Evidence map›Paper›PMID 29971044›Full record

ReviewFrontiers in endocrinology2018

The Role of Semaphorin 4D in Bone Remodeling and Cancer Metastasis.

Konstantinos Lontos, Juraj Adamik, Anastasia Tsagianni, Deborah L Galson, John M Chirgwin, Attaya Suvannasankha

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  9. Extracellular derivatives for bone metabolism.Journal of advanced research · 2024
    Review
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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 5 institutions in 1 country.

Konstantinos LontosHematology-Oncology Division, Department of Medicine, UPMC Hillman Cancer Center, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
Juraj AdamikHematology-Oncology Division, Department of Medicine, UPMC Hillman Cancer Center, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
Anastasia TsagianniDepartment of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, United States.
Deborah L GalsonHematology-Oncology Division, Department of Medicine, UPMC Hillman Cancer Center, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, United States.
John M ChirgwinHematology and Oncology Division, Department of Medicine, Indiana University School of Medicine, Richard L. Roudebush VA Medical Center, Indianapolis, IN, United States.
Attaya SuvannasankhaHematology and Oncology Division, Department of Medicine, Indiana University School of Medicine, Richard L. Roudebush VA Medical Center, Indianapolis, IN, United States.
University of Pittsburgh · USIndiana University School of MedicineMcGowan Institute for Regenerative Medicine · USRichard L. Roudebush VA Medical Center · USUniversity of Pittsburgh Medical Center · US

Funding

GFI-1 and Osteoblast Suppression in Multiple MyelomaR01AR059679 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GALSON, DEBORAH LYNN, ROODMAN, GARSON DAVID · 2010 to 2014
$1.4M
Role of Osteocytes in Myeloma Bone DiseaseI01CX000977 · VA · RLR VA MEDICAL CENTER · PI CHIRGWIN, JOHN M, SUVANNASANKHA, ATTAYA · 2014 to 2017
–
BLRD VA I01 BX004514CSRD VA I01 CX000977NIAMS NIH HHS R01 AR059679
6 · The paper itself

Abstract

Semaphorin 4D (Sema4D; CD100) is a transmembrane homodimer 150-kDa glycoprotein member of the Semaphorin family. Semaphorins were first identified as chemorepellants that guide neural axon growth. Sema4D also possesses immune regulatory activity. Recent data suggest other Sema4D functions: inactivation of platelets, stimulation of angiogenesis, and regulation of bone formation. Sema4D is a coupling factor expressed on osteoclasts that inhibits osteoblast differentiation. Blocking Sema4D may, therefore, be anabolic for bone. Sema4D and its receptor Plexin-B1 are commonly dysregulated in cancers, suggesting roles in cancer progression, invasion, tumor angiogenesis, and skeletal metastasis. This review focuses on Sema4D in bone and cancer biology and the molecular pathways involved, particularly Sema4D-Plexin-B1 signaling crosstalk between cancer cells and the bone marrow microenvironment-pertinent areas since a humanized Sema4D-neutralizing antibody is now in early phase clinical trials in cancers and neurological disorders.

Indexed as

cancerosteoblastsosteoclastsplexinPlexin-B1Sema4Dsemaphorin 4D

Identifiers

PMID29971044
PMCPMC6018527
OpenAlexW2807064947

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.