Evidence map›Paper›PMID 28484276›Full record

ArticleScientific reports2017

Tumor protein 53 mutations are enriched in diffuse large B-cell lymphoma with irregular CD19 marker expression.

Marina Kazantseva, Noelyn A Hung, Sunali Mehta, Imogen Roth, Ramona Eiholzer, Alison M Rich, Benedict Seo, Margaret A Baird, Antony W Braithwaite, Tania L Slatter

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. 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

10 authors at 1 institution in 1 country.

Marina KazantsevaDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Noelyn A HungDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Sunali MehtaDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Imogen RothDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Ramona EiholzerDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Alison M RichSir John Walsh Research Institute, Faculty of Dentistry, University of Otago, Dunedin, New Zealand.
Benedict SeoSir John Walsh Research Institute, Faculty of Dentistry, University of Otago, Dunedin, New Zealand.ORCID 0000-0002-5887-2448
Margaret A BairdDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Antony W BraithwaiteDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Tania L SlatterDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand. tania.slatter@otago.ac.nz.
University of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests tumor protein 53 (p53) promotes correct cellular differentiation. Thus, mutant TP53 may be more frequent in tumors with irregular differentiation. This study investigated whether TP53 mutations were more frequent in diffuse large B cell lymphoma (DLBCL) that lacked the B cell lineage marker CD19. Sixteen CD19 negative and 78 CD19 positive DLBCL were sequenced for TP53 mutations. Twenty nine tumors had TP53 mutations and were associated with poorer survival. Mutant TP53 was more frequent in CD19 negative lymphomas (81% versus 21%, p < 0.0001). Analysis of other B cell markers revealed a lack of paired box 5 (PAX5) in CD19 positive lymphomas with mutant TP53 (50%), which was more frequent compared to tumors with wild-type TP53 (15%, p = 0.002). In summary, DLBCL lacking CD19 or PAX5 expression were more likely to have mutant TP53, suggesting irregular B cell marker phenotypes are associated with TP53 mutation.

Indexed as

Amino Acid SequenceAntigens, CD19Base SequenceBiomarkers, TumorCell DifferentiationDemographyFemaleHumansLymphoma, Large B-Cell, DiffuseMaleMiddle AgedMutationTumor Suppressor Protein p53Antigens, CD19Biomarkers, TumorTumor Suppressor Protein p53

Identifiers

PMID28484276
PMCPMC5431468
OpenAlexW2611880966

What OpenQuestion holds

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LicenceCC BY
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.