Evidence map›Paper›PMID 27702824›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016

Significance of TP53 Mutation in Wilms Tumors with Diffuse Anaplasia: A Report from the Children's Oncology Group.

Ariadne H A G Ooms, Samantha Gadd, Daniela S Gerhard, Malcolm A Smith, Jaime M Guidry Auvil, Daoud Meerzaman, Qing-Rong Chen, Chih Hao Hsu, Chunhua Yan, Cu Nguyen and 21 more

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

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  13. Actinomycin D and bortezomib disrupt protein homeostasis in Wilms tumor.bioRxiv : the preprint server for biology · 2024
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1 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

31 authors at 1 institution in 1 country.

Ariadne H A G OomsDepartment of Pathology and Laboratory Medicine, Ann and Robert H. Lurie Children's Hospital of Chicago, Robert H. Lurie Cancer Center, Northwestern University, Chicago, Illinois.
Samantha GaddDepartment of Pathology and Laboratory Medicine, Ann and Robert H. Lurie Children's Hospital of Chicago, Robert H. Lurie Cancer Center, Northwestern University, Chicago, Illinois.
Daniela S GerhardOffice of Cancer Genomics, National Cancer Institute, Bethesda, Maryland.
Malcolm A SmithCancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland.
Jaime M Guidry AuvilOffice of Cancer Genomics, National Cancer Institute, Bethesda, Maryland.
Daoud MeerzamanCenter for Biomedical Informatics and Information Technology, National Cancer Institute, Bethesda, Maryland.
Qing-Rong ChenCenter for Biomedical Informatics and Information Technology, National Cancer Institute, Bethesda, Maryland.
Chih Hao HsuCenter for Biomedical Informatics and Information Technology, National Cancer Institute, Bethesda, Maryland.
Chunhua YanCenter for Biomedical Informatics and Information Technology, National Cancer Institute, Bethesda, Maryland.
Cu NguyenCenter for Biomedical Informatics and Information Technology, National Cancer Institute, Bethesda, Maryland.
Ying HuCenter for Biomedical Informatics and Information Technology, National Cancer Institute, Bethesda, Maryland.
Yussanne MaCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency (BCCA), Vancouver, British Columbia, Canada.
Zusheng ZongCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency (BCCA), Vancouver, British Columbia, Canada.
Andrew J MungallCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency (BCCA), Vancouver, British Columbia, Canada.
Richard A MooreCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency (BCCA), Vancouver, British Columbia, Canada.
Marco A MarraCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency (BCCA), Vancouver, British Columbia, Canada.
Vicki HuffDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jeffrey S DomeDivision of Pediatric Hematology/Oncology, Children's National Medical Center, Washington, DC.
Yueh-Yun ChiDepartment of Biostatistics, University of Florida, Gainesville, Florida.
Jing TianDepartment of Biostatistics, University of Florida, Gainesville, Florida.
James I GellerDivision of Pediatric Oncology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio.
Charles G MullighanDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee.
Jing MaDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee.
David A WheelerDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.
Oliver A HamptonDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.
Amy L WalzDivision of Hematology-Oncology and Transplantation, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University's Feinberg School of Medicine, Chicago, Illinois.
Marry M van den Heuvel-EibrinkPrincess Maxima Centre for Pediatric Oncology, Utrecht, the Netherlands.
Ronald R de KrijgerPrincess Maxima Centre for Pediatric Oncology, Utrecht, the Netherlands.
Nicole RossDepartment of Pathology and Laboratory Medicine, Nationwide Children's Hospital, Ohio State University College of Medicine, Columbus, Ohio.
Julie M Gastier-FosterDepartment of Pathology and Laboratory Medicine, Nationwide Children's Hospital, Ohio State University College of Medicine, Columbus, Ohio.
Elizabeth J PerlmanDepartment of Pathology and Laboratory Medicine, Ann and Robert H. Lurie Children's Hospital of Chicago, Robert H. Lurie Cancer Center, Northwestern University, Chicago, Illinois. Eperlman@luriechildrens.org.
National Cancer Institute · US

