Telomere biology in neuroblastoma: telomere binding proteins and alternative strengthening of telomeres

Onitake, Yoshiyuki; Hiyama, Eiso; Kamei, Naosuke; Yamaoka, Hiroaki; Sueda, Taijiro; Hiyama, Keiko

doi:10.1016/j.jpedsurg.2009.07.046

Cited by 39 publications

(41 citation statements)

References 31 publications

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“…As shown in our previous study [9], 121 cases that were followed for more than 2 years and had high quality isolated DNA and RNA were selected for further study. Mean age at initial diagnosis was 22.2 months (range, 0-168 months).…”

Section: Samplesmentioning

confidence: 99%

Clinical features of ATRX or DAXX mutated neuroblastoma

Kurihara

Hiyama

Onitake

et al. 2014

Journal of Pediatric Surgery

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Section: Samplesmentioning

confidence: 99%

Clinical features of ATRX or DAXX mutated neuroblastoma

Kurihara

Hiyama

Onitake

et al. 2014

Journal of Pediatric Surgery

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“…The expression levels of TERT, BRG1, and Wnt/β-catenin target genes including MYC, CCND1, ABCB1, MMP7, AXIN2, and BIRC5 in each tumor and the corresponding liver tissue were estimated by the quantitative reverse transcription-PCR as described previously [25]. For BRG1 mRNA expression analysis, wild type and splicing variant types are usually detectable in human somatic cells.…”

Section: Quantitative Reverse Transcription-pcr For Tert Brg1 and Wmentioning

confidence: 99%

Wnt signaling and telomerase activation of hepatoblastoma: correlation with chemosensitivity and surgical resectability

Ueda

Hiyama

Kamimatsuse

et al. 2011

Journal of Pediatric Surgery

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“…16 The estimated frequency of ALT tumors varies from 25 to 34% in grade 2Ϫ4 astrocytomas, 35% in smooth muscle sarcomas, 47 to 66% in osteosarcomas, 11% in melanomas, 9% in neuroblastoma, and 0% in papillary thyroid and lung carcinomas. 13,[17][18][19][20] Measurement of APBs, the co-localization of PML and telomere DNA by fluorescence in situ hybridization, is a "robust" assay for identification of ALT tumors that can be used in paraffin-embedded tissues. 17 To date, all ALT tumors 17 and ALT cell lines (with two exceptions, VA13-C3-c16 and AG11395 cells) have APBs, 14,21,22 and APBs are absent in normal cells and absent or rare in telomerasepositive cells.…”

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confidence: 99%

Pilocytic Astrocytomas Have Telomere-Associated Promyelocytic Leukemia Bodies without Alternatively Lengthened Telomeres

Slatter

Gifford-Garner

Wiles

et al. 2010

The American Journal of Pathology

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Telomere maintenance by either telomerase activity or the recombination-mediated alternative lengthening of telomeres (ALT) mechanism is a hallmark of cancer. Tumors that use ALT as their telomere maintenance mechanism are characterized by long telomeres of great heterogeneity in length and by specific nuclear structures of co-localized promyelocytic leukemia protein and telomere DNA, called ALT-associated promyelocytic leukemia bodies (APBs). Recent advances have revealed a direct role for APBs in telomere recombination in ALT-positive cells. In this study, we investigated the possibility that APBs could occur before the long 'alternatively' lengthened telomeres arise, particularly in low-grade tumors. We measured APBs , telomere length , and telomerase activity in 64 astrocytomas inclusive of grade 1؊4 tumors. Almost all grade 1؊3 tumors (93%) were APBpositive using published criteria. Grade 2؊3 APB-positive tumors also had long telomeres and were confirmed as ALT positive. However, grade 1 tumors lacked long telomeres and were therefore classified as ALT negative, but positive for telomere-associated promyelocytic leukemia bodies (TPB). This is the first report of a TPB-positive but ALT-negative tumor, and suggests that low-grade tumors have the foundation for recombinational telomere repair, as in ALT. Further work is warranted to characterize the TPB-positive phenotype in other early malignancies, as well as The proliferative life span of somatic cells is controlled by telomere length.1 Telomeres are repeatedly shortened with each cell division until the telomere is too short, and the cell ceases proliferation and goes into senescence.2,3 Acquisition of a telomere maintenance mechanism allows malignant cells to evade senescence and continue proliferation. 4 Known telomere maintenance mechanisms include telomerase 5 and the alternative lengthening of telomeres mechanism (ALT) that describes the elongation of telomeres by any telomeraseindependent mechanism.6 Tumors that use ALT are distinguished by their low, or lack of, detectable telomerase activity, 7 increased recombination at telomeres, 8 long and heterogeneous telomere length distributions by terminal restriction fragment (TRF) Southern blotting, 9 -13 and the presence of a specific type of aggregate that contains the promyelocytic leukemia (PML) protein and telomere DNA called ALT-associated PML bodies (APBs) in 5 to 10% of asynchronized dividing cells.14,15 The prevalence of the ALT telomere maintenance mechanism has been studied less extensively than telomerase, which is the predominant telomere maintenance mechanism used in over 85% of tumors collectively. 16 The estimated frequency of ALT tumors varies from 25 to 34% in grade 2Ϫ4 astrocytomas, 35% in smooth muscle sarcomas, 47

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Telomere biology in neuroblastoma: telomere binding proteins and alternative strengthening of telomeres

Cited by 39 publications

References 31 publications

Clinical features of ATRX or DAXX mutated neuroblastoma

Clinical features of ATRX or DAXX mutated neuroblastoma

Wnt signaling and telomerase activation of hepatoblastoma: correlation with chemosensitivity and surgical resectability

Pilocytic Astrocytomas Have Telomere-Associated Promyelocytic Leukemia Bodies without Alternatively Lengthened Telomeres

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