Evidence map›Paper›PMID 20332657›Full record

ArticleORL; journal for oto-rhino-laryngology and its related specialties2010

Inactivation of the tumor suppressor genes causing the hereditary syndromes predisposing to head and neck cancer via promoter hypermethylation in sporadic head and neck cancers.

Ian M Smith, Suhail K Mithani, Wojciech K Mydlarz, Steven S Chang, Joseph A Califano

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ORL; journal for oto-rhino-laryngology and its related specialties, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. DNA Methylation of Telomere-Related Genes and Cancer Risk.Cancer prevention research (Philadelphia, Pa.) · 2018
    Article
  3. Article
  4. Article
  5. Review
  6. Defects in the Fanconi Anemia Pathway in Head and Neck Cancer Cells Stimulate Tumor Cell Invasion through DNA-PK and Rac1 Signaling.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  7. Article
  8. Genome stability pathways in head and neck cancers.International journal of genomics · 2013
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Fanconi anaemia: from a monogenic disease to sporadic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2011
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Ian M SmithDepartment of Otolaryngology-Head and Neck Surgery, Head and Neck Cancer Division, Johns Hopkins Medical Institutions, Baltimore, MD 21287-0910, USA.
Suhail K Mithani
Wojciech K Mydlarz
Steven S Chang
Joseph A Califano
Johns Hopkins University · US

Funding

RESEARCH TRAINING IN OTOLARYNGOLOGYT32DC000027 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI CAREY, JOHN PATRICK · 1989 to 2023
$5.5M
Molecular progression model for HNSCCR37DE012588 · NIDCR · JOHNS HOPKINS UNIVERSITY · PI SIDRANSKY, DAVID · 2004 to 2012
$3.3M
Molecular Anatomy of Mitochondria in HNSCR01DE015939 · NIDCR · JOHNS HOPKINS UNIVERSITY · PI CALIFANO, JOSEPH A · 2004 to 2006
$1.2M
NIDCD NIH HHS T32 DC000027NIDCD NIH HHS T32DC00027NIDCR NIH HHS 1R01DE015939-01NIDCR NIH HHS 5R37DE012588NIDCR NIH HHS R01 DE015939NIDCR NIH HHS R37 DE012588
6 · The paper itself

Abstract

Fanconi anemia (FA) and dyskeratosis congenita (DC) are rare inherited syndromes that cause head and neck squamous cell cancer (HNSCC). Prior studies of inherited forms of cancer have been extremely important in elucidating tumor suppressor genes inactivated in sporadic tumors. Here, we studied whether sporadic tumors have epigenetic silencing of the genes causing the inherited forms of HNSCC. Using bisulfite sequencing, we investigated the incidence of promoter hypermethylation of the 17 Fanconi- and DC-associated genes in sporadic HNSCC. Genes that only showed methylation in the tumor patients were chosen for quantitative methylation-specific PCR (qMSP) in a set of 45 tumor and 16 normal patients. Three gene promoters showed differences in methylation: FancB (FAAP95, FA core complex), FancJ (BRIP1, DNA Helicase/ATPase), and DKC1 (dyskeratin). Bisulfite sequencing revealed that only FancB and DKC1 showed no methylation in normal patients, yet the presence of promoter hypermethylation in tumor patients. On qMSP, 1/16 (6.25%) of the normal mucosal samples from non-cancer patients and 14/45 (31.1%) of the tumor patients demonstrated hypermethylation of the FancB locus (p < 0.05). These results suggest that inactivation of FancB may play a role in the pathogenesis of sporadic HNSCC.

Indexed as

Genes, Tumor SuppressorBasic-Leucine Zipper Transcription FactorsBiopsyCarcinoma, Squamous CellCell Cycle ProteinsChi-Square DistributionDNA MethylationDyskeratosis CongenitaEpigenesis, GeneticFanconi AnemiaFanconi Anemia Complementation Group ProteinsGene SilencingGenetic Predisposition to DiseaseHead and Neck NeoplasmsHumansNuclear ProteinsBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsCell Cycle ProteinsDKC1 protein, humanFANCB protein, humanFanconi Anemia Complementation Group ProteinsNuclear Proteins

Identifiers

PMID20332657
PMCPMC2881891
OpenAlexW2045936922

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.