Evidence map›Paper›PMID 18767147›Full record

ArticleGenes, chromosomes & cancer2009

Oncogenetic tree model of somatic mutations and DNA methylation in colon tumors.

Carol Sweeney, Kenneth M Boucher, Wade S Samowitz, Roger K Wolff, Hans Albertsen, Karen Curtin, Bette J Caan, Martha L Slattery

Open access · bronzeAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Assessing tumor mutations to gain insight into base excision repair sequence polymorphisms and smoking in colon cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2009
    Trial
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  9. Intrinsic cancer subtypes--next steps into personalized medicine.Cellular oncology (Dordrecht, Netherlands) · 2015
    Review
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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

8 authors at 2 institutions in 1 country.

Carol SweeneyHealth Sciences Center, University of Utah, Salt Lake City, UT, USA. carol.sweeney@hsc.utah.edu
Kenneth M Boucher
Wade S Samowitz
Roger K Wolff
Hans Albertsen
Karen Curtin
Bette J Caan
Martha L Slattery
University of Utah · USKaiser Permanente · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
DIET, ACTIVITY &REPRODUCTION--RISKS FOR RECTAL CANCERR01CA048998 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA L · 1991 to 2012
$7.9M
DIET AND SOMATIC MUTATIONS IN COLON CANCERR01CA061757 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA L · 1995 to 2007
$3.8M
Growth Factors and Colon CancerR01CA085846 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA L · 2001 to 2006
$2.2M
DIET, ACTIVITY &REPRODUCTION--RISKS FOR RECTAL CANCERU01CA048998 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA OR MARTY L · 1997 to 1999
–
NCI NIH HHS CA48998NCI NIH HHS CA85846NCI NIH HHS P30 CA042014NCI NIH HHS P30CA042014NCI NIH HHS R01 CA048998NCI NIH HHS R01 CA061757NCI NIH HHS U01 CA048998
6 · The paper itself

Abstract

Our understanding of somatic alterations in colon cancer has evolved from a concept of a series of events taking place in a single sequence to a recognition of multiple pathways. An oncogenetic tree is a model intended to describe the pathways and sequence of somatic alterations in carcinogenesis without assuming that tumors will fall in mutually exclusive categories. We applied this model to data on colon tumor somatic alterations. An oncogenetic tree model was built using data on mutations of TP53, KRAS2, APC, and BRAF genes, methylation at CpG sites of MLH1 and TP16 genes, methylation in tumor (MINT) markers, and microsatellite instability (MSI) for 971 colon tumors from a population-based series. Oncogenetic tree analysis resulted in a reproducible tree with three branches. The model represents methylation of MINT markers as initiating a branch and predisposing to MSI, methylation of MHL1 and TP16, and BRAF mutation. APC mutation is the first alteration in an independent branch and is followed by TP53 mutation. KRAS2 mutation was placed a third independent branch, implying that it neither depends on, nor predisposes to, the other alterations. Individual tumors were observed to have alteration patterns representing every combination of one, two, or all three branches. The oncogenetic tree model assumptions are appropriate for the observed heterogeneity of colon tumors, and the model produces a useful visual schematic of the sequence of events in pathways of colon carcinogenesis.

Indexed as

DNA MethylationMutationAdaptor Proteins, Signal TransducingAdultAgedAlgorithmsColonic NeoplasmsCpG IslandsGenes, APCGenes, p16Genes, p53HumansMicrosatellite InstabilityMiddle AgedModels, GeneticMutL Protein Homolog 1Adaptor Proteins, Signal TransducingBRAF protein, humanKRAS protein, humanMLH1 protein, humanMutL Protein Homolog 1Nuclear ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID18767147
PMCPMC3742107
OpenAlexW2095268740

What OpenQuestion holds

Textmetadata
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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.