Evidence map›Paper›PMID 27034505›Full record

ArticleGenes & development2016

An African-specific polymorphism in the TP53 gene impairs p53 tumor suppressor function in a mouse model.

Matthew Jennis, Che-Pei Kung, Subhasree Basu, Anna Budina-Kolomets, Julia I-Ju Leu, Sakina Khaku, Jeremy P Scott, Kathy Q Cai, Michelle R Campbell, Devin K Porter and 8 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 251 papers.

0numbers the graph read from it
0cells of the map it votes in
251citing papers in PubMed
–field-weighted citation impact
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

251 citing papers in PubMed, 352 citations in OpenAlex.

  1. The Emerging Role of Ferroptosis in Pediatric Cancer Biology and Therapy.International journal of molecular sciences · 2026
    Review
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  6. Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
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  20. Ferroptosis-related signaling pathways in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025
    Review

191 more citing papers are in PubMed but not listed here.

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

18 authors at 6 institutions in 2 countries.

Matthew JennisProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA; Program in Molecular and Cellular Biology and Genetics, Drexel University College of Medicine, Philadelphia, Pennsylvania 19102, USA;
Che-Pei KungProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA;
Subhasree BasuProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA;
Anna Budina-KolometsProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA;
Julia I-Ju LeuDepartment of Genetics, The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Sakina KhakuProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA;
Jeremy P ScottProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA;
Kathy Q CaiFox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA;
Michelle R CampbellNational Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Devin K PorterNational Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Xuting WangNational Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Douglas A BellNational Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Xiaoxian LiDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA;
David S GarlickThe Wistar Institute Cancer Center, Philadelphia, Pennsylvania 19104, USA;
Qin LiuProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA;
Monica HollsteinUniversity of Leeds, Leeds LS2 9JT, United Kingdom.
Donna L GeorgeDepartment of Genetics, The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Maureen E MurphyProgram in Molecular and Cellular Oncogenesis, The Wistar Institute, Philadelphia, Pennsylvania 19104, USA;ORCID http://orcid.org/0000-0001-7644-7296
The Wistar Institute · USNational Institute of Environmental Health Sciences · USUniversity of Pennsylvania · USEmory University · USFox Chase Cancer Center · USUniversity of Leeds · GB

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Targeting the MAP and PI3 Kinase Pathways in MelanomaP01CA114046 · NCI · WISTAR INSTITUTE · PI MURPHY, MAUREEN E. · 2008 to 2023
$37.1M
Functional Analysis of p53 Polymorphic Variants - Diversity SupplementR01CA102184 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 2005 to 2026
$7.4M
Discovery And Genetics Of Environmental Response GenesZ01ES100475 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BELL, DOUGLAS · 2002 to 2008
$2.9M
p53 Variants in Cancer Risk and TherapyR01CA201430 · NCI · WISTAR INSTITUTE · PI MURPHY, MAUREEN E. · 2016 to 2020
$2.2M
Intramural NIH HHS Z01 ES100475NCI NIH HHS CA010815NCI NIH HHS P01 CA114046NCI NIH HHS P30 CA010815NCI NIH HHS P30 CA016520NCI NIH HHS R01 CA102184NCI NIH HHS R01 CA201430NIEHS NIH HHS Z01-ES-100475
6 · The paper itself

Abstract

A nonsynonymous single-nucleotide polymorphism at codon 47 in TP53 exists in African-descent populations (P47S, rs1800371; referred to here as S47). Here we report that, in human cell lines and a mouse model, the S47 variant exhibits a modest decrease in apoptosis in response to most genotoxic stresses compared with wild-type p53 but exhibits a significant defect in cell death induced by cisplatin. We show that, compared with wild-type p53, S47 has nearly indistinguishable transcriptional function but shows impaired ability to transactivate a subset of p53 target genes, including two involved in metabolism:Gls2(glutaminase 2) and Sco2 We also show that human and mouse cells expressing the S47 variant are markedly resistant to cell death by agents that induce ferroptosis (iron-mediated nonapoptotic cell death). We show that mice expressing S47 in homozygous or heterozygous form are susceptible to spontaneous cancers of diverse histological types. Our data suggest that the S47 variant may contribute to increased cancer risk in individuals of African descent, and our findings highlight the need to assess the contribution of this variant to cancer risk in these populations. These data also confirm the potential relevance of metabolism and ferroptosis to tumor suppression by p53.

Indexed as

Polymorphism, Single NucleotideAnimalsBlack PeopleCarcinoma, HepatocellularCell DeathCell LineCisplatinCodonDisease Models, AnimalGenes, p53HumansMiceMice, Inbred C57BLNeoplasmsProtein BindingRisk FactorsCisplatinCodonTumor Suppressor Protein p53ferroptosismetabolismp53polymorphismSer46 phosphorylationtumor suppression

Identifiers

PMID27034505
PMCPMC4840298
OpenAlexW2327775625

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.