Evidence map›Paper›PMID 18758463›Full record

ArticleNature genetics2008

Kras regulatory elements and exon 4A determine mutation specificity in lung cancer.

Minh D To, Christine E Wong, Anthony N Karnezis, Reyno Del Rosario, Roberto Di Lauro, Allan Balmain

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.2field-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

70 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Review
  3. Differential functions of the KRAS splice variants.Biochemical Society transactions · 2023
    Review
  4. Article
  5. Article
  6. The role of KRAS splice variants in cancer biology.Frontiers in cell and developmental biology · 2022
    Review
  7. A role for club cells in smoking-associated lung adenocarcinoma.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  8. Review
  9. Article
  10. RAS interaction with Sin1 is dispensable for mTORC2 assembly and activity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Article
  12. Review
  13. KRAS4A induces metastatic lung adenocarcinomas in vivo in the absence of the KRAS4B isoform.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Article
  15. Review
  16. K-RAS4A: Lead or Supporting Role in Cancer Biology?Frontiers in molecular biosciences · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Minh D ToUniversity of California San Francisco, Helen Diller Family Comprehensive Cancer Center, Cancer Research Institute, San Francisco, California 94115, USA.
Christine E Wong
Anthony N Karnezis
Reyno Del Rosario
Roberto Di Lauro
Allan Balmain
Cancer Research Institute · USUCSF Helen Diller Family Comprehensive Cancer Center · USBiogem · ITUniversity of California, San Francisco · US

Funding

Identification of epithelial tumor susceptiility genesU01CA084244 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 1999 to 2013
$13.3M
The role of the Kras4A isoform in epithelial carcinogenesisR01CA111834 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 2006 to 2016
$2.6M
NCI NIH HHS CA084244NCI NIH HHS CA111834NCI NIH HHS R01 CA111834NCI NIH HHS U01 CA084244
6 · The paper itself

Abstract

Kras is the most frequently mutated ras family member in lung carcinomas, whereas Hras mutations are common in tumors from stratified epithelia such as the skin. Using a Hras knock-in mouse model, we demonstrate that specificity for Kras mutations in lung and Hras mutations in skin tumors is determined by local regulatory elements in the target ras genes. Although the Kras 4A isoform is dispensable for mouse development, it is the most important isoform for lung carcinogenesis in vivo and for the inhibitory effect of wild-type (WT) Kras on the mutant allele. Kras 4A expression is detected in a subpopulation of normal lung epithelial cells, but at very low levels in lung tumors, suggesting that it may not be required for tumor progression. The two Kras isoforms undergo different post-translational modifications; therefore, these findings can have implications for the design of therapeutic strategies for inhibiting oncogenic Kras activity in human cancers.

Indexed as

AnimalsCarcinogensDisease Models, AnimalExonsGenes, rasHumansLungLung NeoplasmsMiceMice, TransgenicMutationProto-Oncogene Proteins p21(ras)Regulatory Sequences, Nucleic AcidSkin NeoplasmsUrethaneCarcinogensHras protein, mouseProto-Oncogene Proteins p21(ras)Urethane

Identifiers

PMID18758463
PMCPMC2654781
OpenAlexW2035394593

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.