Evidence map›Paper›PMID 19738040›Full record

ArticleCancer research2009

Atypical protein kinase C{iota} is required for bronchioalveolar stem cell expansion and lung tumorigenesis.

Roderick P Regala, Rebecca K Davis, Alyssa Kunz, Andras Khoor, Michael Leitges, Alan P Fields

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Cancers · 2022
    Article
  8. PRKCI Mediates RadiosensitivityFrontiers in oncology · 2022
    Article
  9. Protein kinase CCell reports · 2021
    Article
  10. Article
  11. Article
  12. Review
  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

6 authors at 2 institutions in 2 countries.

Roderick P RegalaDepartments of Cancer Biology and Pathology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, Florida, USA.
Rebecca K Davis
Alyssa Kunz
Andras Khoor
Michael Leitges
Alan P Fields
Sylvester Comprehensive Cancer Center · USUniversity of Oslo · NO

Funding

Three-Dimensional Organoid Cultures to Investigate 3q26 Driver Functions in Multiple Lung Cancer Cells of OriginR01CA081436 · NCI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI FIELDS, ALAN P. · 1999 to 2022
$9.9M
PKC iota is an oncogene in non-small cell lung cancerF32CA115160 · NCI · MAYO CLINIC JACKSONVILLE · PI REGALA, RODERICK PAUL · 2006 to 2008
$156k
NCI NIH HHS CA084136-12NCI NIH HHS CA115160NCI NIH HHS F32 CA115160NCI NIH HHS R01 CA081436
6 · The paper itself

Abstract

Protein kinase Ciota (PKCiota) is an oncogene required for maintenance of the transformed phenotype of non-small cell lung cancer cells. However, the role of PKCiota in lung tumor development has not been investigated. To address this question, we established a mouse model in which oncogenic Kras(G12D) is activated by Cre-mediated recombination in the lung with or without simultaneous genetic loss of the mouse PKCiota gene, Prkci. Genetic loss of Prkci dramatically inhibits Kras-initiated hyperplasia and subsequent lung tumor formation in vivo. This effect correlates with a defect in the ability of Prkci-deficient bronchioalveolar stem cells to undergo Kras-mediated expansion and morphologic transformation in vitro and in vivo. Furthermore, the small molecule PKCiota inhibitor aurothiomalate inhibits Kras-mediated bronchioalveolar stem cell expansion and lung tumor growth in vivo. Thus, Prkci is required for oncogene-induced expansion and transformation of tumor-initiating lung stem cells. Furthermore, aurothiomalate is an effective antitumor agent that targets the tumor-initiating stem cell niche in vivo. These data have important implications for PKCiota as a therapeutic target and for the clinical use of aurothiomalate for lung cancer treatment.

Indexed as

AnimalsBronchiolesCarcinoma, Non-Small-Cell LungCell Transformation, NeoplasticGenes, rasGold Sodium ThiomalateHumansIsoenzymesLung NeoplasmsMaleMiceMice, TransgenicProtein Kinase CProtein Kinase C-lambdaPulmonary AlveoliStem CellsGold Sodium ThiomalateIsoenzymesProtein Kinase CProtein Kinase C-lambda

Identifiers

PMID19738040
PMCPMC2756303
OpenAlexW2165068298

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.