ArticleHuman genetics2004
Novel microsatellite markers and single nucleotide polymorphisms refine the tylosis with oesophageal cancer (TOC) minimal region on 17q25 to 42.5 kb: sequencing does not identify the causative gene.
Article in Human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 40 citations in OpenAlex.
- The cytoglobin-dependent transcriptome in melanoma indicates a protective function associated with oxidative stress, inflammation and cancer-associated pathways.Scientific reports · 2024Article
- Copy number gains of chromosome 17 identified by dual in situ hybridization in non-small cell lung cancer tissue correlate with overexpression of c-Myc.Translational cancer research · 2022Article
- Lessons from the post-genomic era: Globin diversity beyond oxygen binding and transport.Redox biology · 2020Review
- Integrative analysis with expanded DNA methylation data reveals common key regulators and pathways in cancers.NPJ genomic medicine · 2019Article
- Analysis of a Finnish family confirms RHBDF2 mutations as the underlying factor in tylosis with esophageal cancer.Familial cancer · 2012Article
- Selected telomere length changes and aberrant three-dimensional nuclear telomere organization during fast-onset mouse plasmacytomas.Neoplasia (New York, N.Y.) · 2012Article
- RHBDF2 mutations are associated with tylosis, a familial esophageal cancer syndrome.American journal of human genetics · 2012Article
- Protection from intracellular oxidative stress by cytoglobin in normal and cancerous oesophageal cells.PloS one · 2012Article
- Cytoglobin: biochemical, functional and clinical perspective of the newest member of the globin family.Cellular and molecular life sciences : CMLS · 2011Review
- Duplication of Subcytoband 11E2 of Chromosome 11 Is Regularly Associated with Accelerated Tumor Development in v-abl/myc-Induced Mouse Plasmacytomas.Genes & cancer · 2010Article
- Genetic heterogeneity of oesophageal cancer in high-incidence areas of southern and northern China.PloS one · 2010Article
- Cytoglobin is upregulated by tumour hypoxia and silenced by promoter hypermethylation in head and neck cancer.British journal of cancer · 2009Article
- Cytoglobin, the newest member of the globin family, functions as a tumor suppressor gene.Cancer research · 2008Article
- Promoter methylation of P16, RARbeta, E-cadherin, cyclin A1 and cytoglobin in oral cancer: quantitative evaluation using pyrosequencing.British journal of cancer · 2006Article
- Rearrangements of the telomeric region of mouse chromosome 11 in Pre-B ABL/MYC cells revealed by mBANDing, spectral karyotyping, and fluorescence in-situ hybridization with a subtelomeric probe.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2004Article
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tylosis (focal non-epidermolytic palmoplantar keratoderma) is associated with the early onset of squamous cell oesophageal cancer in three families. Linkage and haplotype analyses have previously mapped the tylosis with oesophageal cancer ( TOC) locus to a 500-kb region on chromosome 17q25 that has also been implicated in sporadically occurring squamous cell oesophageal cancer. In the current study, 17 additional putative microsatellite markers were identified within this 500-kb region by using sequence data and seven of these were shown to be polymorphic in the UK and US families. In addition, our complete sequence analysis of the non-repetitive parts of the TOC minimal region identified 53 novel and six known single nucleotide polymorphisms (SNPs) in one or both of these families. Further fine mapping of the TOC disease locus by haplotype analysis of the seven polymorphic markers and 21 of the 59 SNPs allowed the reduction of the minimal region to 42.5 kb. One known and two putative genes are located within this region but none of these genes shows tylosis-specific mutations within their protein-coding regions. Alternative mechanisms of disease gene action must therefore be considered.
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