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Journal articles on the topic 'Sarcomagenesis'

Author: Grafiati

Published: 5 June 2025

Last updated: 16 July 2025

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1

Cardona, Andrés Felipe, Jairo Zuluaga, Hernán Carranza, Jorge Miguel Otero, and Carlos Vargas. "Sarcomagenesis." Revista Colombiana de Hematología y Oncología 1, no. 4 (2012): 30–38. http://dx.doi.org/10.51643/22562915.321.

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Los sarcomas representan un número heterogéneo de neoplasias que surgen de la transformación de algunas células mesenquimales primitivas. La evidencia ha aumentado de forma considerable respecto de las células pluripotenciales que dan origen a estos tumores y que parecen ser responsables de la iniciación, el mantenimiento, la diferenciación y la proliferación del osteosarcoma, sarcoma sinovial, rabdomiosarcoma y del sarcoma de Ewing. Se han adoptado diferentes métodos para la identificación de células primitivas en los sarcomas, tales como el uso de marcadores de superficie, la citometría de f

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2

Matushansky, Igor, and Robert G. Maki. "Mechanisms of Sarcomagenesis." Hematology/Oncology Clinics of North America 19, no. 3 (2005): 427–49. http://dx.doi.org/10.1016/j.hoc.2005.03.006.

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3

Hayashi, Takuma. "Genomic Analysis of Sarcomagenesis." Journal of Gynecology and Obstetrics Bulletin 1, no. 1 (2016): 1–2. http://dx.doi.org/10.24218/jgob.2016.01.

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4

Underhill, T. Michael. "Abstract IA004: Mesenchymal progenitors and sarcomagenesis." Clinical Cancer Research 28, no. 18_Supplement (2022): IA004. http://dx.doi.org/10.1158/1557-3265.sarcomas22-ia004.

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Abstract Synovial sarcoma (SS) is an aggressive soft-tissue malignancy that can arise in any area of the body, and most frequently affects adolescents and young adults. The 10-year survival rate has been estimated at 50%. SS is characterized by a pathognomonic t(X;18)(p11.2;q11.2) translocation which produces a fusion oncogene named SS18-SSX. In mouse models, expression of SS18-SSX is sufficient to drive the development of SS-like tumors. Despite recent advancements in our understanding of SS biology, the cell of origin remains undefined. In most instances, it is likely mesenchymal in nature.

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5

Alba-Castellón, Lorena, Raquel Batlle, Clara Francí, et al. "Snail1 Expression Is Required for Sarcomagenesis." Neoplasia 16, no. 5 (2014): 413–21. http://dx.doi.org/10.1016/j.neo.2014.05.002.

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6

Esperança-Martins, Miguel, Iola F.Duarte, Mara Rodrigues, et al. "On the Relevance of Soft Tissue Sarcomas Metabolic Landscape Mapping." International Journal of Molecular Sciences 23, no. 19 (2022): 11430. http://dx.doi.org/10.3390/ijms231911430.

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Soft tissue sarcomas (STS) prognosis is disappointing, with current treatment strategies being based on a “fit for all” principle and not taking distinct sarcoma subtypes specificities and genetic/metabolic differences into consideration. The paucity of precision therapies in STS reflects the shortage of studies that seek to decipher the sarcomagenesis mechanisms. There is an urge to improve STS diagnosis precision, refine STS classification criteria, and increase the capability of identifying STS prognostic biomarkers. Single-omics and multi-omics studies may play a key role on decodifying sa

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7

Rodriguez, Rene, Ruth Rubio, and Pablo Menendez. "Modeling sarcomagenesis using multipotent mesenchymal stem cells." Cell Research 22, no. 1 (2011): 62–77. http://dx.doi.org/10.1038/cr.2011.157.

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8

Radons, Jürgen. "Inflammatory stress and sarcomagenesis: a vicious interplay." Cell Stress and Chaperones 19, no. 1 (2013): 1–13. http://dx.doi.org/10.1007/s12192-013-0449-4.

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9

Miller, Henry E., Aparna Gorthi, Nicklas Bassani, Liesl A. Lawrence, Brian S. Iskra, and Alexander J. R. Bishop. "Reconstruction of Ewing Sarcoma Developmental Context from Mass-Scale Transcriptomics Reveals Characteristics of EWSR1-FLI1 Permissibility." Cancers 12, no. 4 (2020): 948. http://dx.doi.org/10.3390/cancers12040948.

