Evidence map›Paper›PMID 26186558›Full record

ReviewBlood cancer journal2015

Targeting the Pim kinases in multiple myeloma.

N A Keane, M Reidy, A Natoni, M S Raab, M O'Dwyer

Open access · goldAbstract readReview
In one paragraph

Review in Blood cancer journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The role of Pim-1 kinases in inflammatory signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. Article
  9. Article
  10. Review
  11. Pim Kinases: Important Regulators of Cardiovascular Disease.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Effects of PIM3 in prognosis of colon cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  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

5 authors at 1 institution in 1 country.

N A KeaneApoptosis Research Centre, National University of Ireland Galway and Department of Haematology, Galway University Hospital, Galway, Ireland.
M ReidyApoptosis Research Centre, National University of Ireland Galway, Galway, Ireland.
A NatoniApoptosis Research Centre, National University of Ireland Galway, Galway, Ireland.
M S RaabMax-Eder Unit "Experimental Therapies for Hematologic Malignancies", Department of Medicine V, Heidelberg University Medical Center, Im Neuenheimer Feld 410 and German Cancer Research Centre (DKFZ), Heidelberg, Germany.
M O'DwyerApoptosis Research Centre, National University of Ireland Galway and Department of Haematology, Galway University Hospital, Galway, Ireland.
Ollscoil na Gaillimhe – University of Galway · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a plasma cell malignancy that remains incurable. Novel treatment strategies to improve survival are urgently required. The Pims are a small family of serine/threonine kinases with increased expression across the hematological malignancies. Pim-2 shows highest expression in MM and constitutes a promising therapeutic target. It is upregulated by the bone marrow microenvironment to mediate proliferation and promote MM survival. Pim-2 also has a key role in the bone destruction typically seen in MM. Additional putative roles of the Pim kinases in MM include trafficking of malignant cells, promoting oncogenic signaling in the hypoxic bone marrow microenvironment and mediating resistance to therapy. A number of Pim inhibitors are now under development with lead compounds entering the clinic. The ATP-competitive Pim inhibitor LGH447 has recently been reported to have single agent activity in MM. It is anticipated that Pim inhibition will be of clinical benefit in combination with standard treatments and/or with novel drugs targeting other survival pathways in MM.

Indexed as

AnimalsAntineoplastic AgentsCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyMultiple MyelomaProtein Kinase InhibitorsProto-Oncogene Proteins c-pim-1Signal TransductionUp-RegulationAntineoplastic AgentsProtein Kinase InhibitorsProto-Oncogene Proteins c-pim-1proto-oncogene proteins pim

Identifiers

PMID26186558
PMCPMC4526774
OpenAlexW1604058700

What OpenQuestion 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 OpenQuestion graph.