Evidence map›Paper›PMID 31128432›Full record

ArticleNeoplasia (New York, N.Y.)2019

Telomere Trimming and DNA Damage as Signatures of High Risk Neuroblastoma.

Eun Young Yu, Irene Y Cheung, Yi Feng, Mohamed O Rabie, Gail J Roboz, Monica L Guzman, Nai-Kong V Cheung, Neal F Lue

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Alternative Lengthening of Telomeres: The Need forInternational journal of molecular sciences · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Eun Young YuDepartment of Microbiology & Immunology, W. R. Hearst Microbiology Research Center, Weill Cornell Medical College, New York, NY, USA.
Irene Y CheungDepartment of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Yi FengDepartment of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Mohamed O RabieDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medical College, New York, NY, USA.
Gail J RobozDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medical College, New York, NY, USA.
Monica L GuzmanDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medical College, New York, NY, USA; Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA; Sandra and Edward Meyer Cancer Center, Weill Cornell Medical College, New York, NY, USA.
Nai-Kong V CheungDepartment of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Neal F LueDepartment of Microbiology & Immunology, W. R. Hearst Microbiology Research Center, Weill Cornell Medical College, New York, NY, USA; Sandra and Edward Meyer Cancer Center, Weill Cornell Medical College, New York, NY, USA. Electronic address: nflue@med.cornell.edu.
Cornell University · USMemorial Sloan Kettering Cancer Center · USHearst (United States) · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Telomeres play important roles in genome stability and cell proliferation. High risk neuroblastoma (HRNB), an aggressive childhood cancer, is especially reliant on telomere maintenance. Three recurrent genetic aberrations in HRNB (MYCN amplification, TERT re-arrangements, and ATRX mutations) are mutually exclusive and each capable of promoting telomere maintenance mechanisms (i.e., through telomerase or ALT). We analyzed a panel of 5 representative HRNB cell lines and 30 HRNB surgical samples using assays that assess average telomere lengths, length distribution patterns, single-stranded DNA on the G- and C-strand, as well as extra-chromosomal circular telomeres. Our analysis pointed to substantial and variable degrees of telomere DNA damage in HRNB, including pervasive oxidative lesions. Moreover, unlike other cancers, neuroblastoma consistently harbored high levels of C-strand ssDNA overhangs and t-circles, which are consistent with active "telomere trimming". This feature is observed in both telomerase- and ALT-positive tumors and irrespective of telomere length distribution. Moreover, evidence for telomere trimming was detected in normal neural tissues, raising the possibility that TMMs in HRNB evolved in the face of a canonical developmental program of telomere shortening. Telomere trimming by itself appears to distinguish neuroectodermal derived tumors from other human cancers, a distinguishing characteristic with both biologic and therapeutic implications.

Indexed as

Cell ProliferationDNA DamageFemaleGenomic InstabilityHeLa CellsHumansMaleMutationNeuroblastomaN-Myc Proto-Oncogene ProteinTelomeraseTelomereTelomere HomeostasisX-linked Nuclear ProteinATRX protein, humanMYCN protein, humanN-Myc Proto-Oncogene ProteinTelomeraseTERT protein, humanX-linked Nuclear Protein

Identifiers

PMID31128432
PMCPMC6535646
OpenAlexW2946822612

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.