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Cancers
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Advances in Molecular Pathology and Biology of Soft Tissue and...
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Advances in Molecular Pathology and Biology of Soft Tissue and Bone Tumors

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 11812

Special Issue Editors

Dr. Frederic Chibon

E-Mail Website
Guest Editor
ONCOSARC-CRCT, Institut Claudius Regaud, ONCOPOLE, Toulouse, France
Interests: sarcoma; genome; prognosis; metastasis; cell fusion; chromosomal instability; tumor genetics
Prof. Dr. Anne Gomez-Brouchet

E-Mail Website
Co-Guest Editor
1. Department of Pathology, IUCT-Oncopole, CHU and University of Toulouse, Toulouse, France
2. National Centre for Scientific Research (CNRS), Toulouse, France
Interests: osteosarcoma; cancer biology; pathology; cytology
Dr. Philippe Rochaix

E-Mail Website
Co-Guest Editor
Department of Pathology, Institut Universitaire du Cancer de Toulouse- Oncopole, Toulouse, France
Interests: soft tissue sarcoma; histopathology; NGS
Dr. Franck Tirode

E-Mail Website
Co-Guest Editor
Le Centre Régional de Lutte Contre le Cancer Léon Bérard, Lyon, France
Interests: sarcomas; genetics; epigenetics; cancer biology

Special Issue Information

Dear Colleagues, 

As you know only too well, the modern management of sarcomas, even by experts, remains a challenge. In fact, we do not currently have a satisfactory therapeutic weapon for management, both outside of and in addition to surgery. We also too often face a lack of markers to decide which patients can potentially benefit from possibly effective treatments, at least in selected patients. Could this challenge be due to our lack of knowledge of this disease, which has a terribly poor prognosis? Sarcomas are heterogenous and comprise more than a hundred subtypes that are regularly redefined by advances in biological characterization, and this further increases the complexity of our understanding and, ultimately, our management of them. Thus, we have decided to increase our knowledge about these oncogeneses. It is still unclear what the driving chromosomal mechanisms, the cells at the origin of development, the metabolic modifications, the interactions with the cells in the microenvironment or with the host in its entirety, the mechanisms of escape from the immune system that make sarcomas poor responders to immunotherapy, and more generally, the biology that governs the initiation, development, progression, and dissemination of these cancers are. There is still much to do before we can fully understand the complex relationships between tumor genetics, cellular interactions, metabolism, and immunity to allow us, in the long run, to develop new innovative and efficient therapeutic strategies.

We are pleased to invite you to submit your papers to this Special Issue to increase our knowledge in the oncogenesis of sarcomas, allowing us to move toward better patient management.

This Special Issue aims to gather the current research in the field of sarcoma research, from molecular pathology to immune and cellular therapies, including sarcoma genetics, biology and metabolism, cancer stem cells, differentiation, circulating tumor cells studies, spontaneous dog/cat models, and pre-clinical research.

We look forward to receiving your contributions

Dr. Frederic Chibon
Prof. Dr. Anne Gomez-Brouchet
Dr. Philippe Rochaix
Dr. Franck Tirode
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 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

  • chromosomes
  • genome
  • metabolism
  • immune system
  • macrophage
  • mesenchymal
  • stem cell
  • metastasis
  • circulating tumor cell (CTC)
  • circulating cell-free DNA (cfDNA)

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Published Papers (4 papers)

