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

Temporal myc dynamics permit mitotic bypass, promoting polyploid phenotypes.

Cancer letters - 31 Mar 2025

Loycano Michael A, Pienta Kenneth J, Amend Sarah R

Abstract excerpt

High Myc phenotypes are extensively documented in the hyperproliferative cell cycle of cancer cells, as well as non-proliferative endoreplication cycles engaged during normal development and stress response. Notably, endoreplication in cancer produces chemotherapy resistant polyploid cells, necessitating a clearer understanding of altered cell cycle regulation that uncouples DNA replication and mitotic cell...

Read the complete abstract on PubMed

Topics

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

Share to Cell Proliferation
Share to DNA Replication
Share to APC gene

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitosis

Share to Neoplasms

Share to Phenotype

Share to Polyploidy

Share to Proto-Oncogene Proteins c-myc

Source

Open in PubMed Open full text

Identifiers

PMID: 39909233
DOI: 10.1016/j.canlet.2025.217526
PMCID: PMC11924244

Genes

APC

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Temporal myc dynamics permit mitotic bypass, promoting polyploid phenotypes.PMID 39909233Read ↗

Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.Semantic proximity Read ↗

The cell cycle and cancerSemantic proximity Read ↗

Polyploidy in Cancer: Causal Mechanisms, Cancer-Specific Consequences, and Emerging TreatmentsSemantic proximity Read ↗

DNA replication and mitotic entry: A brake model for cell cycle progressionSemantic proximity Read ↗

MYC Dysregulates Mitosis, Revealing Cancer VulnerabilitiesSemantic proximity Read ↗

Cancer regeneration: Polyploid cells are the key drivers of tumor progressionSemantic proximity Read ↗

“The Octet”: Eight Protein Kinases that Control Mammalian DNA ReplicationSemantic proximity Read ↗

FOXM1 is critical for the fitness recovery of chromosomally unstable cellsSemantic proximity Read ↗

To cycle or not to cycle: a critical decision in cancer.Semantic proximity Read ↗

Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.Semantic proximity Read ↗

Profilin 1 maintains cell cycle fidelity to prevent unscheduled genome doubling and polyploidy in cancerSemantic proximity Read ↗

Cyclin B1–Cdk1 Activation Continues after Centrosome Separation to Control Mitotic ProgressionSemantic proximity Read ↗

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