Evidence map›Paper›PMID 19383825›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009

Protein acetylation and histone deacetylase expression associated with malignant breast cancer progression.

Junko Suzuki, Yunn-Yi Chen, Gary K Scott, Sandy Devries, Koei Chin, Christopher C Benz, Frederic M Waldman, E Shelley Hwang

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 134 citations in OpenAlex.

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  19. Targeting epigenetic mechanisms to overcome venetoclax resistance.Biochimica et biophysica acta. Molecular cell research · 2021
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1 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 2 countries.

Junko SuzukiDepartment of Laboratory Medicine, University of California, San Francisco, CA, USA.
Yunn-Yi Chen
Gary K Scott
Sandy Devries
Koei Chin
Christopher C Benz
Frederic M Waldman
E Shelley Hwang
Buck Institute for Research on Aging · USJuntendo University · JPMolecular Oncology (United States) · USUniversity of California, San Francisco · US

Funding

Tissue and Outcomes CoreP50CA058207 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRAY, JOE W. · 1992 to 2012
$32.7M
Primary Hormonal Therpay for DCIS of the BreastK23CA097181 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HWANG, E.SHELLEY · 2004 to 2008
$636k
NCI NIH HHS CA367763NCI NIH HHS K23 CA097181NCI NIH HHS K23 CA0977181-01A10NCI NIH HHS P50 CA058207NCI NIH HHS P50 CA58207
6 · The paper itself

Abstract

purposeExcess histone deacetylase (HDAC) activity can induce hypoacetylation of histone and nonhistone protein substrates, altering gene expression patterns and cell behavior potentially associated with malignant transformation. However, HDAC expression and protein acetylation have not been studied in the context of breast cancer progression. EXPERIMENTAL

designWe assessed expression levels of acetylated histone H4 (ac-H4), ac-H4K12, ac-tubulin, HDAC1, HDAC2, and HDAC6 in 22 reduction mammoplasties and in 58 specimens with synchronous normal epithelium, ductal carcinoma in situ (DCIS), and invasive ductal carcinoma (IDC) components. Differences among groups were tested for significance using nonparametric tests.

resultsFrom normal epithelium to DCIS, there was a marked reduction in histone acetylation (P < 0.0001). Most cases showed similar levels of acetylation in DCIS and IDC, although some showed further reduction of ac-H4 and ac-H4K12 from DCIS to IDC. Expression of HDAC1, HDAC2, and HDAC6 was also significantly reduced but by a smaller magnitude. Greater reductions of H4 acetylation and HDAC1 levels were observed from normal to DCIS in estrogen receptor-negative compared with estrogen receptor-positive, and in high-grade compared with non-high-grade tumors.

conclusionOverall, there was a global pattern of hypoacetylation associated with progression from normal to DCIS to IDC. These findings suggest that the reversal of this hypoacetylation in DCIS and IDC could be an early measure of HDAC inhibitor activity.

Indexed as

AcetylationAdultAgedAged, 80 and overBreastBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, Intraductal, NoninfiltratingDisease ProgressionErb-b2 Receptor Tyrosine KinasesFemaleHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase 6Histone DeacetylasesHistonesErb-b2 Receptor Tyrosine KinasesHDAC1 protein, humanHDAC6 protein, humanHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase 6Histone DeacetylasesHistonesReceptors, EstrogenReceptors, ProgesteroneRepressor ProteinsTubulin

Identifiers

PMID19383825
PMCPMC3746548
OpenAlexW2123649043

What OpenQuestion holds

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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.