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Molecular Biomarkers in Cancer and Chronic Inflammation: New Therapeutic Approaches
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Molecular Biomarkers in Cancer and Chronic Inflammation: New Therapeutic Approaches

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 (31 August 2024) | Viewed by 14523

Special Issue Editors

Prof.Dr. Antonio Filippini

E-Mail Website
Guest Editor
Dipartimento di Scienze Anatomiche, Istologiche, Medico Legali e dell’Apparato Locomotore, Unità di Istologia ed Embriologia Medica, Sapienza Università di Roma, 00161 Roma, Italy
Interests: angiogenesis; calcium; endothelial cells; endothelial dysfunction; second messengers, autophagy; differentiation
Dr. Alessandra Micera

E-Mail Website
Guest Editor
Research and Development Laboratory for Biochemical, Molecular and Cellular Applications in Ophthalmological Sciences, Research Laboratories in Ophthalmology, IRCCS-Fondazione Bietti, 00184 Rome, Italy
Interests: neuromediators; ocular diseases; biomarkers; epigenetics; genetic variants
Special Issues, Collections and Topics in MDPI journals
Dr. Filippo Biamonte

E-Mail Website
Guest Editor
Dipartimento di Scienze, Laboratoristiche ed Infettivologiche, UOC Chimica, Biochimica e Biologia Molecolare Clinica, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
Interests: neurodegeneration; cerebellum; testosterone; cell migration; immunohistochemistry; cellular neuroscience molecular neurobiology; neural plasticity; steroids; brain; estrogens; neuroscience; biochemistry stereology; neurobiology; nutritional medicine

Special Issue Information

Dear Colleagues,

This Special Issue will deal with the role of molecular biomarkers in cancer and chronic inflammation. As is already known, inflammatory pathways play a pivotal role in the development and progression of cancer and promote all steps of tumorigenesis.

Cancer cells, as well as peritumoral and inflammatory ones, engage in well-orchestrated interplays to form an inflammatory tumor-driven microenvironment, often associated with drug resistance during treatment. The crosstalk between inflammatory biomarkers and the intrinsic properties of tumor cells have been identified as a pivotal regulator of tumor initiation and progression.

This Special Issue will include some of the current and interesting advances on molecular and biochemical markers/targets in different tissues and will include gene expression, protein, and biochemical pathways, such as key regulators in inflammation and cancer signaling.

Finally, the latest developments in how molecular biomarkers can be exploited in the development of new targeted therapies and in patients’ follow-up will be considered.

Dr. Antonio Filippini
Dr. Alessandra Micera
Dr. Filippo Biamonte
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

  • cancer
  • inflammation
  • cell signaling
  • gene expression
  • protein expression
  • tumor escape mechanisms

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Published Papers (4 papers)

