Cancer Biomarker and Molecular Oncology

A Special Issue of Journal of Personalized Medicine (ISSN 2075-4426) belonging to the section "Disease Biomarkers".

Deadline for manuscript submissions: 25 November 2026 | Viewed by 7514

Editor


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Guest Editor
Department of Health Management, Economics and Policy, The Graduate School, Augusta University, Augusta, GA, USA
Interests: biomarkers; obesity; nutrition; cancer; genomics

Special Issue Information

Dear Colleagues,

Advances in cancer biomarker research and molecular oncology are driving precision medicine by enabling tailored therapies through tumor molecular profiling. These fields focus on identifying biological indicators and molecular pathways that inform diagnosis, prognosis, and treatment strategies, addressing challenges such as tumor heterogeneity and therapeutic resistance.

This Special Issue highlights cutting-edge research at the intersection of biomarker discovery, molecular mechanisms, and clinical translation. It explores topics such as liquid biopsies, multi-omics integration, and computational approaches to characterize tumor profiles and predict treatment responses. By synthesizing basic science and clinical insights, this Special Issue will foster innovations that enhance patient stratification and optimize targeted interventions.

We welcome submissions of original research and reviews that advance our understanding of cancer biomarkers and molecular pathways, particularly those with the potential to improve diagnostic accuracy and treatment efficacy. Together, these contributions will shape the future of personalized oncology, guiding the development of more precise and effective therapeutic strategies.

Dr. Jeane Silva
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer biomarkers
  • molecular oncology
  • precision medicine
  • liquid biopsies
  • therapeutic resistance

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Published Papers (4 papers)

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Research

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10 pages, 1306 KB  
Article
Clinical Utility of an Ex Vivo Functional Test in Personalized Cancer Treatment
by Vered Bar, Adi Zundelevich, Nancy Gavert, Sara Aharon, Bassima Ibrahim, Anna Kosenko, Guy Neev, Ronen Viner, Ravid Straussman, Raanan Berger and Seth J. Salpeter
J. Pers. Med. 2026, 16(6), 298; https://doi.org/10.3390/jpm16060298 - 31 May 2026
Viewed by 814
Abstract
Background/Objectives: Providing optimized and accurate treatment to cancer patients remains a major challenge in oncology care. The emergence of precision medicine tools to match the correct therapy to the patient has significantly advanced treatment modalities in the last few years. While genomics has [...] Read more.
Background/Objectives: Providing optimized and accurate treatment to cancer patients remains a major challenge in oncology care. The emergence of precision medicine tools to match the correct therapy to the patient has significantly advanced treatment modalities in the last few years. While genomics has been shown to be critical in selecting targeted therapies for a specific somatic mutation, the overall clinical benefit of broad genomic sequencing has been found lacking. Here, we evaluate the utility of our previously clinically validated ex vivo functional assay across different treatment scenarios, demonstrating its ability to transform predicted non-responders into predicted responders, rule out ineffective treatments, provide multiple treatment options, and validate physician choices. Methods: The evaluation was performed on a post-market surveillance study analyzing 312 patients, from which 278 patients had successful test reports (an 89.1% test success rate), with clinical outcomes available from 45 of those patients. Results: We show that in the group of patients with clinical response data, the tests yield a PPV of 91.18% and NPV of 90.91% with clinical utility impacting physician decision in 51.1% of cases. Further analysis of the entire cohort showed the potential of clinical utility to reach up to 59.3% on a large group of patients. Conclusions: The accurate prediction of patient response using the test suggests the potential for the platform to improve patient treatment in clinical practice by reducing ineffective drug use and optimizing personalized patient drug regiments. Full article
(This article belongs to the Special Issue Cancer Biomarker and Molecular Oncology)
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26 pages, 4187 KB  
Article
Small Extracellular Vesicles Secreted by Cisplatin-Resistant Neuroblastoma Cells Increase Lactate Secretion and Alter Metabolic Pathways in Primary Human Umbilical Vein Endothelial Cells (HUVECs)
by Thomas Frawley, Lin Ma, Muhammad Zainul Arifin, Dan Wu, Alysia Scott, Brenton Cavanagh, Donal F. O’Shea, Vadim Zhernovkov, Mi Liu, Marco P. Monopoli and Olga Piskareva
J. Pers. Med. 2025, 15(12), 584; https://doi.org/10.3390/jpm15120584 - 1 Dec 2025
Cited by 1 | Viewed by 1213
Abstract
Background: Chemoresistance, particularly to cisplatin, remains a significant challenge in treating high-risk neuroblastoma, resulting in a mere 20% five-year overall survival rate. Tumour-derived small extracellular vesicles (sEVs) have been implicated in cancer progression by promoting angiogenesis, invasion, and proliferation in recipient cells. [...] Read more.
Background: Chemoresistance, particularly to cisplatin, remains a significant challenge in treating high-risk neuroblastoma, resulting in a mere 20% five-year overall survival rate. Tumour-derived small extracellular vesicles (sEVs) have been implicated in cancer progression by promoting angiogenesis, invasion, and proliferation in recipient cells. This study investigated alterations in the protein cargo of sEVs secreted by cisplatin-sensitive and resistant neuroblastoma cells and their impact on reprogramming non-cancerous recipient cells. Methods: sEVs from cisplatin-resistant (KellyCis83) and its cisplatin-sensitive parental cell line (Kelly) were isolated and characterised, followed by proteomic profiling and Gene Set Enrichment Analysis. Functional assays using human umbilical vein endothelial cells (HUVECs) evaluated the effects of sEVs on proliferation, migration, tube formation, and metabolism. The clinical relevance of the shortlisted sEV glycolytic proteins was evaluated using the R2 Genomics Analysis and Visualisation Platform. Results: Proteomic analysis revealed dysregulated metabolic pathways in KellyCis83 sEVs. While Kelly’s and KellyCis83’s sEV-induced aerobic glycolytic rates were similar, oxidative phosphorylation (OXPHOS) was significantly reduced in HUVECs treated with Kelly’s sEVs compared to KellyCis83’s sEVs, which might have been due to an altered balance of glycolytic enzymes in sEVs. Under angiogenic-factor-deprived conditions, the uptake of sEVs by HUVECs reduced their proliferation and increased anchorage-dependent differentiation. Our study demonstrated the enrichment of the MYCN oncogene and clinically relevant glycolytic proteins in neuroblastoma cell-derived sEVs. Conclusions: This study reports a potential mechanism by which sEVs derived from cisplatin-resistant neuroblastoma cells modulate endothelial cell function through alterations in metabolic pathways and provides an opportunity to explore exosomal MYCN and glycolytic proteins as circulating biomarkers for progression and treatment response signatures, using less invasive methods and enabling personalised treatment approaches for neuroblastoma patients. Full article
(This article belongs to the Special Issue Cancer Biomarker and Molecular Oncology)
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14 pages, 2426 KB  
Article
Molecular Profiling of SYT-SSX Fusion Transcripts for Enhanced Diagnosis of Synovial Sarcomas
by Sara Louati, Kaoutar Bentayebi, Ibtissam Saad, Yvonne Gloor, Nadia Senhaji, Abdelmajid Elmrini, Lahcen Belyamani, Rachid Eljaoudi, Marc Ansari, Sanae Bennis and Youssef Daali
J. Pers. Med. 2025, 15(10), 455; https://doi.org/10.3390/jpm15100455 - 29 Sep 2025
Viewed by 1646
Abstract
Background/Objectives: Synovial sarcoma (SS) is an aggressive soft-tissue tumor characterized by the chromosomal translocation t(X;18) (p11.2;q11.2), most commonly involving the fusion of the SYT gene on chromosome 18 with the SSX1 or SSX2 genes on chromosome X. This study aims to explore [...] Read more.
Background/Objectives: Synovial sarcoma (SS) is an aggressive soft-tissue tumor characterized by the chromosomal translocation t(X;18) (p11.2;q11.2), most commonly involving the fusion of the SYT gene on chromosome 18 with the SSX1 or SSX2 genes on chromosome X. This study aims to explore the clinicopathological and molecular characteristics of synovial sarcoma in a cohort of Moroccan patients. Methods: We analyzed 48 cases of synovial sarcoma using formalin-fixed, paraffin-embedded (FFPE) tissue samples. Histological grading was performed according to the FNCLCC system. Immunohistochemical staining was employed to detect cytokeratin (CK) and epithelial membrane antigen (EMA). Molecular analysis included fluorescence in situ hybridization (FISH) to identify SS18 gene rearrangements and reverse transcription–polymerase chain reaction (RT-PCR) to detect SYT-SSX fusion transcripts. Results: Among the cohort, 56% of cases showed SS18 gene rearrangements via FISH, while RT-PCR confirmed the presence of SS18-SSX1 and SS18-SSX2 transcripts in 60% and 32% of cases, respectively. The remainder was classified as undifferentiated sarcoma. Notably, no significant associations were observed between SYT-SSX fusion type and clinicopathological features. Conclusions: These findings underscore the importance of integrating molecular techniques for precise diagnosis in synovial sarcoma. The results align with global patterns, emphasizing the necessity for molecular testing to enhance diagnostic accuracy and informing potential therapeutic advancements. Full article
(This article belongs to the Special Issue Cancer Biomarker and Molecular Oncology)
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Review

