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

Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

8 Jan 2025

Abstract excerpt

Despite adjuvant treatment with endocrine therapies, estrogen receptor-positive (ER+) breast cancers recur in a significant proportion of patients. Recurrences are attributable to clinically undetectable endocrine-tolerant persister cancer cells that retain tumor-forming potential. Therefore, strategies targeting such persister cells may prevent recurrent disease. Using CRISPR-Cas9 genome-wide knockout screening...

Read the complete abstract on PubMed

Topics

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

Share to Cancer Cells and Metastasis
Share to DNA Repair Mechanisms
Share to Mitochondrial Function and Pathology

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 39777474
DOI: 10.1158/0008-5472.can-24-1204

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast CancerPMID 39777474Read ↗

Endocrine persistence in ER+ breast cancer is accompanied by metabolic vulnerability in oxidative phosphorylationSemantic proximity Read ↗

Metabolic orchestration of drug-tolerant persister cells in cancerSemantic proximity Read ↗

Drug-tolerant persister cell in cancer: reversibility, microenvironmental interplay, and therapeutic strategiesSemantic proximity Read ↗

AMPK activation by metformin promotes survival of dormant ER+ breast cancer cellsSemantic proximity Read ↗

Adenosine triphosphate citrate lyase alters cellular myelocytomatosis oncogene signaling and fatty acid oxidation in residual breast cancer tumor tissues after neoadjuvant treatmentSemantic proximity Read ↗

Cycling cancer persister cells arise from lineages with distinct transcriptional and metabolic programsSemantic proximity Read ↗

Metabolic reprogramming in breast cancer results in distinct mitochondrial bioenergetics between luminal and basal subtypesSemantic proximity Read ↗

Optical imaging reveals chemotherapy-induced metabolic reprogramming of residual disease and recurrenceSemantic proximity Read ↗

Ontogeny and Vulnerabilities of Drug-Tolerant Persisters in HER2+ Breast CancerSemantic proximity Read ↗

ONC201/TIC10 enhances durability of mTOR inhibitor everolimus in metastatic ER+ breast cancerSemantic proximity Read ↗

Single-cell transcriptomics reveals age-specific epithelial evolution and metabolic vulnerability in young breast cancerSemantic proximity Read ↗

The Flick of a Switch: Conferring Survival Advantage to Breast Cancer Stem Cells Through Metabolic PlasticitySemantic proximity Read ↗

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