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Ewing sarcoma is an aggressive pediatric cancer of enigmatic cellular origins typically resulting from a single translocation event t (11; 22) (q24; q12). The resulting fusion gene, EWSR1-FLI1, is toxic or unstable in most primary tissues. Consequently, attempts to model Ewing sarcomagenesis have proven unsuccessful thus far, highlighting the need to identify the cellular features which permit stable EWSR1-FLI1 expression. By re-analyzing publicly available RNA-Sequencing data with manifold learning techniques, we uncovered a group of Ewing-like tissues belonging to a developmental trajectory

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10

Kannan, Sarmishta, Ian Lock, Benjamin B. Ozenberger, and Kevin B. Jones. "Genetic drivers and cells of origin in sarcomagenesis." Journal of Pathology 254, no. 4 (2021): 474–93. http://dx.doi.org/10.1002/path.5617.

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11

Watson, Sarah, Collette A. LaVigne, Lin Xu, et al. "VGLL2-NCOA2 leverages developmental programs for pediatric sarcomagenesis." Cell Reports 42, no. 1 (2023): 112013. http://dx.doi.org/10.1016/j.celrep.2023.112013.

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12

Jones, Kevin B. "What’s in a Name? Cell Fate Reprogramming in Sarcomagenesis." Cancer Cell 33, no. 1 (2018): 5–7. http://dx.doi.org/10.1016/j.ccell.2017.12.005.

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13

Martin, Daniel, Rebeca Galisteo, Alfredo A. Molinolo, Reinhard Wetzker, Emilio Hirsch та J. Silvio Gutkind. "PI3Kγ Mediates Kaposi's Sarcoma-Associated Herpesvirus vGPCR-Induced Sarcomagenesis". Cancer Cell 19, № 6 (2011): 805–13. http://dx.doi.org/10.1016/j.ccr.2011.05.005.

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14

Li, Luyuan, Josiane E. Eid, Ana C. Paz, and Jonathan C. Trent. "Metabolic Enzymes in Sarcomagenesis: Progress Toward Biology and Therapy." BioDrugs 31, no. 5 (2017): 379–92. http://dx.doi.org/10.1007/s40259-017-0237-2.

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15

Weber, Achim, Annette Strehl, Erik Springer, Torsten Hansen, Arno Schad, and C. James Kirkpatrick. "Biomaterial-induced sarcomagenesis is not associated with microsatellite instability." Virchows Archiv 454, no. 2 (2008): 195–201. http://dx.doi.org/10.1007/s00428-008-0705-7.

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16

Tanaka, Miwa, Mizuki Homme, Yukari Yamazaki, et al. "Cooperation between SS18-SSX1 and miR-214 in Synovial Sarcoma Development and Progression." Cancers 12, no. 2 (2020): 324. http://dx.doi.org/10.3390/cancers12020324.

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SS18-SSX fusion proteins play a central role in synovial sarcoma development, although, the genetic network and mechanisms of synovial sarcomagenesis remain unknown. We established a new ex vivo synovial sarcoma mouse model through retroviral-mediated gene transfer of SS18-SSX1 into mouse embryonic mesenchymal cells followed by subcutaneous transplantation into nude mice. This approach successfully induced subcutaneous tumors in 100% recipients, showing invasive proliferation of short spindle tumor cells with occasional biphasic appearance. Cytokeratin expression was observed in epithelial com

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17

Fujino, Takashi, Kimie Nomura, Yuichi Ishikawa, et al. "Function of EWS-POU5F1 in Sarcomagenesis and Tumor Cell Maintenance." American Journal of Pathology 176, no. 4 (2010): 1973–82. http://dx.doi.org/10.2353/ajpath.2010.090486.

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18

Siddiqi, S., M. Terry, and I. Matushansky. "The role of HIWI in stem cell maintenance and sarcomagenesis." Journal of Clinical Oncology 29, no. 15_suppl (2011): e20500-e20500. http://dx.doi.org/10.1200/jco.2011.29.15_suppl.e20500.

