Evidence map›Paper›PMID 28591600›Full record

ArticleBiophysical journal2017

Elastic-Fluid Model for DNA Damage and Mutation from Nuclear Fluid Segregation Due to Cell Migration.

Rachel R Bennett, Charlotte R Pfeifer, Jerome Irianto, Yuntao Xia, Dennis E Discher, Andrea J Liu

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 21 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

6 authors at 1 institution in 1 country.

Rachel R BennettPhysical Sciences Oncology Center at Penn, University of Pennsylvania, Philadelphia, Pennsylvania; Department of Physics and Astronomy, University of Pennsylvania, Philadelphia, Pennsylvania.
Charlotte R PfeiferPhysical Sciences Oncology Center at Penn, University of Pennsylvania, Philadelphia, Pennsylvania; Department of Physics and Astronomy, University of Pennsylvania, Philadelphia, Pennsylvania; Molecular and Cell Biophysics Lab, University of Pennsylvania, Philadelphia, Pennsylvania.
Jerome IriantoPhysical Sciences Oncology Center at Penn, University of Pennsylvania, Philadelphia, Pennsylvania; Molecular and Cell Biophysics Lab, University of Pennsylvania, Philadelphia, Pennsylvania.
Yuntao XiaPhysical Sciences Oncology Center at Penn, University of Pennsylvania, Philadelphia, Pennsylvania; Molecular and Cell Biophysics Lab, University of Pennsylvania, Philadelphia, Pennsylvania.
Dennis E DischerPhysical Sciences Oncology Center at Penn, University of Pennsylvania, Philadelphia, Pennsylvania; Department of Physics and Astronomy, University of Pennsylvania, Philadelphia, Pennsylvania; Molecular and Cell Biophysics Lab, University of Pennsylvania, Philadelphia, Pennsylvania.
Andrea J LiuPhysical Sciences Oncology Center at Penn, University of Pennsylvania, Philadelphia, Pennsylvania; Department of Physics and Astronomy, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: ajliu@physics.upenn.edu.
University of Pennsylvania · US

Funding

PSOC@Penn Education and OutreachU54CA193417 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DISCHER, DENNIS E. · 2015 to 2020
$10.5M
NCI NIH HHS U54 CA193417
6 · The paper itself

Abstract

When cells migrate through constricting pores, they incur DNA damage and develop genomic variation. Experiments show that this damage is not due to DNA breakage from mechanical stress on chromatin in the deformed nucleus. Here we propose a model for a mechanism by which nuclear deformation can lead to DNA damage. We treat the nucleus as an elastic-fluid system with an elastic component (chromatin) and fluid component that can be squeezed out when the nucleus is deformed. We couple the elastic-fluid model to the kinetics of DNA breakage and repair by assuming that the local volume fraction of the elastic component controls the rate of damage per unit volume due to naturally occurring DNA breaks, whereas the volume fraction of the fluid component controls the rate of repair of DNA breaks per unit volume by repair factors, which are soluble in the fluid. By comparing our results to a number of experiments on controlled migration through pores, we show that squeeze-out of the fluid, and hence of the mobile repair factors, is sufficient to account for the extent of DNA damage and genomic variation observed experimentally. We also use our model for migration through a cylindrical pore to estimate the variation with tissue stiffness of the mutation rate in tumors.

Indexed as

DNA DamageModels, BiologicalMutationAnimalsCell MovementCell NucleusElasticityKineticsNeoplasms

Identifiers

PMID28591600
PMCPMC5474726
OpenAlexW2622875644

What OpenQuestion holds

Textmetadata
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.