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Research

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17 pages, 3978 KiB  
Article
Prediction of Overall Survival by Thymidine Kinase 1 Combined with Prostate-Specific Antigen in Men with Prostate Cancer
by Bernhard Tribukait, Per-Olof Lundgren, Anders Kjellman, Ulf Norming, Claes R. Nyman, Kiran Jagarlmundi and Ove Gustafsson
Int. J. Mol. Sci. 2023, 24(6), 5160; https://doi.org/10.3390/ijms24065160 - 8 Mar 2023
Cited by 3 | Viewed by 4566
Abstract
Thymidine kinase 1 (TK1) is an intracellular enzyme involved in DNA-precursor synthesis. Increased serum TK1 levels are used as a biomarker in various malignancies. We combined serum TK1 with PSA and evaluated its capacity to predict overall survival (OS) in 175 men with [...] Read more.
Thymidine kinase 1 (TK1) is an intracellular enzyme involved in DNA-precursor synthesis. Increased serum TK1 levels are used as a biomarker in various malignancies. We combined serum TK1 with PSA and evaluated its capacity to predict overall survival (OS) in 175 men with prostate cancer (PCa), detected by screening in 1988–1989 (n = 52) and during follow-up (median 22.6 years) (n = 123). TK1 was measured in frozen serum, age was stratified into four groups, and dates of PCa diagnosis and dates of death were obtained from Swedish population-based registries. The median concentration of TK1 and PSA was 0.25 and 3.8 ng/ml. TK1 was an independent variable of OS. In the multivariate analysis, PSA was not statistically significant in combination with age whereas the significance remained for TK1 + PSA. Measured once, TK1 + PSA predicted a difference of up to 10 years (depending on patient subgroup) in OS at a median of 9 years before PCa diagnosis. The TK1 concentration in 193 controls without malignancies did not differ from that of the PCa patients, hence TK1 was likely not released from incidental PCa. Thus, TK1 in the blood circulation may indicate the release of TK1 from sources other than cancers, nonetheless associated with OS. Full article
(This article belongs to the Special Issue Molecular Biomarkers in Cancer and Chronic Inflammation: New Therapeutic Approaches)
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13 pages, 3233 KiB  
Article
Spatial Profile of Tumor Microenvironment in PD-L1-Negative and PD-L1-Positive Triple-Negative Breast Cancer
by Liubov A. Tashireva, Anna Yu. Kalinchuk, Tatiana S. Gerashchenko, Maksim Menyailo, Anna Khozyainova, Evgeniy V. Denisov and Vladimir M. Perelmuter
Int. J. Mol. Sci. 2023, 24(2), 1433; https://doi.org/10.3390/ijms24021433 - 11 Jan 2023
Cited by 5 | Viewed by 2902
Abstract
The problem of finding more precise stratification criteria for identifying the cohort of patients who would obtain the maximum benefit from immunotherapy is acute in modern times. In our study were enrolled 18 triple-negative breast cancer patients. The Ventana SP142 test was used [...] Read more.
The problem of finding more precise stratification criteria for identifying the cohort of patients who would obtain the maximum benefit from immunotherapy is acute in modern times. In our study were enrolled 18 triple-negative breast cancer patients. The Ventana SP142 test was used for PD-L1 detection. Spatial transcriptomic analysis by 10x Genomics was used to compare PD-L1-positive and PD-L1-negative tumors. The seven-color multiplex immunofluorescence (by Akoya) was used for the detection of the type of cells that carried the PD1 receptor and the PD-L1 ligand. Using pathway analysis, we showed that PD-L1-positive tumors demonstrate signatures of a cell response to cytokines, among others, and PD-L1-negative tumors demonstrate signatures of antigen presentation. PD-L1-positive and PD-L1-negative tumors have different tumor microenvironment (TME) compositions according to CIBERSORT analysis. Multiplex immunohistochemistry (IHC) confirmed the prevalence of PD1-negative M2 macrophages and PD1-negative T lymphocytes in PD-L1-positive tumors. PD-L1-positive tumors are not characterized by direct contact between cells carrying the PD1 receptor and the PD-L1 ligand. So, the absence of specific immune reactions against the tumor, predominance of pro-tumor microenvironment, and rare contact between PDL1 and PD1-positive cells may be the potential reasons for the lack of an immune checkpoint inhibitor (ICI) effect in triple-negative breast cancer patients. Full article
(This article belongs to the Special Issue Molecular Biomarkers in Cancer and Chronic Inflammation: New Therapeutic Approaches)
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20 pages, 4249 KiB  
Article
Secretory SERPINE1 Expression Is Increased by Antiplatelet Therapy, Inducing MMP1 Expression and Increasing Colon Cancer Metastasis
by Won-Tae Kim, Jeong-Yeon Mun, Seung-Woo Baek, Min-Hye Kim, Gi-Eun Yang, Mi-So Jeong, Sun Young Choi, Jin-Yeong Han, Moo Hyun Kim and Sun-Hee Leem
Int. J. Mol. Sci. 2022, 23(17), 9596; https://doi.org/10.3390/ijms23179596 - 24 Aug 2022
Cited by 18 | Viewed by 2598
Abstract
Contrary to many reports that antiplatelet agents inhibit cancer growth and metastasis, new solid tumors have been reported in patients receiving long-term antiplatelet therapy. We investigated the effects of these agents directly on cancer cells in the absence of platelets to mimic the [...] Read more.
Contrary to many reports that antiplatelet agents inhibit cancer growth and metastasis, new solid tumors have been reported in patients receiving long-term antiplatelet therapy. We investigated the effects of these agents directly on cancer cells in the absence of platelets to mimic the effects of long-term therapy. When four antiplatelet agents (aspirin, clopidogrel, prasugrel, and ticagrelor) were administered to colon cancer cells, cancer cell proliferation was inhibited similarly to a previous study. However, surprisingly, when cells were treated with a purinergic P2Y12 inhibitor (purinergic antiplatelet agent), the motility of the cancer cells was significantly increased. Therefore, gene expression profiles were identified to investigate the effect of P2Y12 inhibitors on cell mobility, and Serpin family 1 (SERPINE1) was identified as a common gene associated with cell migration and cell death in three groups. Antiplatelet treatment increased the level of SERPINE1 in cancer cells and also promoted the secretion of SERPINE1 into the medium. Increased SERPINE1 was found to induce MMP1 and, thus, increase cell motility. In addition, an increase in SERPINE1 was confirmed using the serum of patients who received these antiplatelet drugs. With these results, we propose that SERPINE1 could be used as a new target gene to prevent the onset and metastasis of cancer in patients with long-term antiplatelet therapy. Full article
(This article belongs to the Special Issue Molecular Biomarkers in Cancer and Chronic Inflammation: New Therapeutic Approaches)
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Review

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22 pages, 1985 KiB  
Review
Carcinoid Syndrome: Preclinical Models and Future Therapeutic Strategies
by Giovanni Vitale, Silvia Carra, Ylenia Alessi, Federica Campolo, Carla Pandozzi, Isabella Zanata, Annamaria Colao, Antongiulio Faggiano and on behalf of the NIKE Group
Int. J. Mol. Sci. 2023, 24(4), 3610; https://doi.org/10.3390/ijms24043610 - 10 Feb 2023
Cited by 6 | Viewed by 2756
Abstract
Carcinoid syndrome represents a debilitating paraneoplastic disease, caused by the secretion of several substances, occurring in about 10–40% of patients with well-differentiated neuroendocrine tumors (NETs). The main signs and symptoms associated with carcinoid syndrome are flushing, diarrhea, hypotension, tachycardia, bronchoconstriction, venous telangiectasia, dyspnea [...] Read more.
Carcinoid syndrome represents a debilitating paraneoplastic disease, caused by the secretion of several substances, occurring in about 10–40% of patients with well-differentiated neuroendocrine tumors (NETs). The main signs and symptoms associated with carcinoid syndrome are flushing, diarrhea, hypotension, tachycardia, bronchoconstriction, venous telangiectasia, dyspnea and fibrotic complications (mesenteric and retroperitoneal fibrosis, and carcinoid heart disease). Although there are several drugs available for the treatment of carcinoid syndrome, the lack of therapeutic response, poor tolerance or resistance to drugs are often reported. Preclinical models are indispensable tools for investigating the pathogenesis, mechanisms for tumor progression and new therapeutic approaches for cancer. This paper provides a state-of-the-art overview of in vitro and in vivo models in NETs with carcinoid syndrome, highlighting the future developments and therapeutic approaches in this field. Full article
(This article belongs to the Special Issue Molecular Biomarkers in Cancer and Chronic Inflammation: New Therapeutic Approaches)
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