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Boundaries of Cancer and Cardiovascular Diseases
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Boundaries of Cancer and Cardiovascular Diseases

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: closed (28 February 2021) | Viewed by 12569

Special Issue Editors

Prof. Dr. Godefridus J. Peters

E-Mail Website
Guest Editor
1. Department of Medical Oncology, Amsterdam University Medical Centers, Amsterdam, The Netherlands
2. Department of Biochemistry, Medical University of Gdansk, Gdansk, Poland
Interests: lung cancer; pharmacology of anticancer; drug development; combination therapies; transporters; drug metabolism
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Ryszard T. Smolenski

E-Mail Website
Guest Editor
Department of Biochemistry, Medical University of Gdansk, 1 Debinki Str, 80–210 Gdansk, Poland
Interests: nucleotides; adenosine; cardioprotection; atherosclerosis; heart failure; xenotransplantation

Special Issue Information

Dear Colleagues,

Cardiovascular diseases and cancer are two life-threatening diseases that are responsible for the majority of deaths worldwide. Both diseases remains a major focus in healthcare and research.  However, clinically and in research they are usually considered as separate entities, which undermines the potential of interaction since exchange of scientific knowledge can benefit each field. Cardiovascular side effects of anticancer drugs is a most obvious interaction, but there are many other. Some treatment strategies have opposite targets. In cardiovascular diseases the focus is on restoring normal vascular function and to increase blood supply. In contrast, cancer treatment aims to destroy or prevent new angiogenesis of a tumor. In all mentioned areas endothelium seems to play a critical role since this tissue could be a target for cancer drug toxicity and it is an essential component that controls blood supply through angiogenesis and flow adjustments. Moreover, there are many common metabolic disturbances such as abnormal one-carbon metabolism. Reduced oxygen supply and hypoxia seem to affect both diseases, although from a different perspective. The importance of these interactions was recently appreciated by establishing cardio-oncology aa a sub-specialty in the medical field. Therefore attempts to summarize and highlight such interactions are fully justified. In this special issue we aim to bring together research on the borderline between cardiology and oncology with the aim to develop cardio-oncology, but also to enhance each area separately.

Prof. Dr. Godefridus J. Peters
Prof. Dr. Ryszard T. Smolenski
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 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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Cardiotoxicity
  • Anthracyclines
  • Reactive oxygen species
  • Hypoxia
  • Metabolic effects
  • Imaging
  • Long-term effects

Published Papers (3 papers)

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Research

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19 pages, 5498 KiB  
Article
Macrophage-Derived Adenosine Deaminase 2 Correlates with M2 Macrophage Phenotype in Triple Negative Breast Cancer
by Barbara Kutryb-Zajac, Gabriela Harasim, Agata Jedrzejewska, Oliwia Krol, Alicja Braczko, Patrycja Jablonska, Paulina Mierzejewska, Jacek Zielinski, Ewa M. Slominska and Ryszard. T. Smolenski
Int. J. Mol. Sci. 2021, 22(7), 3764; https://doi.org/10.3390/ijms22073764 - 05 Apr 2021
Cited by 17 | Viewed by 3036
Abstract
Several lines of evidence suggest that altered adenosine deaminase (ADA) activity, especially its ADA2 iso-enzyme, is associated with malignant breast cancer (BC) development. Triple-negative breast cancer (TNBC) is currently the most challenging BC subtype due to its metastatic potential and recurrence. Herein, we [...] Read more.
Several lines of evidence suggest that altered adenosine deaminase (ADA) activity, especially its ADA2 iso-enzyme, is associated with malignant breast cancer (BC) development. Triple-negative breast cancer (TNBC) is currently the most challenging BC subtype due to its metastatic potential and recurrence. Herein, we analyzed the sources of ADA iso-enzymes in TNBC by investigating the effects of cell-to-cell interactions between TNBC cells, macrophages, lymphocytes, and endothelial cells. We also examined the potential relationship between ADA activity and cancer progression in TNBC patients. In vitro analyses demonstrated that the interactions of immune and endothelial cells with MDA-MB-231 triple negative BC cells modulated their extracellular adenosine metabolism pattern. However, they caused an increase in the ADA1 activity, and did not alter ADA2 activity in cancer cells. In turn, the co-culture of MDA-MB-231 cells with THP-1 monocyte/macrophages, Jurkat cells, and human lung microvascular endothelial cells (HULEC) caused the increase in ADA2 activity on THP-1 cells and ADA1 activity on Jurkat cells and HULEC. Clinical sample analysis revealed that TNBC patients had higher plasma ADA2 activities and lower ADA1/ADA2 ratio at advanced stages of cancer development than in the initial stages, while patients with hormone receptor positive, HER2 negative (HR+HER2-), and triple positive (HR+HER2+) breast cancers at the same stages showed opposite trends. TNBC patients also demonstrated positive associations between plasma ADA2 activity and pro-tumor M2 macrophage markers, as well as between ADA1 activity and endothelial dysfunction or inflammatory parameters. The analysis of TNBC patients, at 6 and 12 months following cancer treatment, did not showed significant changes in plasma ADA activities and macrophage polarization markers, which may be the cause of their therapeutic failure. We conclude that alterations in both ADA iso-enzymes can play a role in breast cancer development and progression by the modulation of extracellular adenosine-dependent pathways. Additionally, the changes in ADA2 activity that may contribute to the differentiation of macrophages into unfavorable pro-tumor M2 phenotype deserve special attention in TNBC. Full article
(This article belongs to the Special Issue Boundaries of Cancer and Cardiovascular Diseases)
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Review

