Evidence map›Paper›PMID 17570678›Full record

ReviewPharmacological research2007

Protein kinase C iota: human oncogene, prognostic marker and therapeutic target.

Alan P Fields, Roderick P Regala

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacological research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Protein Kinase C as a Therapeutic Target in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
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  19. Article
  20. FXR1 is elevated in colorectal cancer and acts as an oncogene.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article

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

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

2 authors at 1 institution in 1 country.

Alan P FieldsDepartment of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL 32224, USA. fields.alan@mayo.edu
Roderick P Regala
Mayo Clinic in Florida · US

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
NCI NIH HHS R01 CA081436
6 · The paper itself

Abstract

The protein kinase C (PKC) family of serine/threonine kinases has been the subject of intensive study in the field of cancer since their initial discovery as major cellular receptors for the tumor promoting phorbol esters nearly 30 years ago. However, despite these efforts, the search for a direct genetic link between members of the PKC family and human cancer has yielded only circumstantial evidence that any PKC isozyme is a true cancer gene. This situation changed in the past year with the discovery that atypical protein kinase C iota (PKC iota) is a bonafide human oncogene. PKC iota is required for the transformed growth of human cancer cells and the PKC iota gene is the target of tumor-specific gene amplification in multiple forms of human cancer. PKC iota participates in multiple aspects of the transformed phenotype of human cancer cells including transformed growth, invasion and survival. Herein, we review pertinent aspects of atypical PKC structure, function and regulation that relate to the role of these enzymes in oncogenesis. We discuss the evidence that PKC iota is a human oncogene, review mechanisms controlling PKC iota expression in human cancers, and describe the molecular details of PKC iota-mediated oncogenic signaling. We conclude with a discussion of how oncogenic PKC iota signaling has been successfully targeted to identify a novel, mechanism-based therapeutic drug currently entering clinical trials for treatment of human lung cancer. Throughout, we identify key unanswered questions and exciting future avenues of investigation regarding this important oncogenic molecule.

Indexed as

OncogenesAnimalsBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Transformation, NeoplasticFemaleGene AmplificationGold Sodium ThiomalateHumansIsoenzymesLung NeoplasmsOvarian NeoplasmsProtein Kinase CProtein Kinase C-lambdaProtein Kinase C zetaProtein Structure, TertiaryBiomarkers, TumorGold Sodium ThiomalateIsoenzymesProtein Kinase CProtein Kinase C-lambdaProtein Kinase C zeta

Identifiers

PMID17570678
PMCPMC2705893
OpenAlexW1972758313

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.