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

Genomic DNA and messenger RNA expression alterations of the CDKN2B and CDKN2 genes in esophageal squamous carcinoma cell lines.

Genes, chromosomes & cancer - 1 Aug 1995

Zhou X, Suzuki H, Shimada Y, Imamura M, Yin J, Jiang H Y, Tarmin L, Abraham J M, Meltzer S J

Abstract excerpt

The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. CDKN2 and CDKN2B belong to a family of cyclin-dependent kinase 4 inhibitors (INK41) and control cell proliferation during the G1 phase of the cell cycle. Their...

Topics

Alleles
Base Sequence
Carcinoma, Squamous Cell
Carrier Proteins
Cell Cycle Proteins
Chromosome Deletion
Chromosomes, Human, Pair 9
Cyclin-Dependent Kinase Inhibitor p15
Cyclin-Dependent Kinase Inhibitor p16
DNA, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Enzyme Inhibitors

Esophageal Neoplasms

Gene Expression

Genes, Tumor Suppressor

Homozygote

Humans

Molecular Sequence Data

Mutation

Source

Identifiers

PMID: 7547637
DOI: 10.1002/gcc.2870130409

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-7547637-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genomic DNA and messenger RNA expression alterations of the CDKN2B and CDKN2 genes in esophageal squamous carcinoma cell lines.PMID 7547637Read ↗

Intragenic mutations of CDKN2B and CDKN2A in primary human esophageal cancersSemantic proximity Read ↗

Frequent mutations of CDKN2 in primary pancreatic adenocarcinomas.Semantic proximity Read ↗

Virtually 100% of melanoma cell lines harbor alterations at the DNA level within CDKN2A, CDKN2B, or one of their downstream targets.Semantic proximity Read ↗

High frequency of CDKN2A alterations in esophageal squamous cell carcinoma from a high-risk Chinese population.Semantic proximity Read ↗

p16/CDKN2 alterations and pRb expression in oesophageal squamous carcinoma.Semantic proximity Read ↗

Cell cycle-related gene abnormalities and product expression in esophageal carcinoma.Semantic proximity Read ↗

Fine-Mapping Loss of Gene Architecture at the CDKN2B (p15INK4b), CDKN2A (p14ARF, p16INK4a), and MTAP Genes in Head and Neck Squamous Cell CarcinomaSemantic 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 ↗

Loss of disabled-2 expression is an early event in esophageal squamous tumorigenesisSemantic proximity Read ↗

Comprehensive analysis of CDKN2A status in microdissected urothelial cell carcinoma reveals potential haploinsufficiency, a high frequency of homozygous co-deletion and associations with clinical phenotype.Semantic proximity Read ↗

Mechanisms of inactivation of p14ARF, p15INK4b, and p16INK4a genes in human esophageal squamous cell carcinoma.Semantic proximity Read ↗

Analysis of CDKN2A, CDKN2B, CDKN2C, and cyclin Ds gene status in hepatoblastomaSemantic proximity Read ↗

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