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19

Lu, C., S. U. Jain, D. Hoelper, et al. "Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape." Science 352, no. 6287 (2016): 844–49. http://dx.doi.org/10.1126/science.aac7272.

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20

Galoian, K., T. Guettouche, B. Issac, L. Navarro, and H. T. Temple. "Lost miRNA surveillance of Notch, IGFR pathway—road to sarcomagenesis." Tumor Biology 35, no. 1 (2013): 483–92. http://dx.doi.org/10.1007/s13277-013-1068-5.

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21

Matushansky, I., N. Socci, E. Hernando, et al. "A putative tumor suppressor role for Wnt-signaling in sarcomagenesis." Journal of Clinical Oncology 24, no. 18_suppl (2006): 9507. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.9507.

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9507 Background: We sought to elucidate the relationship between the human adult mesenchymal stem cell (hMSC), Wnt signaling and sarcomagenesis. Methods: In vitro hMSC differentiation, microarray gene expression analysis, distance correlation analysis, and standard molecular biology techniques were used to explore the role of Wnt in controlling the differentiation of both hMSCs and high grade undifferentiated sarcoma (HGUS; MFH, malignant fibrous histiocytoma), a common form of adult soft tissue sarcoma. Results: We determined that 1) hMSCs appear to be the progenitor cells of HGUS/MFH; 2) Dic

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22

Barrott, Jared J., Ju-Fen Zhu, Kyllie Smith-Fry, et al. "The Influential Role of BCL2 Family Members in Synovial Sarcomagenesis." Molecular Cancer Research 15, no. 12 (2017): 1733–40. http://dx.doi.org/10.1158/1541-7786.mcr-17-0315.

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23

Watson, Sarah, Collette A. LaVigne, Lin Xu, et al. "Abstract 3525: VGLL2-NCOA2 leverages developmental programs for pediatric sarcomagenesis." Cancer Research 83, no. 7_Supplement (2023): 3525. http://dx.doi.org/10.1158/1538-7445.am2023-3525.

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Abstract Clinical sequencing efforts are rapidly identifying sarcoma gene fusions that have not been functionally validated for their transformation capacity and biological activity. An example is the new fusion of transcriptional coactivators, VGLL2-NCOA2, found in infantile rhabdomyosarcoma. To delineate VGLL2-NCOA2 tumorigenic mechanisms and identify therapeutic vulnerabilities, we implemented a cross-species comparative oncology approach with zebrafish, mouse allograft, and patient samples. We found that in our transgenic zebrafish and mouse allograft models, VGLL2-NCOA2 is sufficient to g

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24

Ye, Shuai, Matthew A. Lawlor, Adrian Rivera-Reyes та ін. "YAP1-Mediated Suppression of USP31 Enhances NFκB Activity to Promote Sarcomagenesis". Cancer Research 78, № 10 (2018): 2705–20. http://dx.doi.org/10.1158/0008-5472.can-17-4052.

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25

Young, Nathan P., Denise Crowley, and Tyler Jacks. "Uncoupling Cancer Mutations Reveals Critical Timing of p53 Loss in Sarcomagenesis." Cancer Research 71, no. 11 (2011): 4040–47. http://dx.doi.org/10.1158/0008-5472.can-10-4563.

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26

Sodhi, Akrit, Silvia Montaner, and J. Silvio Gutkind. "Does dysregulated expression of a deregulated viral GPCR trigger Kaposi's sarcomagenesis?" FASEB Journal 18, no. 3 (2004): 422–27. http://dx.doi.org/10.1096/fj.03-1035hyp.

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27

Arconada-Luque, Elena, Jaime Jiménez-Suarez, Raquel Pascual-Serra, et al. "ERK5 Is a Major Determinant of Chemical Sarcomagenesis: Implications in Human Pathology." Cancers 14, no. 14 (2022): 3509. http://dx.doi.org/10.3390/cancers14143509.

