Challenges and New Developments in the Diagnosis and Treatment of Sarcoma

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 350

Special Issue Editor


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Guest Editor
1. Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada
2. Department of Medical Oncology, Arthur J.E. Child Comprehensive Cancer Centre, Calgary, AB T2N 5G2, Canada
Interests: prognostic and predictive biomarkers; novel therapeutic intervention through genomic and transcriptome sequencing; clinical, translational research, and clinical trials (breast/sarcoma)
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Special Issue Information

Dear Colleagues,

Due to its extreme rarity, heterogeneity, and complexity, sarcoma is considered one of the most challenging diseases and cancers to diagnose and treat, and it therefore presents a poor prognosis in most advanced or metastatic settings. We are currently facing many challenges in the diagnosis and treatment of sarcoma. With the availability of next-generation sequencing technology, novel fusions have been identified, facilitating the evolution of WHO classification, but the biology of these new fusions is not yet understood. Despite the fact that molecular targeted treatments and immunotherapy have revolutionized treatment in the majority of hematological and solid cancer types, they have not yet been applied to sarcoma. The purpose of this Special Issue is to provide opportunities for sarcoma research communities to contribute new ideas and options to promote better diagnosis and treatment in this deadly disease. For this Special Issue, we welcome the submission of reviews and original research articles, with a deadline of 31 December 2025.

Dr. Xiaolan Feng
Guest Editor

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Keywords

  • bone and soft tissue sarcoma
  • prognostic and predictive biomarker
  • transcriptomic/genomic profiling
  • immunotherapy
  • targeted treatment

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Published Papers (1 paper)

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Research

25 pages, 20466 KiB  
Article
Exploratory Analysis of Molecular Subtypes in Early-Stage Osteosarcoma: Identifying Resistance and Optimizing Therapy
by Luka Bojic, Mina Peric, Jelena Karanovic, Emilija Milosevic, Natasa Kovacevic Grujicic and Milena Milivojevic
Cancers 2025, 17(10), 1677; https://doi.org/10.3390/cancers17101677 - 16 May 2025
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Abstract
Background: Osteosarcoma (OS) is a highly aggressive bone malignancy with limited treatment options and poor prognosis. This exploratory study aimed to identify molecular subtypes of early-stage, treatment-naive OS to guide precise therapeutic strategies. Methods: We analyzed RNA-seq data obtained from tumor tissues from [...] Read more.
Background: Osteosarcoma (OS) is a highly aggressive bone malignancy with limited treatment options and poor prognosis. This exploratory study aimed to identify molecular subtypes of early-stage, treatment-naive OS to guide precise therapeutic strategies. Methods: We analyzed RNA-seq data obtained from tumor tissues from 102 OS patients using a non-negative matrix factorization algorithm (NMF) to classify the tumors into three subtypes: S1, S2, and S3. Differential gene expression was evaluated using DESeq2, followed by functional enrichment analysis with clusterProfiler and CancerHallmarks. The tumor microenvironment was assessed through ESTIMATE and CIBERSORT, and drug sensitivity was predicted using OncoPredict. SAOS-2 and MG63 cells, representing the S1 subtype, were used in the viability essays to determine the effect of hesperidin, a natural phenolic compound noted for its anti-cancer potential, alone and in combination with doxorubicin and 5-fluorouracil. Results: This study revealed three OS subtypes: S1 was enriched in cell cycle regulation, vesicular transport, and RNA metabolism while S2 and S3 were enriched in pathways related to extracellular matrix organization and protein translation, respectively. S1 displayed high tumor purity, significant chemoresistance, and overexpression of KIF20 A, correlating with poor prognosis. AURKB, a hesperidin target, was implicated in S1 pathogenesis. In vitro, hesperidin significantly reduced the viability of SAOS-2 and MG63 cells and enhanced doxorubicin efficacy. Conclusions: Our findings support the molecular subclassification of OS, emphasizing subtype-specific mechanisms of tumor progression and chemoresistance, with hesperidin offering potential as a therapeutic adjunct for high-risk OS patients. Full article
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