Evidence map›Paper›PMID 20731666›Full record

ReviewCancer science2010

Global genomic and RNA profiles for novel risk stratification of neuroblastoma.

Miki Ohira, Akira Nakagawara

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Downregulation of tumor suppressor menin by miR-421 promotes proliferation and migration of neuroblastoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  13. Article
  14. Article
  15. Review
  16. Clinical significance of tumor-associated inflammatory cells in metastatic neuroblastoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012
    Article
  17. Metastatic neuroblastoma of the mandible: a cytogenetic and molecular genetic study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2012
    Article
  18. Neuroblastoma: issues in transplantation.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2012
    Review
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

2 authors at 2 institutions in 2 countries.

Miki OhiraDivision of Biochemistry and Innovative Cancer Therapeutics Laboratory of Cancer Genomics, Chiba Cancer Center Research Institute, Chuoh-ku, Chiba, Japan.
Akira Nakagawara
Advanced Cancer Therapeutics · USChiba Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma is one of the most common solid tumors in children. Its clinical behavior ranges widely from spontaneous regression to life-threatening aggressive growth. The molecular etiology of neuroblastoma is still enigmatic and the overall cure rate of advanced disease is still very poor. Recent microarray-based technology provided us with important information such as comprehensive genomic alterations and gene expression profiles to help us understand the molecular characteristics of each tumor in detail. Several retrospective studies have revealed that these signatures are strongly correlated with patient prognoses and led to the construction of new risk stratification systems, some of which are considered for evaluation in upcoming clinical studies in a prospective way. Large-scale analyses using a variety of genetic tools also discovered a major familial neuroblastoma predisposition gene ALK, as well as new candidate susceptibility genes at 6q22 and 2q35 for sporadic neuroblastoma. Of note, ALK is mutated in 6-9% of sporadic cases, and is either amplified or constitutively activated through mutations mainly within the kinase domain, promoting the possibility of new therapeutic strategies using ALK inhibitors. Additional candidates for outcome predictors such as the methylation phenotype of tumor DNA and expression profiles of microRNA have also been proposed. Such variety of information will help us understand the heterogeneity of neuroblastoma biology and further, the combined use of these signatures will be beneficial in predicting prognosis with high accuracy, as well as choosing a suitable therapy for the individual patient.

Indexed as

Chromosome AberrationsGene Expression ProfilingAnaplastic Lymphoma KinaseGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMutationNeuroblastomaProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesRisk FactorsALK protein, humanAnaplastic Lymphoma KinaseProtein-Tyrosine KinasesReceptor Protein-Tyrosine Kinases

Identifiers

PMID20731666
PMCPMC11159775
OpenAlexW1969970944

What OpenQuestion holds

Textmetadata
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.