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Sarcomas are a heterogeneous group of tumors in which the role of ERK5 is poorly studied. To clarify the role of this MAPK in sarcomatous pathology, we used a murine 3-methyl-cholanthrene (3MC)-induced sarcoma model. Our data show that 3MC induces pleomorphic sarcomas with muscle differentiation, showing an increased expression of ERK5. Indeed, this upregulation was also observed in human sarcomas of muscular origin, such as leiomyosarcoma or rhabdomyosarcoma. Moreover, in cell lines derived from these 3MC-induced tumors, abrogation of Mapk7 expression by using specific shRNAs decreased in vit

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28

Matushansky, Igor, Eva Hernando, Nicholas D. Socci, et al. "A Developmental Model of Sarcomagenesis Defines a Differentiation-Based Classification for Liposarcomas." American Journal of Pathology 172, no. 4 (2008): 1069–80. http://dx.doi.org/10.2353/ajpath.2008.070284.

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29

Barrott, Jared J., Benjamin E. Illum, Huifeng Jin та ін. "Paracrine osteoprotegerin and β-catenin stabilization support synovial sarcomagenesis in periosteal cells". Journal of Clinical Investigation 128, № 1 (2017): 207–18. http://dx.doi.org/10.1172/jci94955.

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30

AbdelMageed, M. A., P. Foltopoulou, and E. A. McNiel. "Feline vaccine-associated sarcomagenesis: Is there an inflammation-independent role for aluminium?" Veterinary and Comparative Oncology 16, no. 1 (2017): E130—E143. http://dx.doi.org/10.1111/vco.12358.

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31

Guarnerio, Jlenia, Luisa Riccardi, Riccardo Taulli, et al. "A Genetic Platform to Model Sarcomagenesis from Primary Adult Mesenchymal Stem Cells." Cancer Discovery 5, no. 4 (2015): 396–409. http://dx.doi.org/10.1158/2159-8290.cd-14-1022.

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32

Charytonowicz, Elizabeth, Igor Matushansky, Mireia Castillo-Martin, Todd Hricik, Carlos Cordon-Cardo, and Mel Ziman. "Alternate PAX3 and PAX7 C-terminal isoforms in myogenic differentiation and sarcomagenesis." Clinical and Translational Oncology 13, no. 3 (2011): 194–203. http://dx.doi.org/10.1007/s12094-011-0640-y.

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33

Cavallin, Lucas E., Qi Ma, Julian Naipauer, et al. "KSHV-induced ligand mediated activation of PDGF receptor-alpha drives Kaposi's sarcomagenesis." PLOS Pathogens 14, no. 7 (2018): e1007175. http://dx.doi.org/10.1371/journal.ppat.1007175.

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34

Maxwell, Matthew B., and Diana C. Hargreaves. "Down, but Not Out: A Role for SMARCB1 in Synovial Sarcoma." Cancer Discovery 11, no. 10 (2021): 2375–77. http://dx.doi.org/10.1158/2159-8290.cd-21-0591.

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Abstract Summary: Reduced protein expression of the BAF complex (also known as SWI/SNF) tumor suppressor SMARCB1 is frequently observed in human synovial sarcoma, a soft-tissue malignancy driven by the oncogenic SS18–SSX fusion, which competes with wild-type SS18 for BAF complex incorporation. In this issue of Cancer Discovery, Li and Mulvihill reveal that low-expressed SMARCB1 has a functional role in synovial sarcomagenesis in mouse models expressing the SS18–SSX2 fusion and present evidence that SMARCB1 reduction in synovial sarcoma is due to wholesale degradation of canonical BAF complexes

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35

Kim, Roger H., Benjamin D. L. Li, and Quyen D. Chu. "The Role of Chemokine Receptor CXCR4 in the Biologic Behavior of Human Soft Tissue Sarcoma." Sarcoma 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/593708.

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The molecular basis of sarcoma remains poorly understood. However, recent studies have begun to uncover some of the molecular pathways involved in sarcomagenesis. The chemokine receptor CXCR4 has been implicated in sarcoma development and has been found to be a prognostic marker for poor clinical outcome. There is growing evidence that overexpression of CXCR4 plays a significant role in development of metastatic disease, especially in directing tumor cells towards the preferential sites of metastases in sarcoma, lung and bone. Although further investigation is necessary to validate these pathw

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36

Zhang, Joyce, Felix Kommoss, Branden Lynch, et al. "Abstract 2611: Cellular origin of DICER1 tumor predisposition syndrome informed by lineage-traceable genetically engineered mouse model." Cancer Research 85, no. 8_Supplement_1 (2025): 2611. https://doi.org/10.1158/1538-7445.am2025-2611.

