Evidence map›Paper›PMID 26982726›Full record

ArticleNature2016

Deletions linked to TP53 loss drive cancer through p53-independent mechanisms.

Yu Liu, Chong Chen, Zhengmin Xu, Claudio Scuoppo, Cory D Rillahan, Jianjiong Gao, Barbara Spitzer, Benedikt Bosbach, Edward R Kastenhuber, Timour Baslan and 8 more

Abstract read
In one paragraph

Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed, 3 pooled it
13.4field-weighted citation impact, top 1% 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

170 citing papers in PubMed, 3 syntheses or guidelines pooled it, 293 citations in OpenAlex.

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  20. The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 2 countries.

Yu Liu *Department of Hematology and Department of Liver Surgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and National Collaborative Innovation Center, Chengdu 610041, China.
Chong Chen *Department of Hematology and Department of Liver Surgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and National Collaborative Innovation Center, Chengdu 610041, China.
Zhengmin XuDepartment of Hematology and Department of Liver Surgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and National Collaborative Innovation Center, Chengdu 610041, China.
Claudio Scuoppoinstitute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA.
Cory D RillahanDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Jianjiong GaoKravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Barbara SpitzerDepartment of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Benedikt BosbachDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Edward R KastenhuberDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Timour BaslanDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Sarah AckermannDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Lihua ChengDepartment of Hematology & Research Laboratory of Hematology, West China Hospital, Sichuan University, Chengdu 610041, China.
Qingguo WangKravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Ting NiuDepartment of Hematology & Research Laboratory of Hematology, West China Hospital, Sichuan University, Chengdu 610041, China.
Nikolaus SchultzKravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Ross L LevineHuman Oncology & Pathogenesis Program and Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Alea A MillsCold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
Scott W LoweDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Memorial Sloan Kettering Cancer Center · USState Key Laboratory of BiotherapyCancer Genetics (United States) · USCold Spring Harbor Laboratory · USHoward Hughes Medical Institute · USSichuan University · CNWest China Hospital of Sichuan University · CN

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI John Edward Moses · 1987 to 2026
$118.9M
Scientific ReagentsP01CA087497 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 2000 to 2021
$35.4M
The role of CHD5 in chromatin-mediated regulation of neural stem cells and gliomaR01CA190997 · NCI · COLD SPRING HARBOR LABORATORY · PI MILLS, ALEA A. · 2014 to 2018
$3.2M
The impact of chromosome 17p lesions on leukemogeneis and therapy responseR01CA190261 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LOWE, SCOTT W. · 2015 to 2019
$2.0M
Intratumoral Heterogeneity and Tumor Evolution in LymphomaF31CA192835 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI KASTENHUBER, EDWARD R · 2015 to 2018
$157k
Howard Hughes Medical InstituteNCI NIH HHS F31 CA192835NCI NIH HHS P01 CA087497NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA016042NCI NIH HHS P30 CA045508NCI NIH HHS R01 CA190261NCI NIH HHS R01 CA190997
6 · The paper itself

Abstract

Mutations disabling the TP53 tumour suppressor gene represent the most frequent events in human cancer and typically occur through a two-hit mechanism involving a missense mutation in one allele and a 'loss of heterozygosity' deletion encompassing the other. While TP53 missense mutations can also contribute gain-of-function activities that impact tumour progression, it remains unclear whether the deletion event, which frequently includes many genes, impacts tumorigenesis beyond TP53 loss alone. Here we show that somatic heterozygous deletion of mouse chromosome 11B3, a 4-megabase region syntenic to human 17p13.1, produces a greater effect on lymphoma and leukaemia development than Trp53 deletion. Mechanistically, the effect of 11B3 loss on tumorigenesis involves co-deleted genes such as Eif5a and Alox15b (also known as Alox8), the suppression of which cooperates with Trp53 loss to produce more aggressive disease. Our results imply that the selective advantage produced by human chromosome 17p deletion reflects the combined impact of TP53 loss and the reduced dosage of linked tumour suppressor genes.

Indexed as

AllelesAnimalsCell Transformation, NeoplasticChromosomes, Human, Pair 17Chromosomes, MammalianDisease Models, AnimalDisease ProgressionEukaryotic Translation Initiation Factor 5AFemaleGenes, p53HeterozygoteHumansLeukemia, Myeloid, AcuteLymphomaMaleMiceEukaryotic Translation Initiation Factor 5APeptide Initiation FactorsRNA-Binding ProteinsTumor Suppressor Protein p53

Identifiers

PMID26982726
PMCPMC4836395
OpenAlexW2302157033

What OpenQuestion holds

Textmetadata
LicenceTDM
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.