Evidence map›Paper›PMID 33051812›Full record

ArticleFamilial cancer2021

The role of TP53 pathogenic variants in early-onset HER2-positive breast cancer.

Carla Escudeiro, Carla Pinto, Joana Vieira, Ana Peixoto, Pedro Pinto, Manuela Pinheiro, Catarina Santos, Joana Guerra, Susana Lisboa, Rui Santos and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Familial cancer, 2021. 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
0.1field-weighted citation impact, top 53% 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, 7 citations in OpenAlex.

  1. Article
  2. Deep learning algorithm on H&E whole slide images to characterizeComputational and structural biotechnology journal · 2024
    Article
  3. Article
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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

17 authors at 4 institutions in 1 country.

Carla EscudeiroDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Carla PintoDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Joana VieiraDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Ana PeixotoDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Pedro PintoDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Manuela PinheiroDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Catarina SantosDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Joana GuerraDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Susana LisboaDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Rui SantosDepartment of Pathology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
João SilvaDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Conceição LealDepartment of Pathology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
Nuno CoimbraDepartment of Pathology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
Paula LopesDepartment of Pathology, Portuguese Oncology Institute of Porto (IPO Porto), Porto, Portugal.
Marco FerreiraDepartment of Pathology, Fernando Fonseca Hospital, Amadora, Portugal.
Ana B SousaDepartment of Genetics, Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, Lisboa, Portugal.
Manuel R TeixeiraDepartment of Genetics, Portuguese Oncology Institute of Porto, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal. manuel.teixeira@ipoporto.min-saude.pt.ORCID 0000-0002-4896-5982
Instituto Português de Oncologia Francisco Gentil · PTCentro Hospitalar Lisboa Norte · PTHospital Prof. Dr. Fernando Fonseca · PTUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the most frequent event in Li-Fraumeni syndrome associated with germline TP53 variants. Some studies have shown that breast cancers in women with Li-Fraumeni syndrome are commonly HER2-positive, suggesting that HER2 amplification or over-expression in a young woman may be a useful criterion to test for germline variants in the TP53 gene. We assessed the prevalence of germline TP53 variants by Sanger sequencing or next-generation sequencing in 149 women with HER2-positive breast cancer diagnosed until age 40. The pattern of HER2 amplification was evaluated with dual-probe FISH in a subset of breast carcinomas from patients with germline TP53 variants as compared with those of noncarriers. Among 149 women tested, three presented a deleterious TP53 germline variant (2%), with one patient diagnosed at age 31 and the other two with bilateral breast cancer at ages 29/33 and 28/32, respectively. Three of the 36 patients (8.3%) with the first breast cancer diagnosed at age 31 or younger presented a pathogenic TP53 variant. Additionally, all TP53 deleterious variant carriers had a first degree relative diagnosed with different early-onset cancers (frequently not belonging to the Li-Fraumeni syndrome tumor spectrum) diagnosed at age 45 or younger. Higher levels of HER2 amplification were found in breast carcinomas of TP53 pathogenic variant carriers than in those of noncarriers. Deleterious germline TP53 variants account for a small proportion of early-onset HER2-positive breast cancers, but these seem to have higher HER2 amplification ratios. All TP53 pathogenic variant carriers found in this study had the first breast carcinoma diagnosed at age 31 or younger and a first-degree relative with early-onset cancer. Further studies are needed to clarify if HER2 status in early-onset breast cancer patients, in combination with other personal and/or familial cancer history, is useful to update the TP53 testing criteria.

Indexed as

Genes, erbB-2Germ-Line MutationAdultAge FactorsBreast NeoplasmsCarcinoma, Ductal, BreastFemaleGene AmplificationGenes, p53Genetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingHumansIn Situ Hybridization, FluorescenceLi-Fraumeni SyndromePedigreeSequence Analysis, DNAHER2-positive breast cancerLi-fraumeni syndromeNext-generation sequencingTP53 germline variants

Identifiers

PMID33051812
OpenAlexW3092121843

What OpenQuestion holds

Textmetadata
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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.