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Cancer Biomarkers and Metabolic Vulnerabilities

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 20 October 2025 | Viewed by 1866

Special Issue Editor


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Guest Editor
Department of Oncology, University of Torino, S. Luigi Gonzaga Hospital, Regione Gonzole 10, 10043 Orbassano, Italy
Interests: cancer biology; translational biochemistry; preclinical models; cancer metabolism; repeat elements; lung cancer; patient-derived organoids; circulating tumor cells

Special Issue Information

Dear Colleagues,

In the precision oncology era, novel and promising biomarkers and potential therapeutic targets are rapidly emerging thanks to unprecedented technological advances and are being sustained through the improvement of existing and new liquid biopsy approaches. A deeper knowledge of cancer cell behaviors and metabolic assets could lead to the identification of key and often undiscovered molecular players that are expected to offer tremendous benefits in clinical care.

We are pleased to invite you to contribute to this Special Issue, “Cancer Biomarkers and Metabolic Vulnerabilities”, which will be focused on the molecular and biochemical circuits exploited by cancer cells, investigating the key molecules that could be exploited as diagnostic, prognostic, stratification, and progression/response biomarkers or as targets of therapeutic relevance.

Within this framework, this Special Issue will collect the latest findings and breakthroughs in the fields of cancer biochemistry and the discovery of molecular and cellular biomarkers, as well as the characterization of novel potential therapeutic targets, with a particular emphasis on metabolic nodes. Original research articles and reviews, including methodological and preclinical papers, are welcome.

We look forward to receiving your contributions.

Dr. Francesca Bersani
Guest Editor

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Keywords

  • cancer metabolism
  • cancer biomarkers
  • liquid biopsy
  • therapeutic targets
  • metabolic rewiring

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Published Papers (1 paper)

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Research

8 pages, 766 KiB  
Communication
Urothelial Urinary Bladder Cancer Is Characterized by Stage-Dependent Aberrations in Metabolism of Bioactive Sphingolipids
by Grzegorz Młynarczyk, Agnieszka Mikłosz, Adrian Chabowski and Marcin Baranowski
Int. J. Mol. Sci. 2024, 25(22), 11889; https://doi.org/10.3390/ijms252211889 - 5 Nov 2024
Cited by 1 | Viewed by 1002
Abstract
Although dysregulated sphingolipid metabolism was observed in many malignant tumors, bladder cancer has not yet been examined in this regard. This study aims to investigate the metabolism of bioactive sphingolipids across different stages of urothelial urinary bladder cancer (UBC). Forty-eight patients with UBC [...] Read more.
Although dysregulated sphingolipid metabolism was observed in many malignant tumors, bladder cancer has not yet been examined in this regard. This study aims to investigate the metabolism of bioactive sphingolipids across different stages of urothelial urinary bladder cancer (UBC). Forty-eight patients with UBC were included in this study. The neoplasms were classified as either non-muscle-invasive (NMIBC, n = 24) or muscle-invasive (MIBC, n = 24). Samples of the healthy bladder tissue were taken from the patients who underwent radical cystectomy. The content of sphingolipids was measured using an HPLC method, and the mRNA expression of sphingolipid transporters and metabolizing enzymes was evaluated using RT-PCR. Compared to the healthy bladder tissue, the UBC, regardless of the stage, showed an elevated expression of SphK1, Spns2, and ABCC1. The changes in the level of bioactive sphingolipids were strongly stage-dependent. MIBC showed accumulation of sphingosine-1-phosphate (S1P) and ceramide, whereas the content of these sphingolipids in the NMIBC tumor was not different from that of healthy tissue. Moreover, MIBC, compared to NMIBC, was characterized by higher levels of sphingosine and dihydroceramide. We conclude that profound alterations in sphingolipid metabolism develop upon UBC transition from non-muscle-invasive to muscle-invasive. They include the accumulation of S1P, resulting from the increased availability of sphingosine generated from ceramide, which also builds up due to a further activation of its de novo synthesis. We hypothesize that the dysregulation of S1P metabolism leading to the accumulation of this tumor-promoting sphingolipid contributes to the progression of UBC. Full article
(This article belongs to the Special Issue Cancer Biomarkers and Metabolic Vulnerabilities)
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