues, Collections and Topics in MDPI journals
Dr. Jimmy Stalin

E-Mail Website
Co-Guest Editor
Pathology, Department of Oncology, Microbiology and Immunology, Section of Medicine, Faculty of Science and Medicine, University of Fribourg, Chemin du Musée 18, CH-1700 Fribourg, Switzerland
Interests: pathological and physiological angiogenesis; anti-angiogenic therapy; anti-metastatic therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Research on tumor angiogenesis has led to the discovery of cellular and molecular mediators, therapeutic targets, and the development of anti-angiogenic drugs, some of which reached clinical practice. In contrast to the high expectations based on preclinical results, the clinical benefits of anti-angiogenic therapies have remained modest. Subsequent research has shed new light on the complex cross-talk between the tumor vasculature, metabolism, immune system, tumor adaptation, and escape, and heralded new prospects for new therapeutic opportunities. This Special Issue presents review and original articles reporting on emerging horizons in the field of tumor angiogenesis and lymphangiogenesis, and opportunities for new therapeutic strategies.

Prof. Curzio R. Rüegg
Dr. Jimmy Stalin
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

  • inflammation
  • metabolism
  • vascular co-option
  • biomarkers
  • immune response
  • microenvironment
  • combination therapies

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Published Papers (3 papers)

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Research

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20 pages, 9239 KiB  
Article
CD147 Promotes Tumor Lymphangiogenesis in Melanoma via PROX-1
by Coralie Reger de Moura, Alexandra Landras, Farah Khayati, Uwe Maskos, Kamel Maouche, Maxime Battistella, Suzanne Menashi, Céleste Lebbé and Samia Mourah
Cancers 2021, 13(19), 4859; https://doi.org/10.3390/cancers13194859 - 28 Sep 2021
Cited by 7 | Viewed by 2283
Abstract
Malignant melanoma is one of the most aggressive skin cancers and is characterized by early lymph node metastasis and the capacity to develop resistance to therapies. Hence, understanding the regulation of lymphangiogenesis through mechanisms contributing to lymphatic vessel formation represents a treatment strategy [...] Read more.
Malignant melanoma is one of the most aggressive skin cancers and is characterized by early lymph node metastasis and the capacity to develop resistance to therapies. Hence, understanding the regulation of lymphangiogenesis through mechanisms contributing to lymphatic vessel formation represents a treatment strategy for metastatic cancer. We have previously shown that CD147, a transmembrane glycoprotein overexpressed in melanoma, regulates the angiogenic process in endothelial cells. In this study, we show a correlation between high CD147 expression levels and the number of lymphatic vessels expressing LYVE-1, Podoplanin, and VEGFR-3 in human melanoma lymph nodes. CD147 upregulates in vitro lymphangiogenesis and its related mediators through the PROX-1 transcription factor. In vivo studies in a melanoma model confirmed that CD147 is involved in metastasis through a similar mechanism as in vitro. This study, demonstrating the paracrine role of CD147 in the lymphangiogenesis process, suggests that CD147 could be a promising target for the inhibition of melanoma-associated lymphangiogenesis. Full article
(This article belongs to the Special Issue New Emerging Connections in Tumor Angiogenesis, Lymphangiogenesis and Their Therapeutic Relevance)
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21 pages, 9108 KiB  
Article
Targeting OLFML3 in Colorectal Cancer Suppresses Tumor Growth and Angiogenesis, and Increases the Efficacy of Anti-PD1 Based Immunotherapy
by Jimmy Stalin, Beat A. Imhof, Oriana Coquoz, Rachel Jeitziner, Philippe Hammel, Thomas A. McKee, Stephane Jemelin, Marine Poittevin, Marc Pocard, Thomas Matthes, Rachid Kaci, Mauro Delorenzi, Curzio Rüegg and Marijana Miljkovic-Licina
Cancers 2021, 13(18), 4625; https://doi.org/10.3390/cancers13184625 - 15 Sep 2021
Cited by 9 | Viewed by 3604
Abstract
The role of the proangiogenic factor olfactomedin-like 3 (OLFML3) in cancer is unclear. To characterize OLFML3 expression in human cancer and its role during tumor development, we undertook tissue expression studies, gene expression analyses of patient tumor samples, in vivo studies in mouse [...] Read more.
The role of the proangiogenic factor olfactomedin-like 3 (OLFML3) in cancer is unclear. To characterize OLFML3 expression in human cancer and its role during tumor development, we undertook tissue expression studies, gene expression analyses of patient tumor samples, in vivo studies in mouse cancer models, and in vitro coculture experiments. OLFML3 was expressed at high levels, mainly in blood vessels, in multiple human cancers. We focused on colorectal cancer (CRC), as elevated expression of OLFML3 mRNA correlated with shorter relapse-free survival, higher tumor grade, and angiogenic microsatellite stable consensus molecular subtype 4 (CMS4). Treatment of multiple in vivo tumor models with OLFML3-blocking antibodies and deletion of the Olfml3 gene from mice decreased lymphangiogenesis, pericyte coverage, and tumor growth. Antibody-mediated blockade of OLFML3 and deletion of host Olfml3 decreased the recruitment of tumor-promoting tumor-associated macrophages and increased infiltration of the tumor microenvironment by NKT cells. Importantly, targeting OLFML3 increased the antitumor efficacy of anti-PD-1 checkpoint inhibitor therapy. Taken together, the results demonstrate that OLFML3 is a promising candidate therapeutic target for CRC. Full article
(This article belongs to the Special Issue New Emerging Connections in Tumor Angiogenesis, Lymphangiogenesis and Their Therapeutic Relevance)
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Review

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17 pages, 1192 KiB  
Review
The Anti-VEGF(R) Drug Discovery Legacy: Improving Attrition Rates by Breaking the Vicious Cycle of Angiogenesis in Cancer
by Domenico Ribatti, Antonio Giovanni Solimando and Francesco Pezzella
Cancers 2021, 13(14), 3433; https://doi.org/10.3390/cancers13143433 - 8 Jul 2021
Cited by 68 | Viewed by 5422
Abstract
Resistance to anti-vascular endothelial growth factor (VEGF) molecules causes lack of response and disease recurrence. Acquired resistance develops as a result of genetic/epigenetic changes conferring to the cancer cells a drug resistant phenotype. In addition to tumor cells, tumor endothelial cells also undergo [...] Read more.
Resistance to anti-vascular endothelial growth factor (VEGF) molecules causes lack of response and disease recurrence. Acquired resistance develops as a result of genetic/epigenetic changes conferring to the cancer cells a drug resistant phenotype. In addition to tumor cells, tumor endothelial cells also undergo epigenetic modifications involved in resistance to anti-angiogenic therapies. The association of multiple anti-angiogenic molecules or a combination of anti-angiogenic drugs with other treatment regimens have been indicated as alternative therapeutic strategies to overcome resistance to anti-angiogenic therapies. Alternative mechanisms of tumor vasculature, including intussusceptive microvascular growth (IMG), vasculogenic mimicry, and vascular co-option, are involved in resistance to anti-angiogenic therapies. The crosstalk between angiogenesis and immune cells explains the efficacy of combining anti-angiogenic drugs with immune check-point inhibitors. Collectively, in order to increase clinical benefits and overcome resistance to anti-angiogenesis therapies, pan-omics profiling is key. Full article
(This article belongs to the Special Issue New Emerging Connections in Tumor Angiogenesis, Lymphangiogenesis and Their Therapeutic Relevance)
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