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 model for random genetic damage directing selection of diploid or aneuploid tumours.

Cell proliferation - 1 Jun 2011

Bazeley P S, Nestor Kalinoski A L, Ways J A, Liu S-T, Ramdath R S, Matsui S-i, Allison D C

Abstract excerpt

OBJECTIVES: To test whether genetic instability may determine whether tumours become aneuploid or diploid. MATERIALS AND METHODS: We have identified genes needed for cell survival or replication by combining Affymetrix gene expression array data from 12 experimental cell lines with in silico GEO+GNF and expO databases. Specific loss of heterozygosis (LOHs), chromosomal abnormalities (called derivative...

Read the complete abstract on PubMed

Topics

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

Share to Aneuploidy
Share to Cell Survival
Share to Chromosomal Instability

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromosome Aberrations

Share to Chromosomes

Share to Diploidy

Share to Loss of Heterozygosity

Share to Stem Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 21535262
DOI: 10.1111/j.1365-2184.2011.00746.x
PMCID: PMC6496868

Genes

APC

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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 model for random genetic damage directing selection of diploid or aneuploid tumours.PMID 21535262Read ↗

Colonic epithelial adaptation to EGFR-independent growth induces chromosomal instability and is accelerated by prior injury.Semantic proximity Read ↗

A model for genetic complementation controlling the chromosomal abnormalities and loss of heterozygosity formation in cancer.Semantic proximity Read ↗

Differential effects of aneuploidy on growth and differentiation in human intestinal stem cellsSemantic proximity Read ↗

Whole-genome duplication shapes the aneuploidy landscape of human cancersSemantic proximity Read ↗

Simple aneuploidy evades p53 surveillance and promotes niche factor-independent growth in human intestinal organoidsSemantic proximity Read ↗

Targeting the DNA Damage Response Pathways and Replication Stress in Colorectal CancerSemantic proximity Read ↗

Carcinogens induce genome-wide loss of heterozygosity in normal stem cells without persistent chromosomal instability.Semantic proximity Read ↗

Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitorsSemantic proximity Read ↗

Negative selection may cause grossly altered but broadly stable karyotypes in metastatic colorectal cancerSemantic proximity Read ↗

Tolerance of whole-genome doubling propagates chromosomal instability and accelerates cancer genome evolution.Semantic proximity Read ↗

The role of chromosome missegregation in cancer development: a theoretical approach using agent-based modelling.Semantic proximity Read ↗

Genome wide expression analysis of radiation-induced DNA damage responses in isogenic HCT116 p53+/+ and HCT116 p53-/- colorectal carcinoma cell lines.Semantic proximity Read ↗

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