Cytogenetic and molecular findings related to rhabdomyosarcoma. An analysis of seven cases

Gil-Benso, Rosario; López‐Ginés, Concha; Cardá, Carmen; López-Guerrero, José Antonio; Ferrer, Jaime; A, Pellín-Pérez; Llombart‐Bosch, Antonio

doi:10.1016/s0165-4608(03)00026-8

Cited by 16 publications

(13 citation statements)

References 34 publications

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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%

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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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Section: Tumor Samplesmentioning

confidence: 99%

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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“…Another member of the p53 pathway is ARF, which blocks MDM2 function and stabilizes the p53 protein. Although mutations of ARF have not been reported in RMS, homozygous deletions of the 9p21 region, which contains the CDKN2A common locus for both P16 INK4A and ARF , were found in 25–33% of ERMS cases (Gil-Benso et al ., 2003; Iolascon et al , 1996). …”

Section: Mutations Seen In Fusion-negative Rmsmentioning

confidence: 99%

Developmental Origins of Fusion-Negative Rhabdomyosarcomas

Kikuchi

Rubin

Keller

2011

Current Topics in Developmental Biology

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Rhabdomyosarcomas (RMS) are very heterogeneous tumors that can be divided into three major groups: alveolar rhabdomyosarcoma, embryonal rhabdomyosarcoma, and pleomorphic rhabdomyosarcoma. Concerted efforts over the past a decade have led to an understanding of the genetic underpinnings of many human tumors through genetically engineered models; however, left largely behind in this effort have been rare tumors with poorly understood chromosomal abnormalities including the vast majority of RMS lacking a pathognomonic translocation, i.e. fusion-negative RMS. In this chapter, we review the characteristic genetic abnormalities associated with human RMS and the genetically engineered animal models for these fusion-negative RMS. We explore not only how specific combinations of mutations and cell of origin give rise to different histologically and biologically distinguishable pediatric and adult RMS subtypes, but we also examine how tumor cell phenotype (and tumor “stem” cell phenotype) can vary markedly from the cell of origin.

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“…Extra copies of chromosome 8 have been referred to in previously reported cases of scERMS. 2,3,5 The role played by these extra copies in scERMS and their influence on drug resistance should be investigated. With reverse transcription polymerase chain reaction, no specific PAX3-FOXO1 or PAX7-FOXO1 fusion transcripts were detected in any of the analysed samples, confirming the embryonal subtype of the tumours.…”

mentioning

confidence: 99%

“…R Gil-Benso 1 T San-Miguel 1 R C Callaghan 1 A Bataller-Calatayud 1 J Caballero 1 A Pell ın-Carcel en 1 J Donat 2 S Navarro 1,3 T Peris 1 M Cerd a-Nicol as 1,3 C L opez-Gin es 1…”

mentioning

confidence: 99%

Chromosomal and genetic changes produced in tumoral progression of embryonal rhabdomyosarcoma

et al. 2013

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Cytogenetic and molecular findings related to rhabdomyosarcoma. An analysis of seven cases

Cited by 16 publications

References 34 publications

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

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

Developmental Origins of Fusion-Negative Rhabdomyosarcomas

Chromosomal and genetic changes produced in tumoral progression of embryonal rhabdomyosarcoma

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