Evidence map›Paper›PMID 26113056›Full record

ArticleHormones & cancer2015

A Role for Histone H2B Variants in Endocrine-Resistant Breast Cancer.

Shweta R Nayak, Emily Harrington, David Boone, Ryan Hartmaier, Jian Chen, Thushangi N Pathiraja, Kristine L Cooper, Jeffrey L Fine, Joseph Sanfilippo, Nancy E Davidson and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Hormones & cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
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  4. Breast Cancer Chemoresistance: Insights into the Regulatory Role of lncRNA.International journal of molecular sciences · 2023
    Review
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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

13 authors at 7 institutions in 2 countries.

Shweta R NayakDivision of Reproductive Endocrinology, Magee-Womens Hospital, University of Pittsburgh Medical Center (UPMC), Pittsburgh, PA, USA.
Emily HarringtonDepartment of Pharmacology and Chemical Biology, Women's Cancer Research Center (WCRC), Magee-Womens Research Institute (MWRI), University of Pittsburgh Cancer Institute (UPCI), 204 Craft Avenue, Pittsburgh, PA, 15213, USA.
David BooneDepartment of Pharmacology and Chemical Biology, Women's Cancer Research Center (WCRC), Magee-Womens Research Institute (MWRI), University of Pittsburgh Cancer Institute (UPCI), 204 Craft Avenue, Pittsburgh, PA, 15213, USA.
Ryan HartmaierDepartment of Pharmacology and Chemical Biology, Women's Cancer Research Center (WCRC), Magee-Womens Research Institute (MWRI), University of Pittsburgh Cancer Institute (UPCI), 204 Craft Avenue, Pittsburgh, PA, 15213, USA.
Jian ChenDepartment of Pharmacology and Chemical Biology, Women's Cancer Research Center (WCRC), Magee-Womens Research Institute (MWRI), University of Pittsburgh Cancer Institute (UPCI), 204 Craft Avenue, Pittsburgh, PA, 15213, USA.
Thushangi N PathirajaGenome Institute of Singapore, Singapore, Singapore.
Kristine L CooperBiostatistics Core Facility at UPCI, Pittsburgh, PA, USA.
Jeffrey L FineDepartment of Pathology, Magee-Womens Hospital, UPMC, Pittsburgh, PA, USA.
Joseph SanfilippoDivision of Reproductive Endocrinology, Magee-Womens Hospital, University of Pittsburgh Medical Center (UPMC), Pittsburgh, PA, USA.
Nancy E DavidsonDepartment of Medicine, UPCI, UPMC, Pittsburgh, PA, USA.
Adrian V LeeDepartment of Pharmacology and Chemical Biology, Women's Cancer Research Center (WCRC), Magee-Womens Research Institute (MWRI), University of Pittsburgh Cancer Institute (UPCI), 204 Craft Avenue, Pittsburgh, PA, 15213, USA.
David DabbsDepartment of Pathology, Magee-Womens Hospital, UPMC, Pittsburgh, PA, USA.
Steffi OesterreichDepartment of Pharmacology and Chemical Biology, Women's Cancer Research Center (WCRC), Magee-Womens Research Institute (MWRI), University of Pittsburgh Cancer Institute (UPCI), 204 Craft Avenue, Pittsburgh, PA, 15213, USA. oesterreichs@upmc.edu.
Magee-Womens Research Institute · USCancer Research Center · USMagee-Womens Hospital · USUniversity of Pittsburgh Medical Center · USGenome Institute of Singapore · SGUPMC Health System · USUPMC Hillman Cancer Center · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
ER Co-Repressor Function of SAFB in Breast CancerR01CA097213 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OESTERREICH, STEFFI · 2002 to 2012
$2.4M
NCI NIH HHS NIH 5P30 CA47904NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA097213NCI NIH HHS R01CA097213
6 · The paper itself

Abstract

Acquired resistance to aromatase inhibitors (AIs) remains a major clinical problem in the treatment of estrogen receptor-positive (ER+) breast cancer. We and others have previously reported widespread changes in DNA methylation using breast cancer cell line models of endocrine resistance. Here, we show that the histone variant HIST1H2BE is hypomethylated in estrogen deprivation-resistant C4-12 and long-term estrogen-deprived (LTED) cells compared with parental MCF-7 cells. As expected, this hypomethylation associates with increased expression of HIST1H2BE in C4-12 and LTED cells. Both overexpression and downregulation of HIST1H2BE caused decreased proliferation in breast cancer cell lines suggesting the need for tightly controlled expression of this histone variant. Gene expression analysis showed varied expression of HIST1H2BE in a large panel of breast cancer cell lines, without restriction to specific molecular subtypes. Analysis of HIST1H2BE messenger RNA (mRNA) expression in ER+ AI-treated breast tumors showed significantly higher expression in resistant (n = 19) compared with sensitive (n = 37) tumors (p = 0.01). Using nanostring analysis, we measured expression of all 61 histone variants in endocrine-resistant and endocrine-sensitive tumors. We found significant overexpression of 22 variant histone genes in tumors resistant to AI therapy. In silico The Cancer Genome Atlas (TCGA) analysis showed frequent amplification of the HIST1 locus. In summary, our studies show, for the first time, that overexpression of histone variants might be important in endocrine response in ER+ breast cancer, and that overexpression is at least in part mediated via epigenetic mechanisms and amplifications. Future studies addressing endocrine response should include a potential role of these currently understudied histone variants.

Indexed as

Genetic VariationAdultAgedAged, 80 and overAnimalsAntineoplastic Agents, HormonalBreast NeoplasmsCase-Control StudiesCell Line, TumorCell ProliferationCluster AnalysisCombined Modality TherapyDNA MethylationDrug Resistance, NeoplasmFemaleGene ExpressionAntineoplastic Agents, HormonalHistones

Identifiers

PMID26113056
PMCPMC4807402
OpenAlexW2214735036

What OpenQuestion holds

Textmetadata
LicenceTDM
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.