Evidence map›Paper›PMID 27498059›Full record

ArticleHuman pathology2016

Sclerostin expression in skeletal sarcomas.

Jia Shen, Carolyn A Meyers, Swati Shrestha, Arun Singh, Greg LaChaud, Vi Nguyen, Greg Asatrian, Noah Federman, Nicholas Bernthal, Fritz C Eilber and 4 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Human pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

14 authors at 2 institutions in 1 country.

Jia ShenDivision of Growth and Development and Section of Orthodontics, School of Dentistry, University of California, Los Angeles, CA 90095; Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Carolyn A MeyersDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Swati ShresthaDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Arun SinghDivision of Hematology/Oncology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Greg LaChaudDivision of Growth and Development and Section of Orthodontics, School of Dentistry, University of California, Los Angeles, CA 90095; Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Vi NguyenDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Greg AsatrianDivision of Growth and Development and Section of Orthodontics, School of Dentistry, University of California, Los Angeles, CA 90095; Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Noah FedermanDepartment of Pediatrics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Nicholas BernthalUCLA and Orthopaedic Hospital Department of Orthopaedic Surgery and the Orthopaedic Hospital Research Center, Los Angeles, CA 90095.
Fritz C EilberDivision of Surgical Oncology, University of California, Los Angeles, CA 90095.
Sarah M DryDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Kang TingDivision of Growth and Development and Section of Orthodontics, School of Dentistry, University of California, Los Angeles, CA 90095.
Chia SooUCLA and Orthopaedic Hospital Department of Orthopaedic Surgery and the Orthopaedic Hospital Research Center, Los Angeles, CA 90095; Division of Plastic and Reconstructive Surgery, Department of Surgery, David Geffen School of Medicine, University of California, Los Angeles, CA 90095.
Aaron W JamesDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095; Division of Plastic and Reconstructive Surgery, Department of Surgery, David Geffen School of Medicine, University of California, Los Angeles, CA 90095; Department of Pathology, Johns Hopkins University, Baltimore, MD 21205. Electronic address: awjames@jhmi.ed.
University of California, Los Angeles · USOrthopaedic Hospital · US

Funding

NELL-1 isoforms for the systemic treatment of osteoporosisK08AR068316 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JAMES, AARON W · 2015 to 2019
$534k
NIAMS NIH HHS K08 AR068316
6 · The paper itself

Abstract

Sclerostin (SOST) is an extracellular Wnt signaling antagonist which negatively regulates bone mass. Despite this, the expression and function of SOST in skeletal tumors remain poorly described. Here, we first describe the immunohistochemical staining pattern of SOST across benign and malignant skeletal tumors with bone or cartilage matrix (n=68 primary tumors). Next, relative SOST expression was compared to markers of Wnt signaling activity and osteogenic differentiation across human osteosarcoma (OS) cell lines (n=7 cell lines examined). Results showed immunohistochemical detection of SOST in most bone-forming tumors (90.2%; 46/51) and all cartilage-forming tumors (100%; 17/17). Among OSs, variable intensity and distribution of SOST expression were observed, which highly correlated with the presence and degree of neoplastic bone. Patchy SOST expression was observed in cartilage-forming tumors, which did not distinguish between benign and malignant tumors or correlate with regional morphologic characteristics. Finally, SOST expression varied widely between OS cell lines, with more than 97-fold variation. Among OS cell lines, SOST expression positively correlated with the marker of osteogenic differentiation alkaline phosphatase and did not correlate well with markers of Wnt/β-catenin signaling activity. In summary, SOST is frequently expressed in skeletal bone- and cartilage-forming tumors. The strong spatial correlation with bone formation and the in vitro expression patterns are in line with the known functions of SOST in nonneoplastic bone, as a feedback inhibitor on osteogenic differentiation. With anti-SOST as a potential therapy for osteoporosis in the near future, its basic biologic and phenotypic consequences in skeletal tumors should not be overlooked.

Indexed as

Adaptor Proteins, Signal TransducingAlkaline PhosphataseBiomarkers, TumorBiopsyBone Morphogenetic ProteinsBone NeoplasmsCell DifferentiationCell Line, TumorChondromaChondrosarcomaGenetic MarkersHumansImmunohistochemistryNeoplasms, Bone TissueOsteoblastomaOsteogenesisAdaptor Proteins, Signal TransducingAlkaline PhosphataseBiomarkers, TumorBone Morphogenetic ProteinsGenetic MarkersSOST protein, humanChondrosarcomaEnchondromaOsteosarcomaSarcomaSOSTWnt signaling

Identifiers

PMID27498059
PMCPMC6560186
OpenAlexW2494205412

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.