Evidence map›Paper›PMID 34971484›Full record

ArticleCancer science2022

Oncogenic FGFR1 mutation and amplification in common cellular origin in a composite tumor with neuroblastoma and pheochromocytoma.

Keiji Tasaka, Hiroo Ueno, Kai Yamasaki, Takahiro Okuno, Tomoya Isobe, Shunsuke Kimura, Katsutsugu Umeda, Junichi Hara, Seishi Ogawa, Junko Takita

Open access · goldAbstract readCase Reports
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

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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

10 authors at 4 institutions in 2 countries.

Keiji TasakaDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-2708-3876
Hiroo UenoDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0001-7617-1672
Kai YamasakiDepartment of Pediatric Hematology and Oncology, Osaka City General Hospital, Osaka, Japan.
Takahiro OkunoDepartment of Pathology, Osaka City General Hospital, Osaka, Japan.
Tomoya IsobeDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Shunsuke KimuraDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Katsutsugu UmedaDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-6844-2011
Junichi HaraCancer Consultation and Support Center, Osaka City General Hospital, Osaka, Japan.ORCID https://orcid.org/0000-0002-6798-1558
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Junko TakitaDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-2452-6520
Kyoto University · JPOsaka City General Hospital · JPHiroshima University · JPThe University of Tokyo · JP

Funding

Core Research for Evolutional Science and Technology JP19gm1110011Japan Agency for Medical Research and Development JP15cm0106056h0005Japan Agency for Medical Research and Development JP16ck0106073h0003Japan Agency for Medical Research and Development JP19ck0106250h0003Japan Agency for Medical Research and Development JP19cm0106501h0004JSPS KAKENHI 20H00528JSPS KAKENHI 21H02880JSPS KAKENHI 21K1905Practical Research for Innovative Cancer Control JP19ck0106468h0001Project for Cancer Research and Therapeutic Evolution JP19cm0106509h9904
6 · The paper itself

Abstract

Neuroblastoma (NB) and pheochromocytoma (PCC) are derived from neural crest cells (NCCs); however, composite tumors with NB and PCC are rare, and their underlying molecular mechanisms remain unknown. To address this issue, we performed exome and transcriptome sequencing with formalin-fixed paraffin-embedded (FFPE) samples from the NB, PCC, and mixed lesions in a patient with a composite tumor. Whole-exome sequencing revealed that most mutations (80%) were shared by all samples, indicating that NB and PCC evolved from the same clone. Notably, all samples harbored both mutation and focal amplification in the FGFR1 oncogene, resulting in an extraordinarily high expression, likely to be the main driver of this tumor. Transcriptome sequencing revealed undifferentiated expression profiles for the NB lesions. Considering that a metastatic lesion was also composite, most likely, the primitive founding lesions should differentiate into both NB and PCC. This is the first reported case with composite-NB and PCC genetically proven to harbor an oncogenic FGFR1 alteration of a common cellular origin.

Indexed as

Adrenal Gland NeoplasmsNeuroblastomaPheochromocytomaHumansMutationOncogenesReceptor, Fibroblast Growth Factor, Type 1FGFR1 protein, humanReceptor, Fibroblast Growth Factor, Type 1common cellular origincomposite tumorFGFR1neuroblastomapheochromocytoma

Identifiers

PMID34971484
PMCPMC8990717
OpenAlexW4206743630

What OpenQuestion holds

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LicenceCC BY
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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.