Chromosomal and genetic changes produced in tumoral progression of embryonal rhabdomyosarcoma

Gil-Benso, Rosario; San-Miguel, Teresa; Callaghan, Robert C.; Bataller-Calatayud, A; Caballero, Javier Martínez; Pellín-Carcelén, Ana; Donat, J; Navarro, Samuel; Peris, Torres; Cerdá-Nicolás, Miguel; López‐Ginés, Concha

doi:10.1111/his.12064

Cited by 5 publications

(7 citation statements)

References 5 publications

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“…The allelotype of ERMS demonstrates a high frequency of LOH on chromosomes 11p, 11q, and 16q [ 28 ]. ERMS tumorigenesis can result from the inactivation of the parental bias of chromosome 11p15, which is the most common rearrangement in ERMS [ 29 ]. The proportion of ERMS with LOH along chromosome 11 is considerably higher than in other subtypes [ 27 ].…”

Section: Novel Discoveries Of Chromosomal Alterations In Rmsmentioning

confidence: 99%

Rhabdomyosarcoma: Advances in Molecular and Cellular Biology

Sun

Guo

Shen

et al. 2015

Sarcoma

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Rhabdomyosarcoma (RMS) is the most common soft tissue malignancy in childhood and adolescence. The two major histological subtypes of RMS are alveolar RMS, driven by the fusion protein PAX3-FKHR or PAX7-FKHR, and embryonic RMS, which is usually genetically heterogeneous. The prognosis of RMS has improved in the past several decades due to multidisciplinary care. However, in recent years, the treatment of patients with metastatic or refractory RMS has reached a plateau. Thus, to improve the survival rate of RMS patients and their overall well-being, further understanding of the molecular and cellular biology of RMS and identification of novel therapeutic targets are imperative. In this review, we describe the most recent discoveries in the molecular and cellular biology of RMS, including alterations in oncogenic pathways, miRNA (miR), in vivo models, stem cells, and important signal transduction cascades implicated in the development and progression of RMS. Furthermore, we discuss novel potential targeted therapies that may improve the current treatment of RMS.

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Section: Novel Discoveries Of Chromosomal Alterations In Rmsmentioning

confidence: 99%

Rhabdomyosarcoma: Advances in Molecular and Cellular Biology

Sun

Guo

Shen

et al. 2015

Sarcoma

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“…As for chromosomal rearrangements, the embryonal subtype is mainly characterized by the presence of loss of heterozygosity (LOH) of the short arm of chromosome 11 (11p15.5) and 16q [14,15]. It has been demonstrated that the most common rearrangements in ERMS are the inactivation of the parental bias of chromosome 11p15 [16] (Figure 1). Novel complex chromosomal rearrangements in PAX3 were rarely reported [17].…”

Section: Overview Rms (Rhabdomyosarcoma)mentioning

confidence: 99%

MiRNAs as Players in Rhabdomyosarcoma Development

Gasparini

Ferrari

Casanova

et al. 2019

IJMS

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Rhabdomyosarcoma (RMS), the most common soft tissue sarcoma of childhood and adolescence, is a rare but aggressive malignancy that originates from immature mesenchymal cells committed to skeletal muscle differentiation. Although RMS is, generally, responsive to the modern multimodal therapeutic approaches, the prognosis of RMS depends on multiple variables and for some patients the outcome remains dismal. Further comprehension of the molecular and cellular biology of RMS would lead to identification of novel therapeutic targets. MicroRNAs (miRNAs) are small non-coding RNAs proved to function as key regulators of skeletal muscle cell fate determination and to play important roles in RMS pathogenesis. The purpose of this review is to better delineate the role of miRNAs as a biomarkers or functional leaders in RMS development, so to possibly elucidate some of RMS molecular mechanisms and potentially therapeutically target them to improve clinical management of pediatric RMS.

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“…The study was performed with the approval from the Institutional Review Board of the University of Valencia. Cases, source, location and additional information are summarized in Table 1; the cytogenetic features of the cases have been previously reported [6,7].…”

Section: Tumor Samplesmentioning

confidence: 99%

“…ARMS is more aggressive and frequently have a bad outcome; cytogenetics show a characteristic t(2;13)(q35;q14) translocation or its variant t(1;13)(p36;q14) in 80 % of cases [2]; these translocations result in fusion genes that encode proteins with increased transcriptional activity [3,4]. ERMS usually shows gain of whole chromosomes but no characteristic structural anomalies [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Expression of the Chemokine Receptors CXCR3, CXCR4, CXCR7 and Their Ligands in Rhabdomyosarcoma

San-Miguel

Pinto

Navarro

et al. 2015

Pathol. Oncol. Res.

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Rhabdomyosarcomas (RMS) are soft tissue malignant tumors of childhood and adolescents. The mechanisms underlying their aggressiveness are still poorly understood. Chemokines are chemotactic proteins involved in pathological processes that have been intensely studied in several types of cancers because of their influence in migration, angiogenesis, or metastases. We analyzed the expression of the chemokine receptors CXCR3, CXCR4 and CXCR7 and their ligands CXCL9, CXCL10, CXCL11 and CXCL12, in 15 RMS samples derived from nine patients. Expression was measured in tumors and primary cultures of RMS by Real-Time Polymerase Chain Reaction, immunostaining and flow cytometry. Our results show that these receptors are widely expressed in RMS. A significant difference between CXCL12/CXCR4, CXCL12/CXCR7, CXCL11/CXCR7 expression ratios was found in alveolar versus embryonal RMS and similarly between CXCL12/CXCR4 and CXCL11/CXCR3 ratios in primary versus recurrent tumors. These findings suggest a possible association between the interrelation of chemokine/chemokine-receptor and an aggressive biological behavior in RMS.

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Chromosomal and genetic changes produced in tumoral progression of embryonal rhabdomyosarcoma

Cited by 5 publications

References 5 publications

Rhabdomyosarcoma: Advances in Molecular and Cellular Biology

Rhabdomyosarcoma: Advances in Molecular and Cellular Biology

MiRNAs as Players in Rhabdomyosarcoma Development

Expression of the Chemokine Receptors CXCR3, CXCR4, CXCR7 and Their Ligands in Rhabdomyosarcoma

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