Evidence map›Paper›PMID 25604078›Full record

ReviewExpert review of anticancer therapy2015

Targeting protein kinase C subtypes in pancreatic cancer.

Peter Storz

Open access · greenAbstract readReview
In one paragraph

Review in Expert review of anticancer therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  4. Review
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  9. Review
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  14. Flow signaling and atherosclerosis.Cellular and molecular life sciences : CMLS · 2017
    Review
  15. Article
  16. 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

1 author at 1 institution in 1 country.

Peter StorzDepartment of Cancer Biology, Mayo Clinic, Griffin Building, Room 306, 4500 San Pablo Road, Jacksonville, FL 32224, USA.
Mayo Clinic in Florida · US

Funding

Protein Kinase D in oncogenic oxidative stress signalingR01CA140182 · NCI · MAYO CLINIC JACKSONVILLE · PI STORZ, PETER · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA140182NCI NIH HHS R01-CA140182
6 · The paper itself

Abstract

In preclinical studies, protein kinase C (PKC) enzymes have been implicated in regulating many aspects of pancreatic cancer development and progression. However, clinical Phase I or Phase II trials with compounds targeting classical PKC isoforms were not successful. Recent studies implicate that mainly atypical and novel PKC enzymes regulate oncogenic signaling pathways in pancreatic cancer. Members of these two subgroups converge signaling induced by mutant Kras, growth factors and inflammatory cytokines. Different approaches for the development of inhibitors for atypical PKC and novel PKC have been described; and new compounds include allosteric inhibitors and inhibitors that block ATP binding.

Indexed as

Adenosine TriphosphateAnimalsAntineoplastic AgentsDrug DesignHumansIsoenzymesPancreatic NeoplasmsProtein Kinase CProtein Kinase InhibitorsSignal TransductionAdenosine TriphosphateAntineoplastic AgentsIsoenzymesProtein Kinase CProtein Kinase Inhibitorsinhibitorpancreatic cancerprotein kinase Ctherapy

Identifiers

PMID25604078
PMCPMC4577234
OpenAlexW2114974183

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.