Evidence map›Paper›PMID 34188043›Full record

ArticleNature communications2021

Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity.

Tamara Isermann, Özge Çiçek Şener, Adrian Stender, Luisa Klemke, Nadine Winkler, Albrecht Neesse, Jinyu Li, Florian Wegwitz, Ute M Moll, Ramona Schulz-Heddergott

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

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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 2 institutions in 2 countries.

Tamara IsermannInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.ORCID http://orcid.org/0000-0002-1866-0221
Özge Çiçek Şener *Institute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.ORCID http://orcid.org/0000-0002-4361-3312
Adrian Stender *Institute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
Luisa KlemkeInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.ORCID http://orcid.org/0000-0003-0368-8771
Nadine WinklerInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
Albrecht NeesseDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Göttingen, Germany.
Jinyu LiDepartment of Pathology, Stony Brook University, Stony Brook, NY, USA.
Florian WegwitzDepartment of Gynecology and Obstetrics, University Medical Center Göttingen, Göttingen, Germany.ORCID http://orcid.org/0000-0003-0750-6998
Ute M MollInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
Ramona Schulz-HeddergottInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany. ramona.schulz-heddergott@med.uni-goettingen.de.ORCID http://orcid.org/0000-0002-6483-4392
Universitätsmedizin Göttingen · DEStony Brook University · US

Funding

Targeting stabilized mutant p53 proteinR01CA176647 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI MOLL, UTE MARTHA · 2013 to 2022
$3.6M
NCI NIH HHS R01 CA176647
6 · The paper itself

Abstract

The vast majority of human tumors with p53 mutations undergo loss of the remaining wildtype p53 allele (loss-of-heterozygosity, p53LOH). p53LOH has watershed significance in promoting tumor progression. However, driving forces for p53LOH are poorly understood. Here we identify the repressive WTp53-HSF1 axis as one driver of p53LOH. We find that the WTp53 allele in AOM/DSS chemically-induced colorectal tumors (CRC) of p53

Indexed as

AnimalsCell Cycle CheckpointsCell Line, TumorColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p21HCT116 CellsHeat Shock Transcription FactorsHEK293 CellsHumansLoss of HeterozygosityMAP Kinase Kinase KinasesMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase Kinase Kinase 11MutationCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Heat Shock Transcription FactorsHSF1 protein, humanMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase Kinase Kinase 11TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID34188043
PMCPMC8242083
OpenAlexW3173770830

What OpenQuestion holds

Textmetadata
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.