Evidence map›Paper›PMID 25749412›Full record

ReviewPharmacology & therapeutics2015

PIM kinase (and Akt) biology and signaling in tumors.

Noel A Warfel, Andrew S Kraft

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
12.4field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Review
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  14. PIM kinase inhibition counters resistance to radiotherapy and chemotherapy in human prostate cancer.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. The role of Pim-1 kinases in inflammatory signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article

53 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 2 institutions in 1 country.

Noel A WarfelDepartment of Cellular and Molecular Medicine, Tucson, AZ 85724, United States; University of Arizona Cancer Center, Tucson, AZ 85724, United States. Electronic address: warfelna@email.arizona.edu.
Andrew S KraftDepartment of Medicine, Tucson, AZ 85724, United States; University of Arizona Cancer Center, Tucson, AZ 85724, United States. Electronic address: Akraft@uacc.arizona.edu.
University of Arizona · USUniversity of Arizona Cancer Center

Funding

Targeting the Pim 1 Protein Kinase to Overcome Resistance to AKT InhibitorsR01CA173200 · NCI · UNIVERSITY OF ARIZONA · PI KRAFT, ANDREW S · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA173200
6 · The paper itself

Abstract

The initiation and progression of human cancer is frequently linked to the uncontrolled activation of survival kinases. Two such pro-survival kinases that are commonly amplified in cancer are PIM and Akt. These oncogenic proteins are serine/threonine kinases that regulate tumorigenesis by phosphorylating substrates that control the cell cycle, cellular metabolism, proliferation, and survival. Growing evidence suggests that cross-talk exists between the PIM and Akt kinases, indicating that they control partially overlapping survival signaling pathways that are critical to the initiation, progression, and metastatic spread of many types of cancer. The PI3K/Akt signaling pathway is activated in many human tumors, and it is well established as a promising anticancer target. Likewise, based on the role of PIM kinases in normal and tumor tissues, it is clear that this family of kinases represents an interesting target for anticancer therapy. Pharmacological inhibition of PIM has the potential to significantly influence the efficacy of standard and targeted therapies. This review focuses on the regulation of PIM kinases, their role in tumorigenesis, and the biological impact of their interaction with the Akt signaling pathway on the efficacy of cancer therapy.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell CycleCell SurvivalDrug Resistance, NeoplasmHumansNeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-pim-1Signal TransductionAntineoplastic AgentsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-pim-1proto-oncogene proteins pimAktCancerOncogenesPIM kinasesTherapeutic resistance

Identifiers

PMID25749412
PMCPMC4957637
OpenAlexW2079410007

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.