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IJMS
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Targeting Blood Vessels in Cancer and Fibrosis
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Targeting Blood Vessels in Cancer and Fibrosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 3309

Special Issue Editor

Dr. José M. Muñoz-Félix

E-Mail Website
Guest Editor
Departamento de Bioquímica y Biología Molecular, Universidad de Salamanca, 37007 Salamanca, Spain
Interests: tumor angiogenesis; vessel co-option; lung metastases; tissue fibrosis; pericytes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Blood vessels are tubes that carry blood throughout an organism. Blood supplies oxygen and nutrients to different tissues. Changes in blood vessels occur in different pathologies such as cancer or tissue fibrosis. Tumors need the formation of a fine network of blood vessels to provide nutrients to cancer cells. However, tumor vasculature is normally immature and leaky and generates hypoxia in tumor cells that mediate therapy resistance and metastasis. For this reason, the modulation of tumor vasculature using different strategies such as anti-angiogenesis or vessel normalization is an interesting approach to enhance the efficacy of cancer therapy. Fibrotic diseases in organs such as the lungs, liver, heart or kidneys are characterized by the accumulation of extracellular matrices in the tissue parenchyma and microvascular rarefaction that also lead to tissue hypoxia. The modulation of microvasculature in fibrotic tissues to eliminate hypoxia and control the buildup of extracellular matrix is also being explored.

This Special Issue welcomes original articles and reviews focused on the novelties in the modulation of blood vessels in cancer and fibrotic diseases.

Dr. José M. Muñoz-Félix
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • blood vessels
  • angiogenesis
  • fibrosis
  • fibroblasts
  • hypoxia
  • pericytes

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Published Papers (2 papers)

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Research

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10 pages, 1557 KiB  
Article
Targeting the Tumor Vascular Supply to Enhance Radiation Therapy Administered in Single or Clinically Relevant Fractionated Schedules
by Michael R. Horsman
Int. J. Mol. Sci. 2024, 25(15), 8078; https://doi.org/10.3390/ijms25158078 - 24 Jul 2024
Viewed by 658
Abstract
This pre-clinical study was designed to demonstrate how vascular disrupting agents (VDAs) should be administered, either alone or when combined with radiation in clinically relevant fractionated radiation schedules, for the optimal anti-tumor effect. CDF1 mice, implanted in the right rear foot with a [...] Read more.
This pre-clinical study was designed to demonstrate how vascular disrupting agents (VDAs) should be administered, either alone or when combined with radiation in clinically relevant fractionated radiation schedules, for the optimal anti-tumor effect. CDF1 mice, implanted in the right rear foot with a 200 mm3 murine C3H mammary carcinoma, were injected with various doses of the most potent VDA drug, combretastatin A-1 phosphate (CA1P), under different schedules. Tumors were also locally irradiated with single-dose, or stereotactic (3 × 5–20 Gy) or conventional (30 × 2 Gy) fractionation schedules. Tumor growth and control were the endpoints used. Untreated tumors had a tumor growth time (TGT5; time to grow to 5 times the original treatment volume) of around 6 days. This increased with increasing drug doses (5–100 mg/kg). However, with single-drug treatments, the maximum TGT5 was only 10 days, yet this increased to 19 days when injecting the drug on a weekly basis or as three treatments in one week. CA1P enhanced radiation response regardless of the schedule or interval between the VDA and radiation. There was a dose-dependent increase in radiation response when the combined with a single, stereotactic, or conventional fractionated irradiation, but these enhancements plateaued at around a drug dose of 25 mg/kg. This pre-clinical study demonstrated how VDAs should be combined with clinically applicable fractionated radiation schedules for the optimal anti-tumor effect, thus suggesting the necessary pre-clinical testing required to ultimately establish VDAs in clinical practice. Full article
(This article belongs to the Special Issue Targeting Blood Vessels in Cancer and Fibrosis)
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Review

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27 pages, 2650 KiB  
Review
The Inhibition of Vessel Co-Option as an Emerging Strategy for Cancer Therapy
by Iván Carrera-Aguado, Laura Marcos-Zazo, Patricia Carrancio-Salán, Elena Guerra-Paes, Fernando Sánchez-Juanes and José M. Muñoz-Félix
Int. J. Mol. Sci. 2024, 25(2), 921; https://doi.org/10.3390/ijms25020921 - 11 Jan 2024
Cited by 2 | Viewed by 2305
Abstract
Vessel co-option (VCO) is a non-angiogenic mechanism of vascularization that has been associated to anti-angiogenic therapy. In VCO, cancer cells hijack the pre-existing blood vessels and use them to obtain oxygen and nutrients and invade adjacent tissue. Multiple primary tumors and metastases undergo [...] Read more.
Vessel co-option (VCO) is a non-angiogenic mechanism of vascularization that has been associated to anti-angiogenic therapy. In VCO, cancer cells hijack the pre-existing blood vessels and use them to obtain oxygen and nutrients and invade adjacent tissue. Multiple primary tumors and metastases undergo VCO in highly vascularized tissues such as the lungs, liver or brain. VCO has been associated with a worse prognosis. The cellular and molecular mechanisms that undergo VCO are poorly understood. Recent studies have demonstrated that co-opted vessels show a quiescent phenotype in contrast to angiogenic tumor blood vessels. On the other hand, it is believed that during VCO, cancer cells are adhered to basement membrane from pre-existing blood vessels by using integrins, show enhanced motility and a mesenchymal phenotype. Other components of the tumor microenvironment (TME) such as extracellular matrix, immune cells or extracellular vesicles play important roles in vessel co-option maintenance. There are no strategies to inhibit VCO, and thus, to eliminate resistance to anti-angiogenic therapy. This review summarizes all the molecular mechanisms involved in vessel co-option analyzing the possible therapeutic strategies to inhibit this process. Full article
(This article belongs to the Special Issue Targeting Blood Vessels in Cancer and Fibrosis)
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