2013
DOI: 10.1038/oncsis.2013.10
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Overexpression of miR-26a-2 in human liposarcoma is correlated with poor patient survival

Abstract: Approximately 90% of well-differentiated/de-differentiated liposarcomas (WDLPS/DDLPS), the most common LPS subtype, have chromosomal amplification at 12q13-q22. Many protein-coding genes in the region, such as MDM2 and , have been studied as potential therapeutic targets for LPS treatment, with minimal success. In the amplified region near the MDM2 gene, our single nucleotide polymorphism (SNP) array analysis of 75 LPS samples identified frequent amplification of miR-26a-2. Besides being in the amplicon, miR-2… Show more

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Cited by 47 publications
(49 citation statements)
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“…11 In a copy number variation study, miR-26a-2 has been found to be amplified and highly expressed in 22 MLS patients and affects cell proliferation and survival by inhibiting a regulator of chromosome condensation and BTB domain containing protein 1. 12 Global miRNA expression analyses using microarrays from high-grade soft tissue sarcomas 13 and various subtypes of LPS 14 have enabled the identification and classification of MLS tumors based on their miRNA expression profiles.…”
Section: Introductionmentioning
confidence: 99%
“…11 In a copy number variation study, miR-26a-2 has been found to be amplified and highly expressed in 22 MLS patients and affects cell proliferation and survival by inhibiting a regulator of chromosome condensation and BTB domain containing protein 1. 12 Global miRNA expression analyses using microarrays from high-grade soft tissue sarcomas 13 and various subtypes of LPS 14 have enabled the identification and classification of MLS tumors based on their miRNA expression profiles.…”
Section: Introductionmentioning
confidence: 99%
“…Previously, tumor suppressive miR-26a has been studied in numerous types of human cancer, and it was revealed to serve a key role as a cancer suppressor gene in liposarcoma (21), thyroid carcinoma (22) and breast cancer (23). miR-26a was demonstrated to be upregulated in glioma, and may enhance cancer cell growth and colony formation (24).…”
Section: Discussionmentioning
confidence: 99%
“…[20][21][22][23] For example, cytogenomic array studies (aCGH or SNP array) have identified recurrent patterns of copy number changes and/or cnLOH in embryonal rhabdomyosarcoma ( þ 2, þ 7, þ 8, þ 11, þ 12, þ 13, þ 20, cnLOH 11p15.5) with acquisition of genomic amplification in lesions distinguished by the presence of anaplasia, benign metastasizing leiomyoma (loss of 1p, 13q, 19q, and 22q material), and dedifferentiated liposarcoma whereby gain of amplicons in 1p32 and 6q23-25 (containing genes involved in the c-jun NH 2 -terminal kinase/mitogen-activated protein kinase pathway) parallels the progression from an atypical lipomatous tumor/well-differentiated liposarcoma to dedifferentiated liposarcoma, Figure 2. [24][25][26][27][28][29][30] …”
Section: Molecular Cytogenetic Analysismentioning
confidence: 99%
“…Dedifferentiated liposarcoma differs by the acquisition of complex secondary chromosomal changes representing coamplifications of other regions/genes such as 1p32 (JUN), 6q23 (ASK1), and 6q25 (MAP3K7IP2). 25,[28][29][30] For clinical purposes, molecular demonstration of MDM2 ( þ CDK4) amplification is recommended when the diagnosis of ALT/WDL or dedifferentiated liposarcoma is not possible based on clinicohistopathologic information alone.…”
Section: Loss Of Immunophenotype or Dedifferentiationmentioning
confidence: 99%