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Research

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19 pages, 4534 KiB  
Article
Analysis of the Peritumoral Tissue Unveils Cellular Changes Associated with a High Risk of Recurrence
by Audrey Michot, Pauline Lagarde, Tom Lesluyes, Elodie Darbo, Agnès Neuville, Jessica Baud, Gaëlle Perot, Iris Bonomo, Mathilde Maire, Maxime Michot, Jean-Michel Coindre, François Le Loarer and Frédéric Chibon
Cancers 2023, 15(13), 3450; https://doi.org/10.3390/cancers15133450 - 30 Jun 2023
Viewed by 1225
Abstract
Background: The management of soft-tissue sarcoma (STS) relies on a multidisciplinary approach involving specialized oncological surgery combined with other adjuvant therapies to achieve optimal local disease control. Purpose and Results: Genomic and transcriptomic pseudocapsules of 20 prospective sarcomas were analyzed and revealed to [...] Read more.
Background: The management of soft-tissue sarcoma (STS) relies on a multidisciplinary approach involving specialized oncological surgery combined with other adjuvant therapies to achieve optimal local disease control. Purpose and Results: Genomic and transcriptomic pseudocapsules of 20 prospective sarcomas were analyzed and revealed to be correlated with a higher risk of recurrence after surgery. Conclusions: A peritumoral environment that has been remodeled and infiltrated by M2 macrophages, and is less expressive of healthy tissue, would pose a significant risk of relapse and require more aggressive treatment strategies. Full article
(This article belongs to the Special Issue Advances in Molecular Pathology and Biology of Soft Tissue and Bone Tumors)
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24 pages, 3973 KiB  
Article
Distinct Cellular Origins and Differentiation Process Account for Distinct Oncogenic and Clinical Behaviors of Leiomyosarcomas
by Elodie Darbo, Gaëlle Pérot, Lucie Darmusey, Sophie Le Guellec, Laura Leroy, Laëtitia Gaston, Nelly Desplat, Noémie Thébault, Candice Merle, Philippe Rochaix, Thibaud Valentin, Gwenaël Ferron, Christine Chevreau, Binh Bui, Eberhard Stoeckle, Dominique Ranchere-Vince, Pierre Méeus, Philippe Terrier, Sophie Piperno-Neumann, Françoise Collin, Gonzague De Pinieux, Florence Duffaud, Jean-Michel Coindre, Jean-Yves Blay and Frédéric Chibonadd Show full author list remove Hide full author list
Cancers 2023, 15(2), 534; https://doi.org/10.3390/cancers15020534 - 15 Jan 2023
Cited by 2 | Viewed by 2734
Abstract
In leiomyosarcoma (LMS), a very aggressive disease, a relatively transcriptionally uniform subgroup of well-differentiated tumors has been described and is associated with poor survival. The question raised how differentiation and tumor progression, two apparently antagonist processes, coexist and allow tumor malignancy. We first [...] Read more.
In leiomyosarcoma (LMS), a very aggressive disease, a relatively transcriptionally uniform subgroup of well-differentiated tumors has been described and is associated with poor survival. The question raised how differentiation and tumor progression, two apparently antagonist processes, coexist and allow tumor malignancy. We first identified the most transcriptionally homogeneous LMS subgroup in three independent cohorts, which we named ‘hLMS’. The integration of multi-omics data and functional analysis suggests that hLMS originate from vascular smooth muscle cells and show that hLMS transcriptional program reflects both modulations of smooth muscle contraction activity controlled by MYOCD/SRF regulatory network and activation of the cell cycle activity controlled by E2F/RB1 pathway. We propose that the phenotypic plasticity of vascular smooth muscle cells coupled with MYOCD/SRF pathway amplification, essential for hLMS survival, concomitant with PTEN absence and RB1 alteration, could explain how hLMS balance this uncommon interplay between differentiation and aggressiveness. Full article
(This article belongs to the Special Issue Advances in Molecular Pathology and Biology of Soft Tissue and Bone Tumors)
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18 pages, 3370 KiB  
Article
Sarcoma Common MHC-I Haplotype Restricts Tumor-Specific CD8+ T Cell Response
by Laura Mosca, Alessandra de Angelis, Andrea Ronchi, Annarosaria De Chiara, Flavio Fazioli, Carlo Ruosi, Lucia Altucci, Mariarosaria Conte and Filomena de Nigris
Cancers 2022, 14(14), 3414; https://doi.org/10.3390/cancers14143414 - 14 Jul 2022
Cited by 8 | Viewed by 2236
Abstract
The major histocompatibility complex (MHC) class I expression in cancer cells has a crucial impact on the outcome of T cell-mediated cancer immunotherapy. We now determined the HLA class I allelic variants and their expression in PD-L1-deficient and positive rare sarcoma tissues. Tumor [...] Read more.
The major histocompatibility complex (MHC) class I expression in cancer cells has a crucial impact on the outcome of T cell-mediated cancer immunotherapy. We now determined the HLA class I allelic variants and their expression in PD-L1-deficient and positive rare sarcoma tissues. Tumor tissues were HLA-I classified based on HLA-A and -B alleles, and for class II, the HLA-DR-B by Taqman genomic PCRs. The HLA-A24*:10-B73*:01 haplotype was the most common. A general down-regulation or deletion of HLA-B mRNA and HLA-A was observed, compared to HLA-DR-B. HLA-I was almost too low to be detectable by immunohistochemistry and 32% of grade III cases were positive to PD-L1. Functional cytotoxic assays co-culturing patient biopsies with autologous T cells were used to assess their ability to kill matched tumor cells. These results establish that deletion of HLA-I loci together with their down-regulation in individual patient restrict the autologous lymphocyte cytotoxic activity, even in the presence of the immune checkpoint blocking antibody, Nivolumab. Additionally, the proposed cytotoxic test suggests a strategy to assess the sensitivity of tumor cells to T cell-mediated attack at the level of the individual patient. Full article
(This article belongs to the Special Issue Advances in Molecular Pathology and Biology of Soft Tissue and Bone Tumors)
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Review

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15 pages, 1167 KiB  
Review
Regulation of Metastasis in Ewing Sarcoma
by Mingli Li and Chunwei Chen
Cancers 2022, 14(19), 4902; https://doi.org/10.3390/cancers14194902 - 7 Oct 2022
Cited by 5 | Viewed by 4968
Abstract
Ewing sarcoma (EwS) is a type of bone and soft tissue tumor in children and adolescents. Over 85% of cases are caused by the expression of fusion protein EWSR1-FLI1 generated by chromosome translocation. Acting as a potent chimeric oncoprotein, EWSR1-FLI1 binds to chromatin, [...] Read more.
Ewing sarcoma (EwS) is a type of bone and soft tissue tumor in children and adolescents. Over 85% of cases are caused by the expression of fusion protein EWSR1-FLI1 generated by chromosome translocation. Acting as a potent chimeric oncoprotein, EWSR1-FLI1 binds to chromatin, changes the epigenetic states, and thus alters the expression of a large set of genes. Several studies have revealed that the expression level of EWSR1-FLI1 is variable and dynamic within and across different EwS cell lines and primary tumors, leading to tumoral heterogeneity. Cells with high EWSR1-FLI1 expression (EWSR1-FLI1-high) proliferate in an exponential manner, whereas cells with low EWSR1-FLI1 expression (EWSR1-FLI1-low) tend to have a strong propensity to migrate, invade, and metastasize. Metastasis is the leading cause of cancer-related deaths. The continuous evolution of EwS research has revealed some of the molecular underpinnings of this dissemination process. In this review, we discuss the molecular signatures that contribute to metastasis. Full article
(This article belongs to the Special Issue Advances in Molecular Pathology and Biology of Soft Tissue and Bone Tumors)
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