Non-angiogenic Tumours: From Cellular Mechanisms to Novel Therapeutic Approaches

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 10861

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Nuffield Division of Clinical Laboratory Science, Nuffield Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK
Interests: relationship between cancer cells and blood vessels
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Special Issue Information

“The great tragedy of science - the slaying of a beautiful hypothesis by an ugly fact.” Thomas Huxley

Dear Colleagues,

In 1996, the European Journal of Cancer published a special issue on angiogenesis in cancer: it was firmly about the idea that angiogenesis, i.e., the formation of new vessels, is essential for a neoplasm to grow bigger than a micro-nodule of cells a few millimeters in diameter. Indeed, four years later, “Inducing angiogenesis” came to be regarded as one of the original six Hallmarks of cancer. As frequently happens, nature is actually by far more complex, as evidence emerged that tumours can also grow in absence of angiogenesis, and this type of growth is also rather aggressive.

Two mains areas of investigation have since developed, one more focused on describing non-angiogenic tumours and investigating why a cell would grow to elicit angiogenesis or rather exploiting by vascular co-option the pre-existing normal vessels of the body. Of course, many overlaps between the two fields occur.

In this collection, we will focus more on the identification and description of non-angiogenic tumours, their biology, and, last but not least, their interaction with cancer treatments, in particular those trying to exploit anti-angiogenic compounds.

It is our sincere hope that all this will attract your attention, and we look forward to your contributions to this Special Issue.

Prof. Francesco Pezzella
Guest Editor

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Keywords

  • cancer
  • angiogenic
  • non-angiogenic
  • vascular co-option
  • hypoxia

Published Papers (2 papers)

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Review

17 pages, 2796 KiB  
Review
Vasculogenic Mimicry in Breast Cancer: Clinical Relevance and Drivers
by Gabriela Morales-Guadarrama, Rocío García-Becerra, Edgar Armando Méndez-Pérez, Janice García-Quiroz, Euclides Avila and Lorenza Díaz
Cells 2021, 10(7), 1758; https://doi.org/10.3390/cells10071758 - 12 Jul 2021
Cited by 31 | Viewed by 6823
Abstract
In solid tumors, vasculogenic mimicry (VM) is the formation of vascular structures by cancer cells, allowing to generate a channel-network able to transport blood and tumor cells. While angiogenesis is undertaken by endothelial cells, VM is assumed by cancer cells. Besides the participation [...] Read more.
In solid tumors, vasculogenic mimicry (VM) is the formation of vascular structures by cancer cells, allowing to generate a channel-network able to transport blood and tumor cells. While angiogenesis is undertaken by endothelial cells, VM is assumed by cancer cells. Besides the participation of VM in tumor neovascularization, the clinical relevance of this process resides in its ability to favor metastasis and to drive resistance to antiangiogenic therapy. VM occurs in many tumor types, including breast cancer, where it has been associated with a more malignant phenotype, such as triple-negative and HER2-positive tumors. The latter may be explained by known drivers of VM, like hypoxia, TGFB, TWIST1, EPHA2, VEGF, matrix metalloproteinases, and other tumor microenvironment-derived factors, which altogether induce the transformation of tumor cells to a mesenchymal phenotype with a high expression rate of stemness markers. This review analyzes the current literature in the field, including the participation of some microRNAs and long noncoding RNAs in VM-regulation and tumorigenesis of breast cancer. Considering the clinical relevance of VM and its association with the tumor phenotype and clinicopathological parameters, further studies are granted to target VM in the clinic. Full article
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13 pages, 3868 KiB  
Review
Overview on the Different Patterns of Tumor Vascularization
by Domenico Ribatti and Francesco Pezzella
Cells 2021, 10(3), 639; https://doi.org/10.3390/cells10030639 - 13 Mar 2021
Cited by 38 | Viewed by 3509
Abstract
Angiogenesis is a crucial event in the physiological processes of embryogenesis and wound healing. During malignant transformation, dysregulation of angiogenesis leads to the formation of a vascular network of tumor-associated capillaries promoting survival and proliferation of the tumor cells. Starting with the hypothesis [...] Read more.
Angiogenesis is a crucial event in the physiological processes of embryogenesis and wound healing. During malignant transformation, dysregulation of angiogenesis leads to the formation of a vascular network of tumor-associated capillaries promoting survival and proliferation of the tumor cells. Starting with the hypothesis formulated by Judah Folkman that tumor growth is angiogenesis-dependent, this area of research has a solid scientific foundation and inhibition of angiogenesis is a major area of therapeutic development for the treatment of cancer. Over this period numerous authors published data of vascularization of tumors, which attributed the cause of neo-vascularization to various factors including inflammation, release of angiogenic cytokines, vasodilatation, and increased tumor metabolism. More recently, it has been demonstrated that tumor vasculature is not necessarily derived by endothelial cell proliferation and sprouting of new capillaries, but alternative vascularization mechanisms have been described, namely vascular co-option and vasculogenic mimicry. In this article, we have analyzed the mechanisms involved in tumor vascularization in association with classical angiogenesis, including post-natal vasculogenesis, intussusceptive microvascular growth, vascular co-option, and vasculogenic mimicry. We have also discussed the role of these alternative mechanism in resistance to anti-angiogenic therapy and potential therapeutic approaches to overcome resistance. Full article
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