UTRN on chromosome 6q24 is mutated in multiple tumors

Li, Y; Huang, Jianmin; Zhao, Yanling; He, Jié; W, Wang; Davies, Kay E.; Nosé, Vânia; Xiao, Sheng

doi:10.1038/sj.onc.1210432

Cited by 41 publications

(40 citation statements)

References 28 publications

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“…For the 6q24 region, which was found to be commonly deleted in our array CGH experiments, two probes flanking UTRN were used (Table 2); this tumor suppressor gene is known to be deleted in several types of neoplasms. 18 FISH was performed on interphase nuclei in 26 cases, on metaphase spreads in five (CMF22, CMF28, CMF29, CMF31 and CMF43), and on both interphase nuclei and metaphase spreads in one tumor (CMF29), giving consistent results. Probe labeling and hybridization were done as previously described.…”

Section: Fish Mappingmentioning

confidence: 57%

“…Deletions may also result in inactivation of genes, and it could be noted that the 6q24 region is reported to be deleted in several other tumors. 18 Two candidate tumor suppressor genes map to 6q24: UTRN and PLAGL1. 18,21 The level of expression of these two genes was, however, not altered in cases with deletion of this region, suggesting that haploinsufficiency alone of PLAGL1 or UTRN is not of pathogenetic significance in CMF.…”

Section: Discussionmentioning

confidence: 99%

“…18 Two candidate tumor suppressor genes map to 6q24: UTRN and PLAGL1. 18,21 The level of expression of these two genes was, however, not altered in cases with deletion of this region, suggesting that haploinsufficiency alone of PLAGL1 or UTRN is not of pathogenetic significance in CMF. For case CMF29 it is difficult to speculate on the consequence of a large 6q deletion.…”

Section: Discussionmentioning

confidence: 99%

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Heterogeneous and Complex Rearrangements of Chromosome Arm 6q in Chondromyxoid Fibroma

Romeo

Duim

Bridge

et al. 2010

The American Journal of Pathology

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Chondromyxoid fibroma (CMF) is an uncommon benign cartilaginous tumor of bone usually occurring during the second decade of life. CMF is associated with recurrent rearrangements of chromosome bands 6p23-25, 6q12-15, and 6q23-27. To delineate further the role and frequency of the involvement of three candidate regions (6q13, 6q23.3 and 6q24) in the pathogenesis of CMF, we studied a group of 43 cases using a molecular cytogenetic approach. Fluorescence in situ hybridization with probe sets bracketing the putative breakpoint regions was performed in 30 cases. The expression level of nearby candidate genes was studied by immunohistochemistry and quantitative RT-PCR in 24 and 23 cases, respectively. Whole-genome copy number screening was performed by array comparative genomic hybridization in 16 cases. Balanced and unbalanced rearrangements of 6q13 and 6q23.3 occurred in six and five cases, respectively, and a hemizygous deletion in 6q24 was found in five cases. Two known tumor suppressor genes map to the latter region: PLAGL1 and UTRN. However, neither of these two genes nor BCLAF1 and COL12A1, respectively located in 6q23.3 and 6q13, showed altered expression. Therefore, although rearrangements of chromosomal regions 6q13, 6q23.3, and 6q24 are common in CMF, the complexity of the changes precludes the use of a single fluorescence in situ hybridization probe set as an adjunct diagnostic tool. These data indicate that the genetic alterations in CMF are heterogeneous and are likely a result of a cryptic rearrangement beyond the resolution level of combined binary ratio fluorescence in situ hybridization or a point mutation.

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Section: Fish Mappingmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Heterogeneous and Complex Rearrangements of Chromosome Arm 6q in Chondromyxoid Fibroma

Romeo

Duim

Bridge

et al. 2010

The American Journal of Pathology

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“…The other two genes, UTRN and RYR1, were not registered in the cancer gene consensus database but were implicated in cancer pathways 30 . Also, UTRN is known to be mutated in multiple cancers 31 .…”

Section: Resultsmentioning

confidence: 99%

DNA replication timing and selection shape the landscape of nucleotide variation in cancer genomes

2012

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Cancer cells evolve from normal cells by somatic mutations and natural selection. Comparing the evolution of cancer cells and that of organisms can elucidate the genetic basis of cancer. Here we analyse somatic mutations in > 400 cancer genomes. We find that the frequency of somatic single-nucleotide variations increases with replication time during the s phase much more drastically than germ-line single-nucleotide variations and somatic large-scale structural alterations, including amplifications and deletions. The ratio of nonsynonymous to synonymous single-nucleotide variations is higher for cancer cells than for germ-line cells, suggesting weaker purifying selection against somatic mutations. Among genes with recurrent mutations only cancer driver genes show evidence of strong positive selection, and late-replicating regions are depleted of cancer driver genes, although enriched for recurrently mutated genes. These observations show that replication timing has a prominent role in shaping the single-nucleotide variation landscape of cancer cells.

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“…Significantly, antisense-mediated gene silencing has been recently shown to provide a powerful tool for the identification of tumor suppressor genes. For instance, Li et al were able to demonstrate the oncosuppressive role for the utrophin gene by a functional assay based on antisense-mediated suppression of the endogenous sense gene transcript from this locus in a cancer cell line (43). Despite this suggestive evidence, to date little effort has been devoted to a better understanding of the role that antisense-mediated regulation of gene expression play in the pathogenesis of cancer.…”

Section: Discussionmentioning

confidence: 99%

In silico prediction and experimental validation of natural antisense transcripts in two cancer-associated regions of human chromosome 6

Monti

Cinquetti

Guffanti³

et al. 2009

Int J Oncol

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Abstract. Antisense transcription has long been recognized as a mechanism involved in the regulation of gene expression. Therefore, several human diseases associated with abnormal patterns of gene expression might display antisense RNAmediated pathogenetic mechanisms. Such issue could be particularly relevant for cancer pathogenesis, since deregulated gene expression has long been established as a hallmark of cancer cells. Herein, we report on a bioinformatic search for antisense transcription in two cancer-associated regions of human chromosome 6 (6q21 and 6q27). Natural antisense transcripts (NATs) for several genes in both genomic regions were predicted in silico and subsequently validated by strand-specific RT-PCR. Detailed experimental validation by quantitative real-time RT-PCR of five putative cancer related sense-antisense transcript pairs revealed a single candidate tumor suppressor gene (RPS6KA2) whose expression levels display marked cancer-related changes that are likely mediated by its antisense RNA in a breast cancer cell line model.

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UTRN on chromosome 6q24 is mutated in multiple tumors

Cited by 41 publications

References 28 publications

Heterogeneous and Complex Rearrangements of Chromosome Arm 6q in Chondromyxoid Fibroma

Heterogeneous and Complex Rearrangements of Chromosome Arm 6q in Chondromyxoid Fibroma

DNA replication timing and selection shape the landscape of nucleotide variation in cancer genomes

In silico prediction and experimental validation of natural antisense transcripts in two cancer-associated regions of human chromosome 6

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