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Abstract Introduction: DICER1 tumor predisposition syndrome is a genetic disorder driven by germline DICER1 pathogenic variants that predisposes pediatric and young adult patients to cancers of various organs. The second, missense mutation in RNase IIIb domain leads to systemic loss of mature 5p-miRNAs. Tumours of various sites are histologically and molecularly similar, suggesting a shared cellular origin and oncogenic mechanisms. To this end, we expanded our first-ever genetically engineered mouse model (GEMM) that recapitulated human Müllerian adenosarcomas, a DICER1 neoplasm, through indu

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37

Teitz, T., T. S. B. Yen, and Y. W. Kan. "Amplification of a SV40 T antigen transgene is associated with sarcomagenesis in mice." Carcinogenesis 15, no. 9 (1994): 2049–51. http://dx.doi.org/10.1093/carcin/15.9.2049.

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38

Jain, Neha, Jyoti Roy, Basudeb Das, and Bibekanand Mallick. "miR‐197‐5p inhibits sarcomagenesis and induces cellular senescence via repression of KIAA0101." Molecular Carcinogenesis 58, no. 8 (2019): 1376–88. http://dx.doi.org/10.1002/mc.23021.

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39

Iomhair, Maura Mhic, and S. M. Lavelle. "Effect of 3 growth control substances on foreign body sarcomagenesis: IFN, IUdR, MGBG." Irish Journal of Medical Science 168, no. 1 (1999): 42–44. http://dx.doi.org/10.1007/bf02939580.

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40

Jones, K. B., J. J. Barrott, M. Xie, et al. "The impact of chromosomal translocation locus and fusion oncogene coding sequence in synovial sarcomagenesis." Oncogene 35, no. 38 (2016): 5021–32. http://dx.doi.org/10.1038/onc.2016.38.

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41

Kohrn, Rachael, and Joyce Ohm. "Abstract A029 Investigating the role of environmental toxicant exposures and STAG2 loss in sarcomagenesis." Cancer Research 84, no. 17_Supplement (2024): A029. http://dx.doi.org/10.1158/1538-7445.pediatric24-a029.

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Abstract Humans are exposed to a variety of environmental toxicants which have been implicated in contributing to cancer development. A possible explanation for this link is that adaptive epigenetic changes occur in stem cell populations upon toxicant exposure. These cells are particularly vulnerable during developmental stages, leading to abnormal gene expression later in life. Environmental exposures have been associated with the initiation of sarcoma development. This study will focus on Ewing Sarcoma (ES), as this malignancy has a low mutational burden relative to other cancer types and is

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42

Shive, Heather R., John S. House, Jordan L. Ferguson, Dereje D. Jima, Aubrie A. Selmek, and Dillon T. Lloyd. "Abstract PR011: Characterization of the precancerous and cancer microenvironment in a zebrafish sarcoma model." Clinical Cancer Research 28, no. 18_Supplement (2022): PR011. http://dx.doi.org/10.1158/1557-3265.sarcomas22-pr011.

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Abstract Contributions of the microenvironment to soft tissue sarcoma progression are relatively undefined, representing a major impediment to identifying essential regulatory networks in sarcomagenesis. Furthermore, genetic and molecular characteristics that distinguish precancerous versus cancerous microenvironments are not well known across human cancer types. While animal models have the potential to reveal these complex processes, significant impediments to such inquiries include (1) the difficulty in distinguishing microenvironmental cells from precancerous or cancer cells in tissue spec

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43

Hai, Yu, Asuka Kawachi, Xiaodong He, and Akihide Yoshimi. "Pathogenic Roles of RNA-Binding Proteins in Sarcomas." Cancers 14, no. 15 (2022): 3812. http://dx.doi.org/10.3390/cancers14153812.

