Evidence map›Paper›PMID 24286018›Full record

ArticleForum on immunopathological diseases and therapeutics2011

Unique Pattern of Overexpression of Raf-1 Kinase Inhibitory Protein in Its Inactivated Phosphorylated Form in Human Multiple Myeloma.

Stavroula Baritaki, Sara Huerta-Yepez, Ma da Lourdas Cabrava-Haimandez, Marialuisa Sensi, Silvana Canevari, Massimo Libra, Manuel Penichet, Haiming Chen, James R Berenson, Benjamin Bonavida

Abstract read
In one paragraph

Article in Forum on immunopathological diseases and therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact, top 90% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026
    Review
  2. Article
  3. Cancer resistance via the downregulation of the tumor suppressorsExploration of targeted anti-tumor therapy · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. RAF Kinase Inhibitor Protein in Myeloid Leukemogenesis.International journal of molecular sciences · 2019
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. 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

10 authors at 6 institutions in 3 countries.

Stavroula BaritakiDepartment of Microbiology, Immunology and Molecular Genetics, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA.
Sara Huerta-Yepez
Ma da Lourdas Cabrava-Haimandez
Marialuisa Sensi
Silvana Canevari
Massimo Libra
Manuel Penichet
Haiming Chen
James R Berenson
Benjamin Bonavida
Fondazione IRCCS Istituto Nazionale dei Tumori · ITHospital Infantil de México Federico Gómez · MXInstitute for Myeloma & Bone Cancer Research · USUniversity of California, Los Angeles · USUCLA Jonsson Comprehensive Cancer CenterUniversity of Catania · IT

Funding

Anti-TfR IgG3-Av: A New Drug Against Multiple MyelomaR01CA107023 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PENICHET, MANUEL L · 2005 to 2009
$1.7M
NCI NIH HHS R01 CA107023
6 · The paper itself

Abstract

Multiple myeloma (MM) is the second most common hematological and incurable malignancy of plasma cells with low proliferative activity in the bone marrow. MM patients initially respond to conventional therapy, however, many develop resistance and recurrences occur. We have identified RKIP as a novel gene product that is differentially overexpressed in MM cell lines and MM tissues compared to other studied tumors and normal bone marrow. This overexpression consisted, in large part, of a phosphorylated inactive form of RKIP at Ser153 (p-Ser153 RKIP). In contrast to RKIP, p-Ser153 RKIP lacks its ability to inhibit the MAPK signaling pathway. The overexpression of p-Ser153 RKIP in MM cell lines and MM tissues was further validated in a mouse model carrying a human MM xenograft, namely, LAGλ-1B. Bioinformatic analyses from databases support the presence of increased RKIP mRNA expression in MM compared to normal plasma cells. In these databases, high RKIP levels in MM are also correlated with the nonhyperdiploid status and the presence of IgH translocations, parameters that generally display more aggressive clinical features and shorter patients' survival irrespective of the treatment. Since RKIP expression regulates both the NF-κB and MAPK survival pathways, the overexpression of "inactive" p-Ser153 RKIP in MM might contribute positively to the overall cell survival/antiapoptotic phenotype and drug resistance of MM through the constitutive activation of survival pathways and downstream the transcription of anti-apoptotic gene products. The overexpression of RKIP and p-Ser153 RKIP in MM is the first demonstration in the literature, since in most tumor tissues the expression of RKIP is very low and the expression of p-Ser153 RKIP is much lower. The relationship between the levels of active RKIP and inactive p-Ser153 RKIP in MM may be of prognostic significance, and the regulation of RKIP activity may be a target for therapeutic intervention.

Indexed as

apoptosismultiple myelomaNF-κBRaf-1 kinase inhibitor protein (RKIP)

Identifiers

PMID24286018
PMCPMC3839863
OpenAlexW2048537216

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.