Evidence map›Paper›PMID 15931363›Full record

ReviewClinical medicine & research2004

Novel management of oral cancer: a paradigm of predictive oncology.

Jon Sudbø

RetractedOpen access · bronzeAbstract readRetracted PublicationReview
In one paragraph

Review in Clinical medicine & research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

3 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Jon SudbøDepartment of Medical Oncology and Radiotherapy, The Norwegian Radium Hospital, Oslo, Norway. jon.sudbo@rh.uio.no
Norwegian Cancer Society · NO

Funding

TARGETING COX-2 AND EGFR SIGNALING IN ORAL CARCINOGENESISP01CA106451 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIPPMAN, SCOTT M · 2004 to 2009
$8.3M
NCI NIH HHS P01 CA106451
6 · The paper itself

Abstract

The rationale for molecular-targeted prevention of oral cancer is strong. Oral cancer is a major global threat to public health with 300,000 new cases diagnosed worldwide on an annual basis. Notably, the great morbidity and mortality rates of this devastating disease have not improved in decades. Oral cancer development is a tobacco-related multistep and multifocal process involving field carcinogenesis and intraepithelial clonal spread. Biomarkers of genomic instability, such as aneuploidy and allelic imbalance, can accurately measure the cancer risk of oral premalignant lesions or intraepithelial neoplasia (IEN). Retinoid-oral IEN studies (e.g., retinoid acid receptor-beta, p53, genetic instability, loss of heterozygosity, and cyclin D1) have advanced the overall understanding of the biology of intraepithelial carcinogenesis and preventive agent molecular mechanisms and targets, important advances for monitoring preventive interventions, assessing cancer risk, and pharmacogenomics. Clinical management of oral IEN varies from watchful waiting to complete resection, although complete resection does not prevent oral cancer in high-risk patients. New approaches, such as interventions with molecular-targeted agents and agent combinations in molecularly defined high-risk oral IEN patients, are urgently needed to reduce the devastating worldwide consequences of oral cancer.

Indexed as

Biomarkers, TumorCarcinoma, Squamous CellGenetic TestingHumansLeukoplakia, OralMouth NeoplasmsPrecancerous ConditionsPredictive Value of TestsRisk FactorsBiomarkers, Tumor

Identifiers

PMID15931363
PMCPMC1069099
OpenAlexW2119655816

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.