Evidence map›Paper›PMID 22588778›Full record

ReviewInternational journal of clinical oncology2012

Molecular and genetic bases of neuroblastoma.

Takehiko Kamijo, Akira Nakagawara

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

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  12. Targeting anaplastic lymphoma kinase in neuroblastoma.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2019
    Review
  13. Associations betweenBioscience reports · 2019
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Takehiko KamijoDivision of Biochemistry and Molecular Carcinogenesis, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuo-ku, Chiba, Chiba, 260-8717, Japan. tkamijo@chiba-cc.jp
Akira Nakagawara

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma, which is derived from the sympathetic nervous system, is the second most common pediatric solid malignant tumor. This pediatric tumor has a heterogeneous course, ranging from spontaneous regression to inexorable progression and death, depending on the biological features of the tumor. Identification of risk groups on the basis of clinical and molecular prognostic variables has allowed tailor-made therapy to improve outcomes and minimize the risk of deleterious consequences of therapy. In Japan, current therapeutic stratification of patients with neuroblastoma is based on risk assessment according to combinations of age, tumor stage, MYCN status, DNA ploidy status, and histopathology; however, unfavorable neuroblastoma is still one of the most difficult tumors to cure, with only 40 % long-term survival despite intensive multimodal therapy. Further refined therapeutic stratification based on newly identified prognostic factors will be required to improve the outcome of patients with unfavorable neuroblastoma and reduce the side effects of therapies for patients with favorable neuroblastoma. In the present review, we describe recent topics on the molecular and genetic bases of neuroblastoma; we hope this review will be helpful for understanding the mechanism of neuroblastoma tumorigenesis and aggressiveness and for developing a new therapeutic stratification and new protocols for neuroblastoma treatments.

Indexed as

ChildDNAHumansNeoplastic Stem CellsNeuroblastomaN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsPloidiesDNAMYCN protein, humanN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene Proteins

Identifiers

What OpenQuestion holds

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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.