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Recent Advances in the Molecular Genetics of Sarcomas

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

Deadline for manuscript submissions: closed (30 November 2025) | Viewed by 1365

Special Issue Editor


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Guest Editor
Department of Pathology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA
Interests: bone and soft tissue sarcoma; diagnostic pathology; molecular pathology

Special Issue Information

Dear Colleagues,

Sarcomas are a heterogeneous group of tumors that arise in bone and soft tissue, encompassing a large spectrum of entities with distinct histogenesis and unique clinical and histomorphological characteristics. With the advancement of molecular genetic studies in recent years, these tumors have been shown to possess unique molecular characteristics that enhance the classification, diagnosis, and treatment of these rare tumors, particularly improving the reservoir for targeted therapies. When overlapping molecular events are identified in seemingly distinct tumor types, questions regarding the optimum classification of these tumors arise, along with questions concerning their genetic makeup. In this Special Issue, we welcome papers that illustrate novel molecular genetic findings with regard to sarcomas, in terms of the diagnosis, classification, and treatment of these tumors. Papers/reviews focusing on new paradigms in classification and treatment are especially welcome.

Dr. Wei Jiang
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 250 words) can be sent to the Editorial Office for assessment.

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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

  • sarcoma, bone and soft tissue
  • molecular genetics
  • molecular pathology
  • classification

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Published Papers (1 paper)

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Research

15 pages, 4859 KB  
Article
The Extracellular Matrix Regulates Invasion in Fusion-Negative Rhabdomyosarcoma via YAP–PIEZO1 Signaling Axis
by Yuanzhong Pan, Juha Kim, Brian M. Wong, Esteban Cobo Espuny and JinSeok Park
Cancers 2026, 18(5), 827; https://doi.org/10.3390/cancers18050827 - 4 Mar 2026
Viewed by 640
Abstract
Background: Fusion-negative rhabdomyosarcoma (FNRMS) represents the most prevalent subtype of rhabdomyosarcoma, the most common pediatric soft-tissue sarcoma. Although its invasion is a leading cause of recurrence and poor prognosis, its underlying mechanism remains unclear. We investigated how extracellular matrix density regulates FNRMS [...] Read more.
Background: Fusion-negative rhabdomyosarcoma (FNRMS) represents the most prevalent subtype of rhabdomyosarcoma, the most common pediatric soft-tissue sarcoma. Although its invasion is a leading cause of recurrence and poor prognosis, its underlying mechanism remains unclear. We investigated how extracellular matrix density regulates FNRMS progression via mechano-transduction. Methods: We used three-dimensional spheroid invasion assays with FNRMS cells embedded in varying collagen concentrations. Mechanistic insights were gained through immunofluorescence, sequencing reanalysis, calcium live-cell imaging, and pharmacological inhibition of the YAP–PIEZO1 axis. Results: High extracellular matrix density significantly enhanced invasive spreading, correlating with increased YAP nuclear localization. YAP overexpression was sufficient to promote invasive spreading, while its inhibition attenuated the matrix-enhanced phenotype. We identified PIEZO1 as a direct transcriptional target of YAP. High extracellular matrix density stimulated PIEZO1-dependent calcium influx, which was required for invasion. Furthermore, elevated PIEZO1 expression was significantly associated with poorer overall survival in FNRMS patients. Targeting YAP effectively suppressed both calcium flux and invasion. Conclusions: Our findings establish a YAP–PIEZO1 axis linking extracellular matrix density to FNRMS invasion. This mechanosensitive pathway represents a potential therapeutic vulnerability in aggressive FNRMS. Full article
(This article belongs to the Special Issue Recent Advances in the Molecular Genetics of Sarcomas)
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