Evidence map›Paper›PMID 24769898›Full record

ArticleOncogene2015

TACC3 deregulates the DNA damage response and confers sensitivity to radiation and PARP inhibition.

G-H Ha, J-L Kim, A Petersson, S Oh, M F Denning, T Patel, E-K Breuer

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  15. The Ran Pathway in Drosophila melanogaster Mitosis.Frontiers in cell and developmental biology · 2015
    Review
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

7 authors at 1 institution in 1 country.

G-H Ha1] Oncology Institute, Cardinal Bernardin Cancer Center, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA [2] Department of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
J-L Kim1] Oncology Institute, Cardinal Bernardin Cancer Center, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA [2] Department of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
A Petersson1] Oncology Institute, Cardinal Bernardin Cancer Center, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA [2] Department of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
S OhDepartment of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
M F Denning1] Oncology Institute, Cardinal Bernardin Cancer Center, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA [2] Department of Pathology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.ORCID 0000000161656925
T PatelDepartment of Molecular Pharmacology and Therapeutics Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
E-K Breuer1] Oncology Institute, Cardinal Bernardin Cancer Center, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA [2] Department of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
Loyola University Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of the transforming acidic coiled-coil protein 3 (TACC3), an important factor in the centrosome-microtubule system, has been linked to a variety of human cancer types. We have recently reported on the oncogenic potential of TACC3; however, the molecular mechanisms by which TACC3 mediates oncogenic function remain to be elucidated. In this study, we show that high levels of TACC3 lead to the accumulation of DNA double-strand breaks (DSBs) and disrupt the normal cellular response to DNA damage, at least in part, by negatively regulating the expression of ataxia telangiectasia mutated (ATM) and the subsequent DNA damage response (DDR) signaling cascade. Cells expressing high levels of TACC3 display defective checkpoints and DSB-mediated homologous recombination (HR) and non-homologous end joining (NHEJ) repair systems, leading to genomic instability. Importantly, high levels of TACC3 confer cellular sensitization to radiation and poly(ADP-ribose) polymerase (PARP) inhibition. Overall, our findings provide critical information regarding the mechanisms by which TACC3 contributes to genomic instability, potentially leading to cancer development, and suggest a novel prognostic, diagnostic and therapeutic strategy for the treatment of cancer types expressing high levels of TACC3.

Indexed as

DNA DamagePoly(ADP-ribose) Polymerase InhibitorsRadiation ToleranceChromosome AberrationsDNA Breaks, Double-StrandedHumansMicrotubule-Associated ProteinsNeoplasmsMicrotubule-Associated ProteinsPoly(ADP-ribose) Polymerase InhibitorsTACC3 protein, human

Identifiers

PMID24769898
OpenAlexW2029420222

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.