Evidence map›Paper›PMID 18592002›Full record

ArticleNeoplasia (New York, N.Y.)2008

RAS signaling in colorectal carcinomas through alteration of RAS, RAF, NF1, and/or RASSF1A.

Terje Ahlquist, Irene Bottillo, Stine A Danielsen, Gunn I Meling, Torleiv O Rognum, Guro E Lind, Bruno Dallapiccola, Ragnhild A Lothe

Abstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Downregulation ofInternational journal of molecular sciences · 2020
    Article
  5. Article
  6. Association between clinicopathological characteristics and RAS mutation in colorectal cancer.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Observational
  7. Article
  8. Article
  9. Review
  10. Methylation status of theOncology letters · 2016
    Article
  11. Article
  12. Observational
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. RAS signaling pathways, mutations and their role in colorectal cancer.World journal of gastrointestinal oncology · 2013
    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

8 authors.

Terje AhlquistDepartment of Cancer Prevention, Institute for Cancer Research, Norwegian Radium Hospital, Rikshospitalet University Hospital, Oslo, Norway.
Irene Bottillo
Stine A Danielsen
Gunn I Meling
Torleiv O Rognum
Guro E Lind
Bruno Dallapiccola
Ragnhild A Lothe

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

More than half of all colorectal carcinomas are known to exhibit an activated mitogen-activated protein kinase pathway. The NF1 gene, a negative regulator of KRAS, has not previously been examined in a series of colorectal cancer. In the present study, primary colorectal carcinomas stratified according to microsatellite instability status were analyzed. The whole coding region of NF1 was analyzed for mutations using denaturing high-performance liquid chromatography and sequencing, and the copy number alterations of NF1 were examined using multiple ligation-dependent probe amplification and real-time polymerase chain reaction. The mutational hot spots in KRAS and BRAF were sequenced, and promoter hypermethylation status of RASSF1A was assessed with a methylation-specific polymerase chain reaction. One sample had two missense mutations in NF1, whereas nine additional tumors had intronic mutations likely to affect exon splicing. Interestingly, 8 of these 10 tumors were microsatellite-unstable. Four other tumors showed a duplication of NF1. Mutations in KRAS and BRAF were mutually exclusive and were present at 40% and 22%, respectively. RASSF1A was hypermethylated in 31% of the samples. We show that the RAS signaling network is extensively dysregulated in colorectal carcinomas, because more than 70% of the tumors had an alteration in one or more of the four examined components.

Indexed as

Genes, Neurofibromatosis 1Genes, rasAdultAgedAged, 80 and overBase SequenceCarcinomaColorectal NeoplasmsDNA Mutational AnalysisFemaleGene Expression Regulation, NeoplasticGene Regulatory NetworksGenetic TestingHumansMaleMiddle Agedraf KinasesRASSF1 protein, humanTumor Suppressor Proteins

Identifiers

PMID18592002
PMCPMC2434205

What Socratic 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 Socratic graph.