Evidence map›Paper›PMID 26915295›Full record

ArticleCell death and differentiation2016

The acetyltransferase Tip60 contributes to mammary tumorigenesis by modulating DNA repair.

C Bassi, Y-T Li, K Khu, F Mateo, P S Baniasadi, A Elia, J Mason, V Stambolic, M A Pujana, T W Mak and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 71 citations in OpenAlex.

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  17. Journal of microbiology and biotechnology · 2022
    Article
  18. Review
  19. BET Proteins as Attractive Targets for Cancer Therapeutics.International journal of molecular sciences · 2021
    Review
  20. Article
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

11 authors at 3 institutions in 2 countries.

C BassiCampbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada.
Y-T LiCampbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada.
K KhuCampbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada.
F MateoProCURE, Catalan Institute of Oncology, IDIBELL, L'Hospitalet del Llobregat, Barcelona, Spain.
P S BaniasadiCampbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada.
A EliaCampbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada.
J MasonCampbell Family Institute for Breast Cancer Research, Therapeutics Group, Toronto, ON, Canada.
V StambolicDepartment of Medical Biophysics, University of Toronto, University Health Network, Toronto, ON, Canada.
M A PujanaProgram Against Cancer Therapeutic Resistance, Breast Cancer and Systems Biology, Catalan Institute of Oncology, Bellvitge Institute for Biomedical Research, L'Hospitalet del Llobregat, Barcelona, Catalonia, Spain.
T W MakCampbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada.
C GorriniCampbell Family Institute for Breast Cancer Research, University Health Network, Toronto, ON, Canada.
University Health Network · CAInstitut Català d'Oncologia · ESPrincess Margaret Cancer Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acetyltransferase Tip60/Kat5 acetylates both histone and non-histone proteins, and is involved in a variety of biological processes. By acetylating p53, Tip60 controls p53-dependent transcriptional activity and so is implicated as a tumor suppressor. However, many breast cancers with low Tip60 also show p53 mutation, implying that Tip60 has a tumor suppressor function independent of its acetylation of p53. Here, we show in a p53-null mouse model of sporadic invasive breast adenocarcinoma that heterozygosity for Tip60 deletion promotes mammary tumorigenesis. Low Tip60 reduces DNA repair in normal and tumor mammary epithelial cells, both under resting conditions and following genotoxic stress. We demonstrate that Tip60 controls homologous recombination (HR)-directed DNA repair, and that Tip60 levels correlate inversely with a gene expression signature associated with defective HR-directed DNA repair. In human breast cancer data sets, Tip60 mRNA is downregulated, with low Tip60 levels correlating with p53 mutations in basal-like breast cancers. Our findings indicate that Tip60 is a novel breast tumor suppressor gene whose loss results in genomic instability leading to cancer formation.

Indexed as

DNA RepairAcetylationAnimalsApoptosis Regulatory ProteinsBRCA1 ProteinBreast NeoplasmsCell LineCisplatinCyclin-Dependent Kinase Inhibitor p21DNA DamageEpithelial CellsFemaleHistonesHomologous RecombinationHumansLysine Acetyltransferase 5Apoptosis Regulatory ProteinsBRCA1 ProteinCisplatinCyclin-Dependent Kinase Inhibitor p21HistonesLysine Acetyltransferase 5PUMA protein, mouseRad51 RecombinaseTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID26915295
PMCPMC4946888
OpenAlexW2287107628

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.