Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

Hormones & cancer - 1 Dec 2015

Nayak Shweta R, Harrington Emily, Boone David, Hartmaier Ryan, Chen Jian, Pathiraja Thushangi N, Cooper Kristine L, Fine Jeffrey L, Sanfilippo Joseph, Davidson Nancy E, Lee Adrian V, Dabbs David, Oesterreich Steffi

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antineoplastic Agents, Hormonal
Share to Combined Modality Therapy

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Gene Knockdown Techniques

Share to Histones

Share to Multigene Family

Share to Neoplasm Grading

Share to Neoplasm Staging

Source

Open in PubMed Open full text

Identifiers

PMID: 26113056
DOI: 10.1007/s12672-015-0230-5
PMCID: PMC4807402

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Role for Histone H2B Variants in Endocrine-Resistant Breast Cancer.PMID 26113056Read ↗

Incorporating histone H2B variants into chromatin modifies chromatin accessibility to induce epithelial-to-mesenchymal transition in breast cancerSemantic proximity Read ↗

Immunohistochemical Profiling of Histone Modification Biomarkers Identifies Subtype-Specific Epigenetic Signatures and Potential Drug Targets in Breast CancerSemantic proximity Read ↗

Emerging Role of Epigenetic Modifiers in Breast Cancer Pathogenesis and Therapeutic ResponseSemantic proximity Read ↗

Development and validation of multivariate predictors of primary endocrine resistance to tamoxifen and aromatase inhibitors in luminal breast cancer reveal drug-specific differencesSemantic proximity Read ↗

Inhibition of EZH2 Catalytic Activity Selectively Targets a Metastatic Subpopulation in Triple-Negative Breast Cancer.Semantic proximity Read ↗

HIST1H1B Promotes Basal-Like Breast Cancer Progression by Modulating CSF2 ExpressionSemantic proximity Read ↗

Amplification of WHSC1L1 regulates expression and estrogen‐independent activation of ERα in SUM‐44 breast cancer cells and is associated with ERα over‐expression in breast cancerSemantic proximity Read ↗

Constitutively Active Androgen Receptor Supports the Metastatic Phenotype of Endocrine-Resistant Hormone Receptor-Positive Breast CancerSemantic proximity Read ↗

Endocrine therapy-specific lineage and partial epithelial-mesenchymal reprogramming defines divergent resistant cell-states in ER+ breast cancerSemantic proximity Read ↗

Combinatorial targeting of a chromatin complex comprising Dot1L, menin and the tyrosine kinase BAZ1B reveals a new therapeutic vulnerability of endocrine therapy-resistant breast cancerSemantic proximity Read ↗

Increased gene expression variability in BRCA1-associated and basal-like breast tumours.Semantic proximity Read ↗

Widespread reorganisation of the regulatory chromatin landscape facilitates resistance to inhibition of oncogenic ERBB2 signallingSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.