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

Combined Inhibition of mTOR and CDK4/6 Is Required for Optimal Blockade of E2F Function and Long-term Growth Inhibition in Estrogen Receptor–positive Breast Cancer

26 Feb 2018

Abstract excerpt

Abstract The cyclin dependent kinase (CDK)–retinoblastoma (RB)–E2F pathway plays a critical role in the control of cell cycle in estrogen receptor–positive (ER+) breast cancer. Small-molecule inhibitors of CDK4/6 have shown promise in this tumor type in combination with hormonal therapies, reflecting the particular dependence of this subtype of cancer on cyclin D1 and E2F transcription factors. mTOR inhibitors...

Read the complete abstract on PubMed

Topics

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

Share to Advanced Breast Cancer Therapies
Share to Cancer-related Molecular Pathways
Share to Chronic Lymphocytic Leukemia Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 29483206
DOI: 10.1158/1535-7163.mct-17-0537

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Combined Inhibition of mTOR and CDK4/6 Is Required for Optimal Blockade of E2F Function and Long-term Growth Inhibition in Estrogen Receptor–positive Breast CancerPMID 29483206Read ↗

Nexus Between PI3K/AKT and Estrogen Receptor Signaling in Breast CancerSemantic proximity Read ↗

Cdk4 and Cdk6 Couple the Cell-Cycle Machinery to Cell Growth via mTORC1Semantic proximity Read ↗

Acquired CDK6 amplification promotes breast cancer resistance to CDK4/6 inhibitors and loss of ER signaling and dependenceSemantic proximity Read ↗

The retinoblastoma tumor suppressor modifies the therapeutic response of breast cancerSemantic proximity Read ↗

CDK4 and CDK6 kinases: From basic science to cancer therapySemantic proximity Read ↗

Targeting mTOR to overcome resistance to hormone and CDK4/6 inhibitors in ER-positive breast cancer models.Semantic proximity Read ↗

Targeting the PI3K/AKT/mTOR Pathway in Hormone-Positive Breast Cancer.Semantic proximity Read ↗

Molecular Pathways: Targeting the Cyclin D–CDK4/6 Axis for Cancer TreatmentSemantic proximity Read ↗

Targeting Transcriptional Regulation with a CDK9 Inhibitor Suppresses Growth of Endocrine- and Palbociclib-Resistant ER+ Breast CancersSemantic proximity Read ↗

An E2F1-dependent gene expression program that determines the balance between proliferation and cell death.Semantic proximity Read ↗

GREB1 regulates proliferation of estrogen receptor positive breast cancer through modulation of PI3K/Akt/mTOR signalingSemantic proximity Read ↗

High CDK6 Protects Cells from Fulvestrant-Mediated Apoptosis and is a Predictor of Resistance to Fulvestrant in Estrogen Receptor–Positive Metastatic Breast CancerSemantic proximity Read ↗

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