Evidence map›Paper›PMID 19568590›Full record

ReviewYonsei medical journal2009

Promoter methylation in the genesis of gastrointestinal cancer.

Clement Richard Boland, Sung Kwan Shin, Ajay Goel

Open access · goldAbstract readReview
In one paragraph

Review in Yonsei medical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Role of PLK4 inhibition in cancer therapy.Cancer metastasis reviews · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Development of a gLCR-based KRAS mutation detection approach and its comparison with other screening methods.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  8. Article
  9. Article
  10. DNA methylation and microRNAs in cancer.World journal of gastroenterology · 2012
    Review
  11. Epigenetics: principles and practice.Digestive diseases (Basel, Switzerland) · 2011
    Review
  12. DNA methylation changes in ex-adenoma carcinoma of the large intestine.Virchows Archiv : an international journal of pathology · 2010
    Article
  13. Review
  14. Nitric oxide: perspectives and emerging studies of a well known cytotoxin.International journal of molecular sciences · 2010
    Review
  15. Review
  16. Article
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

3 authors at 1 institution in 2 countries.

Clement Richard BolandDivision of Gastroenterology, Department of Internal Medicine, Sammons Cancer Center, Baylor Research Institute, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX 75246, USA. RickBo@BaylorHealth.edu
Sung Kwan Shin
Ajay Goel
Baylor University Medical Center · US

Funding

The Biology and Diagnosis of HNPCCR01CA072851 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI GOEL, AJAY · 1996 to 2019
$6.6M
JC Virus and Tumor Formation in the Human ColonR01CA098572 · NCI · BAYLOR RESEARCH INSTITUTE · PI BOLAND, CLEMENT RICHARD · 2004 to 2014
$2.7M
NCI NIH HHS CA 72851NCI NIH HHS CA 98572NCI NIH HHS R01 CA072851NCI NIH HHS R01 CA098572
6 · The paper itself

Abstract

Colorectal cancers (CRC)--and probably all cancers--are caused by alterations in genes. This includes activation of oncogenes and inactivation of tumor suppressor genes (TSGs). There are many ways to achieve these alterations. Oncogenes are frequently activated by point mutation, gene amplification, or changes in the promoter (typically caused by chromosomal rearrangements). TSGs are typically inactivated by mutation, deletion, or promoter methylation, which silences gene expression. About 15% of CRC is associated with loss of the DNA mismatch repair system, and the resulting CRCs have a unique phenotype that is called microsatellite instability, or MSI. This paper reviews the types of genetic alterations that can be found in CRCs and hepatocellular carcinoma (HCC), and focuses upon the epigenetic alterations that result in promoter methylation and the CpG island methylator phenotype (CIMP). The challenge facing CRC research and clinical care at this time is to deal with the heterogeneity and complexity of these genetic and epigenetic alterations, and to use this information to direct rational prevention and treatment strategies.

Indexed as

Colorectal NeoplasmsDNA MethylationGastrointestinal NeoplasmsHumansMicrosatellite InstabilityPromoter Regions, Geneticchromosomal instabilityCIMPColorectal cancerhepatocellular carcinomaHNPCCLynch syndromemicrosatellite instabilitypromoter methylation

Identifiers

PMID19568590
PMCPMC2703751
OpenAlexW2121641866

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.