Evidence map›Paper›PMID 26190113›Full record

ArticleCell reports2015

CXCR4 Regulates Extra-Medullary Myeloma through Epithelial-Mesenchymal-Transition-like Transcriptional Activation.

Aldo M Roccaro, Yuji Mishima, Antonio Sacco, Michele Moschetta, Yu-Tzu Tai, Jiantao Shi, Yong Zhang, Michaela R Reagan, Daisy Huynh, Yawara Kawano and 12 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
9.1field-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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
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  8. Anti-myeloma activity of the CXCR4 antagonist WZ811.Journal of molecular medicine (Berlin, Germany) · 2026
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29 more citing papers are in PubMed but not listed here.

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

22 authors at 4 institutions in 3 countries.

Aldo M RoccaroDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Yuji MishimaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan.
Antonio SaccoDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Michele MoschettaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Yu-Tzu TaiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Jiantao ShiDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02215, USA.
Yong ZhangDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Michaela R ReaganDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Maine Medical Center Research Institute (MMCRI), Scarborough, ME 04074, USA.
Daisy HuynhDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Yawara KawanoDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Ilyas SahinDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Marco ChiariniDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Spedali Civili di Brescia, Centro per la Ricerca Onco-ematologica AIL (CREA), 25123 Brescia, Italy.
Salomon ManierDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Michele CeaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Yosra AljawaiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Siobhan GlaveyDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Elizabeth MorganDepartment of Pathology, Brigham & Women's Hospital, Boston, MA 02215, USA.
Chin PanBristol-Myers Squibb, Redwood City, CA 94063, USA.
Franziska MichorDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02215, USA.
Pina CardarelliBristol-Myers Squibb, Redwood City, CA 94063, USA.
Michelle KuhneBristol-Myers Squibb, Redwood City, CA 94063, USA.
Irene M GhobrialDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Electronic address: irene_ghobrial@dfci.harvard.edu.
Dana-Farber Cancer Institute · USHarvard University · USBristol-Myers Squibb (United States) · USBrigham and Women's Hospital · US

Funding

The Cell-Of-Origin of Human CancersU54CA143798 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI MICHOR, FRANZISKA · 2009 to 2014
$11.2M
Stroma-mediated clonal evolution in Multiple MyelomaR01CA181683 · NCI · DANA-FARBER CANCER INST · PI GHOBRIAL, IRENE M. · 2014 to 2018
$1.8M
NCI NIH HHS R01 CA181683NCI NIH HHS R01CA181683NCI NIH HHS U54 CA143798NCI NIH HHS U54CA143798
6 · The paper itself

Abstract

Extra-medullary disease (EMD) in multiple myeloma (MM) is associated with poor prognosis and resistance to chemotherapy. However, molecular alterations that lead to EMD have not been well defined. We developed bone marrow (BM)- and EMD-prone MM syngeneic cell lines; identified that epithelial-to-mesenchymal transition (EMT) transcriptional patterns were significantly enriched in both clones compared to parental cells, together with higher levels of CXCR4 protein; and demonstrated that CXCR4 enhanced the acquisition of an EMT-like phenotype in MM cells with a phenotypic conversion for invasion, leading to higher bone metastasis and EMD dissemination in vivo. In contrast, CXCR4 silencing led to inhibited tumor growth and reduced survival. Ulocuplumab, a monoclonal anti-CXCR4 antibody, inhibited MM cell dissemination, supported by suppression of the CXCR4-driven EMT-like phenotype. These results suggest that targeting CXCR4 may act as a regulator of EMD through EMT-like transcriptional modulation, thus representing a potential therapeutic strategy to prevent MM disease progression.

Indexed as

Epithelial-Mesenchymal TransitionTranscriptional ActivationAnimalsAntibodies, MonoclonalBone NeoplasmsCells, CulturedHumansMiceMice, SCIDReceptors, CXCR4Sarcoma, MyeloidAntibodies, MonoclonalReceptors, CXCR4

Identifiers

PMID26190113
PMCPMC4961259
OpenAlexW1579890940

What OpenQuestion holds

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Registered trials

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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.