Evidence map›Paper›PMID 19147983›Full record

ArticleThe Journal of clinical investigation2009

PIM-1-specific mAb suppresses human and mouse tumor growth by decreasing PIM-1 levels, reducing Akt phosphorylation, and activating apoptosis.

Xiu Feng Hu, Jie Li, Scott Vandervalk, Zeping Wang, Nancy S Magnuson, Pei Xiang Xing

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.9field-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

60 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Imparting aromaticity to 2-pyridone derivatives byJournal of enzyme inhibition and medicinal chemistry · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Pim1 promotes IFN-β production by interacting with IRF3.Experimental & molecular medicine · 2022
    Article
  10. Synthesis of 2-Oxoquinoline Derivatives as Dual Pim and mTORC Protein Kinase Inhibitors.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. The role of Pim kinase in immunomodulation.American journal of cancer research · 2020
    Review
  18. Article
  19. Article
  20. PIM Kinase as an Executional Target in Cancer.Journal of cancer prevention · 2018
    Review
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

6 authors at 3 institutions in 3 countries.

Xiu Feng HuCancer Immunotherapy Laboratory, Burnet Institute Incorporating Austin Research Institute, Heidelberg, Victoria, Australia.
Jie Li
Scott Vandervalk
Zeping Wang
Nancy S Magnuson
Pei Xiang Xing
Burnet Institute · AUWashington State University · USQilu Hospital of Shandong University · CN

Funding

Contribution of Pim-1 kinase to cell surivalR01CA104470 · NCI · WASHINGTON STATE UNIVERSITY · PI MAGNUSON, NANCY S · 2003 to 2007
$1.2M
NCI NIH HHS R01 CA104470
6 · The paper itself

Abstract

Provirus integration site for Moloney murine leukemia virus (PIM1) is a proto-oncogene that encodes a serine/threonine kinase with multiple cellular functions. Overexpression of PIM-1 plays a critical role in progression of prostatic and hematopoietic malignancies. Here we describe the generation of a mAb specific for GST-PIM-1, which reacted strongly with most human and mouse cancer tissues and cell lines of prostate, breast, and colon origin but only weakly (if at all) with normal tissues. The mAb binds to PIM-1 in the cytosol and nucleus as well as to PIM-1 on the surface of human and murine cancer cells. Treatment of human and mouse prostate cancer cell lines with the PIM-1-specific mAb resulted in disruption of PIM-1/Hsp90 complexes, decreased PIM-1 and Hsp90 levels, reduced Akt phosphorylation at Ser473, reduced phosphorylation of Bad at Ser112 and Ser136, and increased cleavage of caspase-9, an indicator of activation of the mitochondrial cell death pathway. The mAb induced cancer cell apoptosis and synergistically enhanced antitumor activity when used in combination with cisplatin and epirubicin. In tumor models, the PIM-1-specific mAb substantially inhibited growth of the human prostate cancer cell line DU145 in SCID mice and the mouse prostate cancer cell TRAMP-C1 in C57BL/6 mice. These findings are important because they provide what we believe to be the first in vivo evidence that treatment of prostate cancer may be possible by targeting PIM-1 using an Ab-based therapy.

Indexed as

ApoptosisAnimalsAntibodies, Monoclonalbcl-Associated Death ProteinCell Line, TumorDrug Resistance, NeoplasmFemaleFlow CytometryHSP90 Heat-Shock ProteinsHumansMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, SCIDNeoplasmsAntibodies, Monoclonalbcl-Associated Death ProteinHSP90 Heat-Shock ProteinsMAS1 protein, humanPhosphatidylinositol 3-KinasesPIM1 protein, humanPim1 protein, mouseProto-Oncogene MasProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-pim-1RNA, Small Interfering

Identifiers

PMID19147983
PMCPMC2631288
OpenAlexW2110620323

What OpenQuestion 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 OpenQuestion graph.