Evidence map›Paper›PMID 30940634›Full record

ArticleBlood advances2019

Citron Rho-interacting kinase silencing causes cytokinesis failure and reduces tumor growth in multiple myeloma.

Ilyas Sahin, Yawara Kawano, Romanos Sklavenitis-Pistofidis, Michele Moschetta, Yuji Mishima, Salomon Manier, Antonio Sacco, Ruben Carrasco, Rafael Fonseca, Aldo M Roccaro and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 28% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  17. Targeting cytoskeletal phosphorylation in cancer.Exploration of targeted anti-tumor therapy · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 3 countries.

Ilyas SahinDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Yawara KawanoDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Romanos Sklavenitis-PistofidisDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Michele MoschettaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Yuji MishimaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Salomon ManierDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Antonio SaccoDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Ruben CarrascoDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Rafael FonsecaDivision of Hematology, Mayo Clinic, Scottsdale, AZ; and.
Aldo M RoccaroDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.ORCID 0000-0002-1872-5128
Thomas WitzigDivision of Hematology, Mayo Clinic, Rochester, MN.ORCID 0000-0002-4215-6500
Irene M GhobrialDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Harvard University · USMayo Clinic in Arizona · US

Funding

Project 4: Targeting Resistance to T-Cell Directed Therapy in Multiple MyelomaP50CA186781 · NCI · MAYO CLINIC ARIZONA · PI Rafael Fonseca · 2015 to 2026
$25.5M
Stroma-mediated clonal evolution in Multiple MyelomaR01CA181683 · NCI · DANA-FARBER CANCER INST · PI GHOBRIAL, IRENE M. · 2014 to 2018
$1.8M
NCI NIH HHS P50 CA186781NCI NIH HHS R01 CA181683
6 · The paper itself

Abstract

Citron Rho-interacting serine/threonine kinase (CIT) is a serine/threonine kinase that acts as a key component of the midbody and is essential for cytokinesis. CIT has been reported to be highly expressed in some tumor tissues and to play a role in cancer proliferation; however, the significance of CIT has not been investigated in multiple myeloma (MM). Here, we identified, by protein microarray and immunohistochemistry, that CIT is 1 of the upregulated proteins in the plasma cells of MM patients compared with healthy controls. Analysis of a gene expression profile data set showed that MM patients with high CIT gene expression had significantly worse overall survival compared with MM patients with low CIT gene expression. CIT silencing in MM cell lines induced cytokinesis failure and resulted in decreased MM cell proliferation in vitro and in vivo.

Indexed as

CytokinesisCase-Control StudiesCell Line, TumorCell ProliferationHumansIntracellular Signaling Peptides and ProteinsMultiple MyelomaPlasma CellsProtein Serine-Threonine KinasesSurvival AnalysisTranscriptomeTumor Cells, CulturedTumor Suppressor Protein p53citron-kinaseIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30940634
PMCPMC6457230
OpenAlexW2926977582

What OpenQuestion holds

Textmetadata
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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.