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13 pages, 246 KB  
Review
Biomarkers in Colorectal Cancer: Clinically Relevant Diagnostic and Prognostic Molecular Features, and the Future of Precision Medicine
by Rebecca Whitmer, Julia Sepulveda, Jason Gandhi, Isha Puri and Rohan Gupta
J. Pers. Med. 2026, 16(3), 132; https://doi.org/10.3390/jpm16030132 - 28 Feb 2026
Cited by 3 | Viewed by 3278
Abstract
Colorectal cancer (CRC) is a major public health concern in the United States. It is currently the fourth most diagnosed cancer and, despite advancements in screening and treatment, the second leading cause of cancer-related deaths. Approximately 153,000 new cases are diagnosed annually, with [...] Read more.
Colorectal cancer (CRC) is a major public health concern in the United States. It is currently the fourth most diagnosed cancer and, despite advancements in screening and treatment, the second leading cause of cancer-related deaths. Approximately 153,000 new cases are diagnosed annually, with over 53,000 deaths reported. Understanding the molecular and genetic underpinnings of CRC biomarkers plays a crucial role in diagnosis, prognosis, and treatment planning. Specific gene mutations, including MMR deficiency leading to high microsatellite instability (MSI), as well as several other common mutations in CRC, including APC, TP53, KRAS, NRAS, SMAD4, PIK3CA and BRAF, provide valuable insights into tumor biology, therapeutic resistance, and response to targeted therapies. This review explores the mutations and co-mutations most relevant to CRC, their prevalence, prognostic significance, and implications for precision oncology. By focusing on these genetic and epigenetic alterations, we aim to contextualize how biomarker-driven strategies are reshaping the management of CRC in both early and advanced disease settings. Full article
(This article belongs to the Special Issue Cancer Biomarker and Molecular Oncology)
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