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Cancers
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Latest Research in Cartilaginous Neoplasms
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Latest Research in Cartilaginous Neoplasms

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

Deadline for manuscript submissions: closed (15 September 2023) | Viewed by 4089

Special Issue Editor

Dr. Benjamin A. Alman

E-Mail Website
Guest Editor
Department of Orthopedic Surgery, Duke University, Durham, NC 27710, USA
Interests: understanding the role of developmentally important processes in repair and pathologies involving the musculoskeletal system; pathobiology of musculoskeletal tumors; bone and skin repair and the role of hematopoietic cells in regeneration, metabolism in musculoskeletal tumors, and the role of cellular heterogeneity in sarcomas

Special Issue Information

Dear Colleagues,

Cartilage tumors are the most common types of bone lesions, occurring in 5% of the population. They range from benign lesions, such an enchondromas and osteochondromas, to malignant chondrosarcomas. Benign cartilaginous lesions can progress to chondrosarcomas. Benign lesions can cause disabilities, due to pain, deformity, and joint dysfunction. There have been significant advances in our understanding of cartilage tumors in the past several years. The identification of the genetic mechanism that causes benign cartilage tumors, modeling these lesions in mice, and understanding how these mutations alter cell behavior have all identified possible new therapeutics. Next-generation sequencing identified novel genetic changes that are common in chondrosarcoma. New findings in epigenetics, metabolism, DNA repair, bioinformatics, and next-generation genetic analysis have identified new therapies, some of which have been translated to clinical trials. This Special Issue will cover many of these recent advances, identifying future directions for translational research.

Dr. Benjamin A. Alman
Guest Editor

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 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • enchondroma
  • chondrosarcoma
  • osteochondroma
  • Ext
  • IDH
  • mouse models
  • epigenetics
  • metabolomics

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Published Papers (2 papers)

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Research

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13 pages, 1493 KiB  
Article
Grade 2, 3 and Dedifferentiated Chondrosarcomas: A Comparative Study of Isocitrate Dehydrogenase-Mutant and Wild-Type Tumors with Implications for Prognosis and Therapy
by Karen Schoedel, Tanya Heim, Anette Duensing, Ines Lohse, Laura Presutti, Rebekah Belayneh, Sumail Bhogal, Anya Singh-Varma, Alexander Chang, Uma Chandran, Daniel Marker, Heather Szabo-Rogers and Kurt Weiss
Cancers 2024, 16(2), 247; https://doi.org/10.3390/cancers16020247 - 5 Jan 2024
Viewed by 1586
Abstract
Background: Grade 2 and 3 and dedifferentiated chondrosarcomas (CS) are frequently associated with isocitrate dehydrogenase (IDH) mutations and often exhibit a poor clinical outcome. Treatment is limited mainly to surgery. Defining IDH status (wild type (WT) and mutant) and the associated [...] Read more.
Background: Grade 2 and 3 and dedifferentiated chondrosarcomas (CS) are frequently associated with isocitrate dehydrogenase (IDH) mutations and often exhibit a poor clinical outcome. Treatment is limited mainly to surgery. Defining IDH status (wild type (WT) and mutant) and the associated transcriptome may prove useful in determining other therapeutic options in these neoplasms. Methods: Formalin-fixed paraffin-embedded material from 69 primary and recurrent grade 2, 3 and dedifferentiated CS was obtained. DNA sequencing for IDH1 and IDH2 mutations (n = 47) and RNA sequencing via Nextseq 2000 (n = 14) were performed. Differentially expressed genes (DEGs) were identified and used to predict aberrant biological pathways with Ingenuity Pathway Analysis (IPA) software (Qiagen). Gene Set Enrichment Analyses (GSEA) using subsets C3, C5 and C7 were performed. Differentially expressed genes were validated by immunohistochemistry. Outcome analysis was performed using the Wilcoxon test. Results: A set of 69 CS (28 females, 41 males), average age 65, distributed among femur, pelvis, humerus, and chest wall were identified from available clinical material. After further selection based on available IDH status, we evaluated 15 IDH WT and 32 IDH mutant tumors as part of this dataset. Out of 15 IDH WT tumors, 7 involved the chest wall/scapula, while 1 of 32 mutants arose in the scapula. There were far more genes overexpressed in IDH WT tumors compared to IDH mutant tumors. Furthermore, IDH WT and IDH mutant tumors were transcriptomically distinct in the IPA and GSEA, with IDH mutant tumors showing increased activity in methylation pathways and endochondral ossification, while IDH WT tumors showed more activity in normal matrix development pathways. Validation immunohistochemistry demonstrated expression of WT1 and AR in IDH WT tumors, but not in IDH mutants. SATB2 was expressed in IDH mutant tumors and not in WT tumors. Outcome analysis revealed differences in overall survival between mutant and WT tumors (p = 0.04), dedifferentiated mutant and higher-grade (2, 3) mutant tumors (p = 0.03), and dedifferentiated mutant and higher-grade (2, 3) WT tumors (p = 0.03). The longest survival times were observed in patients with higher-grade WT tumors, while patients with dedifferentiated mutant tumors showed the lowest survival. Generally, patients with IDH WT tumors displayed longer survival in both the higher-grade and dedifferentiated groups. Conclusions: Grade 2, 3 and dedifferentiated chondrosarcomas are further characterized by IDH status, which in turn informs transcriptomic phenotype and overall survival. The transcriptome is distinct depending on IDH status, and implies different treatment targets. Full article
(This article belongs to the Special Issue Latest Research in Cartilaginous Neoplasms)
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Review

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12 pages, 742 KiB  
Review
IDH Mutations in Chondrosarcoma: Case Closed or Not?
by Sanne Venneker and Judith V. M. G. Bovée
Cancers 2023, 15(14), 3603; https://doi.org/10.3390/cancers15143603 - 13 Jul 2023
Cited by 7 | Viewed by 2138
Abstract
Chondrosarcomas are malignant cartilage-producing tumours that frequently harbour isocitrate dehydrogenase 1 and -2 (IDH) gene mutations. Several studies have confirmed that these mutations are key players in the early stages of cartilage tumour development, but their role in later stages remains [...] Read more.
Chondrosarcomas are malignant cartilage-producing tumours that frequently harbour isocitrate dehydrogenase 1 and -2 (IDH) gene mutations. Several studies have confirmed that these mutations are key players in the early stages of cartilage tumour development, but their role in later stages remains ambiguous. The prognostic value of IDH mutations remains unclear and preclinical studies have not identified effective treatment modalities (in)directly targeting these mutations. In contrast, the IDH mutation status is a prognostic factor in other cancers, and IDH mutant inhibitors as well as therapeutic strategies targeting the underlying vulnerabilities induced by IDH mutations seem effective in these tumour types. This discrepancy in findings might be ascribed to a difference in tumour type, elevated D-2-hydroxyglutarate levels, and the type of in vitro model (endogenous vs. genetically modified) used in preclinical studies. Moreover, recent studies suggest that the (epi)genetic landscape in which the IDH mutation functions is an important factor to consider when investigating potential therapeutic strategies or patient outcomes. These findings imply that the dichotomy between IDH wildtype and mutant is too simplistic and additional subgroups indeed exist within chondrosarcoma. Future studies should focus on the identification, characterisation, and tailoring of treatments towards these biological subgroups within IDH wildtype and mutant chondrosarcoma. Full article
(This article belongs to the Special Issue Latest Research in Cartilaginous Neoplasms)
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