Evidence map›Paper›PMID 21035469›Full record

ArticleMutation research2011

Genetic variation in RPS6KA1, RPS6KA2, RPS6KB1, RPS6KB2, and PDK1 and risk of colon or rectal cancer.

Martha L Slattery, Abbie Lundgreen, Jennifer S Herrick, Roger K Wolff

Abstract read
In one paragraph

Article in Mutation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Genome-Wide Association Study of Immune Indices in Yaks.Animals : an open access journal from MDPI · 2025
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  5. Influence of CCancers · 2023
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  7. Review
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  9. MicroRNA-486-5p Suppresses Lung CancerFrontiers in oncology · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Martha L SlatteryDepartment of Medicine, University of Utah, Salt Lake City, UT 84108, USA. marty.slattery@hss.utah.edu
Abbie Lundgreen
Jennifer S Herrick
Roger K Wolff
University of Utah · US

Funding

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
SURVEILLANCE EPIDEMIOLOGY &END RESULTS PROGRAMN01PC067000 · PC · UNIVERSITY OF UTAH · PI WIGGINS, CHARLES L · 1996 to 2000
$1.3M
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 CA61757NCI NIH HHS N01-PC-67000NCI NIH HHS R01 CA048998NCI NIH HHS R01 CA061757NCI NIH HHS U01 CA048998
6 · The paper itself

Abstract

RPS6KA1, RPS6KA2, RPS6KB1, RPS6KB2, and PDK1 are involved in several pathways central to the carcinogenic process, including regulation of cell growth, insulin, and inflammation. We evaluated genetic variation in their candidate genes to obtain a better understanding of their association with colon and rectal cancer. We used data from two population-based case-control studies of colon (n=1574 cases, 1940 controls) and rectal (n=791 cases, 999 controls) cancer. We observed genetic variation in RPS6KA1, RPS6KA2, and PRS6KB2 were associated with risk of developing colon cancer while only genetic variation in RPS6KA2 was associated with altering risk of rectal cancer. These genes also interacted significantly with other genes operating in similar mechanisms, including Akt1, FRAP1, NFκB1, and PIK3CA. Assessment of tumor markers indicated that these genes and this pathway may importantly contributed to CIMP+ tumors and tumors with KRAS2 mutations. Our findings implicate these candidate genes in the etiology of colon and rectal cancer and provide information on how these genes operate with other genes in the pathway. Our data further suggest that this pathway may lead to CIMP+ and KRAS2-mutated tumors.

Indexed as

Polymorphism, Single NucleotideAdultAgedCase-Control StudiesColonic NeoplasmsEpistasis, GeneticFemaleGene FrequencyGenetic Predisposition to DiseaseGenetic VariationGenotypeHumansMaleMiddle AgedProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktAKT1 protein, humanPDK1 protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring Kinaseribosomal protein S6 kinase, 70kD, polypeptide 1ribosomal protein S6 kinase, 70kD, polypeptide 2ribosomal protein S6 kinase, 90kDa, polypeptide 3Ribosomal Protein S6 Kinases, 70-kDaRibosomal Protein S6 Kinases, 90-kDaRPS6KA1 protein, human

Identifiers

PMID21035469
PMCPMC3038588
OpenAlexW1970883381

What OpenQuestion holds

Textmetadata
LicenceTDM
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.