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18 pages, 562 KiB  
Review
Visceral Obesity and Its Shared Role in Cancer and Cardiovascular Disease: A Scoping Review of the Pathophysiology and Pharmacological Treatments
by Erika Aparecida Silveira, Golnaz Vaseghi, Annelisa Silva de Carvalho Santos, Nathalie Kliemann, Farzad Masoudkabir, Matias Noll, Noushin Mohammadifard, Nizal Sarrafzadegan and Cesar de Oliveira
Int. J. Mol. Sci. 2020, 21(23), 9042; https://doi.org/10.3390/ijms21239042 - 27 Nov 2020
Cited by 32 | Viewed by 4508
Abstract
The association between obesity, cancer and cardiovascular disease (CVD) has been demonstrated in animal and epidemiological studies. However, the specific role of visceral obesity on cancer and CVD remains unclear. Visceral adipose tissue (VAT) is a complex and metabolically active tissue, that can [...] Read more.
The association between obesity, cancer and cardiovascular disease (CVD) has been demonstrated in animal and epidemiological studies. However, the specific role of visceral obesity on cancer and CVD remains unclear. Visceral adipose tissue (VAT) is a complex and metabolically active tissue, that can produce different adipokines and hormones, responsible for endocrine-metabolic comorbidities. This review explores the potential mechanisms related to VAT that may also be involved in cancer and CVD. In addition, we discuss the shared pharmacological treatments which may reduce the risk of both diseases. This review highlights that chronic inflammation, molecular aspects, metabolic syndrome, secretion of hormones and adiponectin associated to VAT may have synergistic effects and should be further studied in relation to cancer and CVD. Reductions in abdominal and visceral adiposity improve insulin sensitivity, lipid profile and cytokines, which consequently reduce the risk of CVD and some cancers. Several medications have shown to reduce visceral and/or subcutaneous fat. Further research is needed to investigate the pathophysiological mechanisms by which visceral obesity may cause both cancer and CVD. The role of visceral fat in cancer and CVD is an important area to advance. Public health policies to increase public awareness about VAT’s role and ways to manage or prevent it are needed. Full article
(This article belongs to the Special Issue Boundaries of Cancer and Cardiovascular Diseases)
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19 pages, 272 KiB  
Review
Immune Checkpoint Inhibitors and Cardiac Toxicity in Patients Treated for Non-Small Lung Cancer: A Review
by Grzegorz Sławiński, Anna Wrona, Alicja Dąbrowska-Kugacka, Grzegorz Raczak and Ewa Lewicka
Int. J. Mol. Sci. 2020, 21(19), 7195; https://doi.org/10.3390/ijms21197195 - 29 Sep 2020
Cited by 51 | Viewed by 4101
Abstract
Lung cancer is a major cause of cancer-related mortality worldwide, both in men and women. The vast majority of patients are diagnosed with non-small-cell lung cancer (NSCLC, 80–85% of lung cancer cases). Therapeutics named immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment in [...] Read more.
Lung cancer is a major cause of cancer-related mortality worldwide, both in men and women. The vast majority of patients are diagnosed with non-small-cell lung cancer (NSCLC, 80–85% of lung cancer cases). Therapeutics named immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment in the last decade. They are monoclonal antibodies, and those directed against PD-1 (programmed cell death protein 1) or PD-L1 (programmed cell death-ligand 1) have been used in the treatment of lung cancer and significantly improved the prognosis of NSCLC patients. However, during treatment with ICIs, immune-related adverse events (irAEs) can occur in any organ and any tissue. At the same time, although cardiac irAEs are relatively rare compared to irAEs in other organs, they have a high mortality rate. The two most common clinical manifestations of immunotherapy-related cardiotoxicity are myocarditis and pericarditis. Various types of arrhythmias have been reported in patients treated with ICIs, including the occurrence of life-threatening complete atrioventricular block or ventricular tachyarrhythmias. Here, we aim to summarize the incidence, clinical manifestations, underlying mechanisms, diagnosis, and treatment strategies for ICI-associated cardiotoxicity as these issues become very important in view of the increasing use of ICI in the treatment of lung cancer. Full article
(This article belongs to the Special Issue Boundaries of Cancer and Cardiovascular Diseases)
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