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Journals
Cancers
Special Issues
Clinical Trials of Sarcoma
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Clinical Trials of Sarcoma

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 25 November 2025 | Viewed by 906

Special Issue Editor

Dr. Patrick Schlegel

E-Mail Website
Guest Editor
University Hospital of Regensburg, Department of Pediatric Hematology, Oncology and Stem Cell Transplantation, 93053 Regensburg, Germany
Interests: cancer; sarcoma; clinical trial
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue focuses on advancements in clinical trials for sarcoma, a rare and diverse group of cancers arising in connective tissues. Despite significant challenges in treatment due to its heterogeneity, recent breakthroughs in targeted therapies, immunotherapy, and precision medicine are reshaping outcomes for sarcoma patients. This collection invites original research, reviews, and case studies highlighting innovative trial designs, biomarker-driven strategies, and translational approaches. By showcasing cutting-edge developments and collaborative efforts, this Special Issue aims at advancing understanding and fostering new therapeutic strategies to improve survival and quality of life for sarcoma patients worldwide.

Dr. Patrick Schlegel
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

  • cancer
  • sarcoma
  • clinical trial

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Published Papers (1 paper)

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Research

23 pages, 2621 KB  
Article
AMPK Signaling Regulates Epithelioid Hemangioendothelioma Cell Growth
by Ryan Kanai, Sarah McMullan, Pukar Baniya, Roselyn S. Dai, Emily Norton, Kaila Lasher, Chloe T. Purello, Caleb N. Seavey, Brian P. Rubin and John M. Lamar
Cancers 2025, 17(17), 2889; https://doi.org/10.3390/cancers17172889 - 2 Sep 2025
Viewed by 649
Abstract
Background/Objectives: Epithelioid Hemangioendothelioma (EHE) is an ultra-rare, metastatic vascular sarcoma with limited therapeutic options. The hallmark of EHE is a chromosomal translocation that produces the WWTR1-CAMTA1 gene fusion, encoding the aberrant transcriptional regulator TAZ-CAMTA1. Given its central role in the EHE initiation and [...] Read more.
Background/Objectives: Epithelioid Hemangioendothelioma (EHE) is an ultra-rare, metastatic vascular sarcoma with limited therapeutic options. The hallmark of EHE is a chromosomal translocation that produces the WWTR1-CAMTA1 gene fusion, encoding the aberrant transcriptional regulator TAZ-CAMTA1. Given its central role in the EHE initiation and progression, TAZ-CAMTA1 represents a compelling therapeutic target. Methods and Results: In this study, we identified AMP-activated protein kinase (AMPK) as one of several proteins capable of repressing the TAZ-CAMTA1 transcriptional activity in NIH3T3 and HEK293 cell lines. The pharmacologic activation of AMPK inhibited the proliferation of EHE cell lines without inducing apoptosis; however, in contrast to the NIH3T3 and HEK293 models, AMPK activation in EHE cells unexpectedly increased the TAZ-CAMTA1 expression and activity. Notably, elevated TAZ-CAMTA1 expression was also associated with reduced EHE cell growth, suggesting that the induction of TAZ-CAMTA1 may be one mechanism by which AMPK suppresses EHE growth. Additionally, we found that AMPK inhibits mTOR activity and that direct mTOR inhibition also suppresses EHE cell growth. Conclusions: Together, these findings demonstrate that AMPK activation impairs EHE viability through dual mechanisms: by promoting TAZ-CAMTA1 expression and by inhibiting mTOR signaling. This work highlights AMPK as a potential therapeutic target in EHE and supports the growing body of evidence favoring mTOR inhibitors as promising treatments for this rare cancer. Full article
(This article belongs to the Special Issue Clinical Trials of Sarcoma)
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