Evidence map›Paper›PMID 33934450›Full record

ArticleCancer science2021

Clonal evidence for the development of neuroblastoma with extensive copy-neutral loss of heterozygosity arising in a mature teratoma.

Rintaro Ono, Hiroo Ueno, Kenichi Yoshida, Satoko Takahashi, Hiroki Yoshihara, Taiki Nozaki, Koyu Suzuki, Atsuko Nakazawa, Ryunosuke Saiki, Masafumi Seki and 4 more

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

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Technologies, strategies, and cautions when deconvoluting genome-wide association signals: FTO in focus.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023
    Review
  5. Article
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

14 authors at 5 institutions in 1 country.

Rintaro OnoDepartment of Pediatrics, St. Luke's International Hospital, Tokyo, Japan.ORCID https://orcid.org/0000-0001-8847-2528
Hiroo UenoDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kenichi YoshidaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Satoko TakahashiDepartment of Pediatrics, St. Luke's International Hospital, Tokyo, Japan.
Hiroki YoshiharaDepartment of Pediatrics, St. Luke's International Hospital, Tokyo, Japan.
Taiki NozakiDepartment of Diagnostic Radiology, St. Luke's International Hospital, Tokyo, Japan.
Koyu SuzukiDepartment of Pathology, St. Luke's International Hospital, Tokyo, Japan.
Atsuko NakazawaDepartment of Clinical Research, Saitama Children's Medical Center, Saitama, Japan.
Ryunosuke SaikiDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masafumi SekiDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Junko TakitaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Atsushi ManabeDepartment of Pediatrics, St. Luke's International Hospital, Tokyo, Japan.
Daisuke HasegawaDepartment of Pediatrics, St. Luke's International Hospital, Tokyo, Japan.
St. Luke's International Hospital · JPKyoto University · JPHokkaido University · JPSaitama Children's Medical Center · JPThe University of Tokyo · JP

Funding

Japan Agency for Medical Research and Development (AMED)Japan Society for the Promotion of Science JP19H05656Japan Society for the Promotion of Science JP26221308Project for Development of Innovative Research on Cancer Therapeutics JP 20cm0106501h0005
6 · The paper itself

Abstract

Mature teratomas are usually benign tumors that rarely undergo malignant transformation. We report an advanced neuroblastoma arising in a mature teratoma of the ovary. Whole-exome sequencing identified extensive copy-neutral loss of heterozygosity (LOH) in both neuroblastoma and teratoma elements, suggesting that the neuroblastoma evolved from the teratoma. In addition, several truncating germline heterozygous variants in tumor suppressor genes, including RBL2 and FBXW12, became homozygous as a result of LOH. Collectively, we speculate that extensive LOH in teratoma cells may force heterozygous germline variants to become homozygous, which, in turn, may contribute to the development of neuroblastoma with the acquisition of additional chromosomal changes.

Indexed as

Germ-Line MutationLoss of HeterozygosityAdolescentExome SequencingF-Box ProteinsFemaleHomozygoteHumansNeoplasms, Multiple PrimaryNeuroblastomaOvarian NeoplasmsRetinoblastoma-Like Protein p130TeratomaF-Box ProteinsFBXW12 protein, humanRBL2 protein, humanRetinoblastoma-Like Protein p130cancer genome/geneticscopy-neutral loss of heterozygositygenomic analysismalignant transformationneuroblastomateratoma

Identifiers

PMID33934450
PMCPMC8253283
OpenAlexW3159097303

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.