Evidence map›Paper›PMID 32296034›Full record

ReviewSignal transduction and targeted therapy2020

PIM kinase inhibition: co-targeted therapeutic approaches in prostate cancer.

Sabina Luszczak, Christopher Kumar, Vignesh Krishna Sathyadevan, Benjamin S Simpson, Kathy A Gately, Hayley C Whitaker, Susan Heavey

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
  2. Review
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  9. Review
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  11. From Hypoxia to Bone: Reprogramming the Prostate Cancer Metastatic Cascade.International journal of molecular sciences · 2025
    Review
  12. Article
  13. 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
  14. Article
  15. Article
  16. Article
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  18. PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024
    Review
  19. Review
  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

7 authors at 3 institutions in 2 countries.

Sabina LuszczakMolecular Diagnostics and Therapeutics Group, University College London, London, UK.
Christopher KumarMolecular Diagnostics and Therapeutics Group, University College London, London, UK.
Vignesh Krishna SathyadevanMolecular Diagnostics and Therapeutics Group, University College London, London, UK.
Benjamin S SimpsonMolecular Diagnostics and Therapeutics Group, University College London, London, UK.ORCID http://orcid.org/0000-0003-3685-6110
Kathy A GatelyTrinity Translational Medicine Institute, St. James's Hospital Dublin, Dublin 8, Dublin, Ireland.
Hayley C WhitakerMolecular Diagnostics and Therapeutics Group, University College London, London, UK.
Susan HeaveyMolecular Diagnostics and Therapeutics Group, University College London, London, UK. s.heavey@ucl.ac.uk.ORCID http://orcid.org/0000-0002-2974-4578
University College London · GBKing's College London · GBSt. James's Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PIM kinases have been shown to play a role in prostate cancer development and progression, as well as in some of the hallmarks of cancer, especially proliferation and apoptosis. Their upregulation in prostate cancer has been correlated with decreased patient overall survival and therapy resistance. Initial efforts to inhibit PIM with monotherapies have been hampered by compensatory upregulation of other pathways and drug toxicity, and as such, it has been suggested that co-targeting PIM with other treatment approaches may permit lower doses and be a more viable option in the clinic. Here, we present the rationale and basis for co-targeting PIM with inhibitors of PI3K/mTOR/AKT, JAK/STAT, MYC, stemness, and RNA Polymerase I transcription, along with other therapies, including androgen deprivation, radiotherapy, chemotherapy, and immunotherapy. Such combined approaches could potentially be used as neoadjuvant therapies, limiting the development of resistance to treatments or sensitizing cells to other therapeutics. To determine which drugs should be combined with PIM inhibitors for each patient, it will be key to develop companion diagnostics that predict response to each co-targeted option, hopefully providing a personalized medicine pathway for subsets of prostate cancer patients in the future.

Indexed as

Molecular Targeted TherapyApoptosisDrug Resistance, NeoplasmHumansMalePhosphatidylinositol 3-KinasesProstatic NeoplasmsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-pim-1TOR Serine-Threonine KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-pim-1proto-oncogene proteins pimTOR Serine-Threonine Kinases

Identifiers

PMID32296034
PMCPMC6992635
OpenAlexW3003589303

What Socratic holds

Textmetadata
LicenceCC BY
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.