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RNA-binding proteins (RBPs) are proteins that physically and functionally bind to RNA to regulate the RNA metabolism such as alternative splicing, polyadenylation, transport, maintenance of stability, localization, and translation. There is accumulating evidence that dysregulated RBPs play an essential role in the pathogenesis of malignant tumors including a variety of types of sarcomas. On the other hand, prognosis of patients with sarcoma, especially with sarcoma in advanced stages, is very poor, and almost no effective standard treatment has been established for most of types of sarcomas so

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44

Chen, Mark, Eric S. Xu, Nathan H. Leisenring, et al. "The Fusion Oncogene FUS-CHOP Drives Sarcomagenesis of High-Grade Spindle Cell Sarcomas in Mice." Sarcoma 2019 (July 25, 2019): 1–14. http://dx.doi.org/10.1155/2019/1340261.

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Myxoid liposarcoma is a malignant soft tissue sarcoma characterized by a pathognomonic t(12;16)(q13;p11) translocation that produces a fusion oncoprotein, FUS-CHOP. This cancer is remarkably sensitive to radiotherapy and exhibits a unique pattern of extrapulmonary metastasis. Here, we report the generation and characterization of a spatially and temporally restricted mouse model of sarcoma driven by FUS-CHOP. Using different Cre drivers in the adipocyte lineage, we initiated in vivo tumorigenesis by expressing FUS-CHOP in Prrx1+ mesenchymal progenitor cells. In contrast, expression of FUS-CHOP

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45

Straessler, Krystal M., Kevin B. Jones, Hao Hu, Huifeng Jin, Matt van de Rijn, and Mario R. Capecchi. "Modeling Clear Cell Sarcomagenesis in the Mouse: Cell of Origin Differentiation State Impacts Tumor Characteristics." Cancer Cell 23, no. 2 (2013): 215–27. http://dx.doi.org/10.1016/j.ccr.2012.12.019.

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46

Scotlandi, Katia, Claudia Maria Hattinger, Evelin Pellegrini, Marco Gambarotti, and Massimo Serra. "Genomics and Therapeutic Vulnerabilities of Primary Bone Tumors." Cells 9, no. 4 (2020): 968. http://dx.doi.org/10.3390/cells9040968.

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Osteosarcoma, Ewing sarcoma and chondrosarcoma are rare diseases but the most common primary tumors of bone. The genes directly involved in the sarcomagenesis, tumor progression and treatment responsiveness are not completely defined for these tumors, and the powerful discovery of genetic analysis is highly warranted in the view of improving the therapy and cure of patients. The review summarizes recent advances concerning the molecular and genetic background of these three neoplasms and, of their most common variants, highlights the putative therapeutic targets and the clinical trials that ar

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47

Kim, Ted, and Nam Q. Bui. "The Next Frontier in Sarcoma: Molecular Pathways and Associated Targeted Therapies." Cancers 15, no. 6 (2023): 1692. http://dx.doi.org/10.3390/cancers15061692.

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Soft tissue sarcomas (STS) are a rare, complex, heterogeneous group of mesenchymal neoplasms with over 150 different histological subtypes. Treatments for this malignancy have been especially challenging due to the heterogeneity of the disease and the modest efficacy of conventional chemotherapy. The next frontier lies in discerning the molecular pathways in which these mesenchymal neoplasms arise, metastasize, and develop drug-resistance, thereby helping guide new therapeutic targets for the treatment of STS. This comprehensive review will discuss the current understanding of tumorigenesis of

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48

Goodwin, Matthew L., Huifeng Jin, Krystal Straessler, et al. "Modeling Alveolar Soft Part Sarcomagenesis in the Mouse: A Role for Lactate in the Tumor Microenvironment." Cancer Cell 26, no. 6 (2014): 851–62. http://dx.doi.org/10.1016/j.ccell.2014.10.003.

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49

Price, J. G., A. J. Wisdom, Y. M. Mowery, H. S. Earp, and D. G. Kirsch. "Deciphering the Role of MerTK in Sarcomagenesis And Response To Radiation Therapy And Immune Checkpoint Blockade." International Journal of Radiation Oncology*Biology*Physics 108, no. 3 (2020): e564. http://dx.doi.org/10.1016/j.ijrobp.2020.07.1743.

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50

Barrott, Jared J., Benjamin E. Illum, Huifeng Jin та ін. "β-catenin stabilization enhances SS18-SSX2-driven synovial sarcomagenesis and blocks the mesenchymal to epithelial transition". Oncotarget 6, № 26 (2015): 22758–66. http://dx.doi.org/10.18632/oncotarget.4283.

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