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

Clonal expansion and loss of heterozygosity at chromosomes 9p and 17p in premalignant esophageal (Barrett's) tissue.

Journal of the National Cancer Institute - 15 Dec 1999

Galipeau P C, Prevo L J, Sanchez C A, Longton G M, Reid B J

Abstract excerpt

BACKGROUND: Abnormalities involving the p16 (also known as cyclin-dependent kinase N2 [CDKN2], p16 [INK4a], or MTS1) and p53 (also known as TP53) tumor suppressor genes are highly prevalent in esophageal adenocarcinomas. Loss of heterozygosity (LOH) at 9p21 and 17p13 chromosomes (locations for p16 and p53 genes, respectively) is frequently observed in the premalignant condition, Barrett's esophagus. We studied...

Read the complete abstract on PubMed

Topics

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

Share to Aneuploidy
Share to Barrett Esophagus

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Chromosomes, Human, Pair 17

Share to Chromosomes, Human, Pair 9

Share to Clone Cells

Share to Esophageal Neoplasms

Share to Loss of Heterozygosity

Share to Precancerous Conditions

Source

Open in PubMed Open full text

Identifiers

PMID: 10601379
DOI: 10.1093/jnci/91.24.2087
PMCID: PMC1559996

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Clonal expansion and loss of heterozygosity at chromosomes 9p and 17p in premalignant esophageal (Barrett's) tissue.PMID 10601379Read ↗

Loss of heterozygosity on chromosome 17p predicts neoplastic progression in Barrett's esophagus.Semantic proximity Read ↗

17p allelic losses in diploid cells of patients with Barrett's esophagus who develop aneuploidy.Semantic proximity Read ↗

17p allelic deletions and p53 protein overexpression in Barrett's adenocarcinoma.Semantic proximity Read ↗

p16(INK4a) lesions are common, early abnormalities that undergo clonal expansion in Barrett's metaplastic epithelium.Semantic proximity Read ↗

Genetic mechanisms in esophageal carcinogenesis: frequent deletion of 3p and 17p in premalignant lesions.Semantic proximity Read ↗

p53 mutations in Barrett's adenocarcinoma and high-grade dysplasia.Semantic proximity Read ↗

Chromosomal Instability in Barrett's Esophagus Is Related to Telomere ShorteningSemantic proximity Read ↗

Genetic Mechanisms of TP53 Loss of Heterozygosity in Barrett's Esophagus: Implications for Biomarker ValidationSemantic proximity Read ↗

Allelic loss of 9p21 and mutation of the CDKN2/p16 gene develop as early lesions during neoplastic progression in Barrett's esophagus.Semantic proximity Read ↗

Single nucleotide polymorphism-based genome-wide chromosome copy change, loss of heterozygosity, and aneuploidy in Barrett's esophagus neoplastic progression.Semantic proximity Read ↗

Fractional allele loss indicates distinct genetic populations in the development of squamous cell carcinoma of the head and neck (SCCHN).Semantic proximity Read ↗

Selectively advantageous mutations and hitchhikers in neoplasms: p16 lesions are selected in Barrett's esophagus.Semantic proximity Read ↗

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