Funding

NCTN BIQSFP ANBL1531 (NRT)U10CA180886 · NCI · PUBLIC HEALTH INSTITUTE · PI Douglas S. Hawkins · 2014 to 2026
$390.6M
COG FOREIGN ACCRUALU10CA098543 · NCI · NATIONAL CHILDHOOD CANCER FOUNDATION · PI ADAMSON, PETER C. · 2003 to 2013
$335.5M
Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
COG SDMC - Statistics CoreU10CA180899 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI TODD A ALONZO · 2014 to 2026
$132.8M
Children's Oncology Group Statistics &Data Center GrantU10CA098413 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DEVIDAS, MEENAKSHI · 2003 to 2013
$67.5M
COG U24 Funding 2026-2027U24CA196173 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI Mignon Lee-Cheun Loh, Nilsa Del Carmen Ramirez Milan · 2015 to 2026
$62.5M
Support for Human Specimen Banking in NCI-Supported Cancer Clinical TrialsU24CA114766 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI RAMIREZ MILAN, NILSA DEL CARMEN · 2005 to 2014
$14.5M
CLINICAL ONCOLOGY RESEARCH TRAINING PROGRAMT32CA079447 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LICHT, JONATHAN D. · 1999 to 2013
$3.1M
CATEGORIZATION OF WILMS TUMOR BY GENETIC EXPRESSIONU01CA088131 · NCI · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI PERLMAN, ELIZABETH J · 2001 to 2006
$1.7M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENCI NIH HHS P30 CA060553NCI NIH HHS T32 CA079447NCI NIH HHS U01 CA088131NCI NIH HHS U10 CA098413NCI NIH HHS U10 CA098543NCI NIH HHS U10 CA180886NCI NIH HHS U10 CA180899NCI NIH HHS U24 CA114766NCI NIH HHS U24 CA196173
6 · The paper itself

Abstract

purposeTo investigate the role and significance of TP53 mutation in diffusely anaplastic Wilms tumors (DAWTs). EXPERIMENTAL

designAll DAWTs registered on National Wilms Tumor Study-5 (n = 118) with available samples were analyzed for TP53 mutations and copy loss. Integrative genomic analysis was performed on 39 selected DAWTs.

resultsFollowing analysis of a single random sample, 57 DAWTs (48%) demonstrated TP53 mutations, 13 (11%) copy loss without mutation, and 48 (41%) lacked both [defined as TP53-wild-type (wt)]. Patients with stage III/IV TP53-wt DAWTs (but not those with stage I/II disease) had significantly lower relapse and death rates than those with TP53 abnormalities. In-depth analysis of a subset of 39 DAWTs showed seven (18%) to be TP53-wt: These demonstrated gene expression evidence of an active p53 pathway. Retrospective pathology review of TP53-wt DAWT revealed no or very low volume of anaplasia in six of seven tumors. When samples from TP53-wt tumors known to contain anaplasia histologically were available, abnormal p53 protein accumulation was observed by immunohistochemistry.

conclusionsThese data support the key role of TP53 loss in the development of anaplasia in WT, and support its significant clinical impact in patients with residual anaplastic tumor following surgery. These data also suggest that most DAWTs will show evidence of TP53 mutation when samples selected for the presence of anaplasia are analyzed. This suggests that modifications of the current criteria to also consider volume of anaplasia and documentation of TP53 aberrations may better reflect the risk of relapse and death and enable optimization of therapeutic stratification. Clin Cancer Res; 22(22); 5582-91. ©2016 AACR.

Indexed as

AdolescentAdultAgedAged, 80 and overAnaplasiaChildFemaleGene ExpressionHumansImmunohistochemistryKidney NeoplasmsMaleMiddle AgedMutationRadiusRetrospective StudiesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID27702824
PMCPMC5290091
OpenAlexW2529309126

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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.