Evidence map›Paper›PMID 34956867›Full record

ArticleFrontiers in oncology2021

Copy Number Alterations in Hepatoblastoma: Literature Review and a Brazilian Cohort Analysis Highlight New Biological Pathways.

Juliana Sobral Barros, Talita Ferreira Marques Aguiar, Silvia Souza Costa, Maria Prates Rivas, Monica Cypriano, Silvia Regina Caminada Toledo, Estela Maria Novak, Vicente Odone, Lilian Maria Cristofani, Dirce Maria Carraro and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 14 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

15 authors at 3 institutions in 2 countries.

Juliana Sobral BarrosHuman Genome and Stem Cell Research Center, Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil.
Talita Ferreira Marques AguiarHuman Genome and Stem Cell Research Center, Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil.
Silvia Souza CostaHuman Genome and Stem Cell Research Center, Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil.
Maria Prates RivasHuman Genome and Stem Cell Research Center, Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil.
Monica CyprianoDepartment of Pediatrics, Institute of Pediatric Oncology, Support Group for Children and Adolescents with Cancer (IOP-GRAACC), Federal University of São Paulo, São Paulo, Brazil.
Silvia Regina Caminada ToledoDepartment of Pediatrics, Institute of Pediatric Oncology, Support Group for Children and Adolescents with Cancer (IOP-GRAACC), Federal University of São Paulo, São Paulo, Brazil.
Estela Maria NovakDepartment of Pediatrics, Institute of Childhood Cancer Treatment (ITACI), Faculty of Medicine, University of São Paulo, São Paulo, Brazil.
Vicente OdoneDepartment of Pediatrics, Institute of Childhood Cancer Treatment (ITACI), Faculty of Medicine, University of São Paulo, São Paulo, Brazil.
Lilian Maria CristofaniDepartment of Pediatrics, Institute of Childhood Cancer Treatment (ITACI), Faculty of Medicine, University of São Paulo, São Paulo, Brazil.
Dirce Maria CarraroInternational Research Center, AC Camargo Cancer Center (ACCCC), São Paulo, Brazil.
Isabela Werneck da CunhaInternational Research Center, AC Camargo Cancer Center (ACCCC), São Paulo, Brazil.
Cecília Maria Lima CostaInternational Research Center, AC Camargo Cancer Center (ACCCC), São Paulo, Brazil.
Angela M Vianna-MorganteHuman Genome and Stem Cell Research Center, Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil.
Carla RosenbergHuman Genome and Stem Cell Research Center, Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil.
Ana Cristina Victorino KrepischiHuman Genome and Stem Cell Research Center, Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, Brazil.
Universidade de São Paulo · BRAC Camargo Hospital · BRSupport group for adolescents and children with cancer · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatoblastoma (HB) is a rare embryonal tumor, although it is the most common pediatric liver cancer. The aim of this study was to provide an accurate cytogenomic profile of this type of cancer, for which information in cancer databases is lacking. We performed an extensive literature review of cytogenetic studies on HBs disclosing that the most frequent copy number alterations (CNAs) are gains of 1q, 2/2q, 8/8q, and 20; and losses at 1p and 4q. Furthermore, the CNA profile of a Brazilian cohort of 26 HBs was obtained by array-CGH; the most recurrent CNAs were the same as shown in the literature review. Importantly, HBs from female patients, high-risk stratification tumors, tumors who developed in older patients (> 3 years at diagnosis) or from patients with metastasis and/or deceased carried a higher diversity of chromosomal alterations, specifically chromosomal losses at 1p, 4, 11q and 18q. In addition, we distinguished three major CNA profiles: no detectable CNA, few CNAs and tumors with complex genomes. Tumors with simpler genomes exhibited a significant association with the epithelial fetal subtype of HBs; in contrast, the complex genome group included three cases with epithelial embryonal histology, as well as the only HB with HCC features. A significant association of complex HB genomes was observed with older patients who developed high-risk tumors, metastasis, and deceased. Moreover, two patients with HBs exhibiting complex genomes were born with congenital anomalies. Together, these findings suggest that a high load of CNAs, mainly chromosomal losses, particularly losses at 1p and 18, increases the tendency to HB aggressiveness. Additionally, we identified six hot-spot chromosome regions most frequently affected in the entire group: 1q31.3q42.3, 2q23.3q37.3, and 20p13p11.1 gains, besides a 5,3 Mb amplification at 2q24.2q24.3, and losses at 1p36.33p35.1, 4p14 and 4q21.22q25. An

Indexed as

array-CGHcopy number alterationcytogenomicshepatoblastomapediatric cancer

Identifiers

PMID34956867
PMCPMC8692715
OpenAlexW4200003526

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.