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

Control of replicative life span in human cells: barriers to clonal expansion intermediate between M1 senescence and M2 crisis.

Molecular and cellular biology - 1 Apr 1999

Bond J A, Haughton M F, Rowson J M, Smith P J, Gire V, Wynford-Thomas D, Wyllie F S

Abstract excerpt

The accumulation of genetic abnormalities in a developing tumor is driven, at least in part, by the need to overcome inherent restraints on the replicative life span of human cells, two of which-senescence (M1) and crisis (M2)-have been well characterized. Here we describe additional barriers to clonal expansion (Mint) intermediate between M1 and M2, revealed by abrogation of tumor-suppressor gene (TSG) pathways...

Read the complete abstract on PubMed

Topics

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

Share to Cell Compartmentation
Share to Cellular Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p16

Share to Cyclin-Dependent Kinase Inhibitor p21

Share to Cyclins

Share to Oncogene Proteins, Viral

Share to Papillomavirus E7 Proteins

Share to Thyroid Gland

Source

Open in PubMed Open full text

Identifiers

PMID: 10082577
DOI: 10.1128/MCB.19.4.3103
PMCID: PMC84104

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

Control of replicative life span in human cells: barriers to clonal expansion intermediate between M1 senescence and M2 crisis.PMID 10082577Read ↗

Telomere-based proliferative lifespan barriers in Werner-syndrome fibroblasts involve both p53-dependent and p53-independent mechanismsSemantic proximity Read ↗

Uncoupling between phenotypic senescence and cell cycle arrest in aging p21-deficient fibroblasts.Semantic proximity Read ↗

Immortalization of normal human mammary epithelial cells in two steps by direct targeting of senescence barriers does not require gross genomic alterationsSemantic proximity Read ↗

E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescenceSemantic proximity Read ↗

The disparity between human cell senescence in vitro and lifelong replication in vivoSemantic proximity Read ↗

Molecular Distinctions between Stasis and Telomere Attrition Senescence Barriers Shown by Long-term Culture of Normal Human Mammary Epithelial CellsSemantic proximity Read ↗

Telomerase activation by the E6 gene product of human papillomavirus type 16.Semantic proximity Read ↗

A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status.Semantic proximity Read ↗

Immortalization of distinct human mammary epithelial cell types by human papilloma virus 16 E6 or E7.Semantic proximity Read ↗

Nek4 Regulates Entry into Replicative Senescence and the Response to DNA Damage in Human FibroblastsSemantic proximity Read ↗

Overcoming cellular senescence in human cancer pathogenesis.Semantic proximity Read ↗

Contribution of p16(INK4a) to replicative senescence of human fibroblasts.Semantic proximity Read ↗

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