Evidence map›Paper›PMID 30385632›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Oncogenic role of SFRP2 in p53-mutant osteosarcoma development via autocrine and paracrine mechanism.

Huensuk Kim, Seungyeul Yoo, Ruoji Zhou, An Xu, Jeffrey M Bernitz, Ye Yuan, Andreia M Gomes, Michael G Daniel, Jie Su, Elizabeth G Demicco and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 52 citations in OpenAlex.

  1. SFRP2Molecular carcinogenesis · 2026
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  7. Decoding cancer etiology with cellular reprogramming.Current opinion in genetics & development · 2025
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  20. Rewired mNature communications · 2023
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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

15 authors at 6 institutions in 4 countries.

Huensuk KimDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Seungyeul YooDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Ruoji ZhouDepartment of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030.
An XuDepartment of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030.
Jeffrey M BernitzDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Ye YuanDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Andreia M GomesDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Michael G DanielDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Jie SuDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Elizabeth G DemiccoDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.ORCID 0000-0003-4144-8824
Jun ZhuDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Kateri A MooreDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Dung-Fang LeeDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029; dung-fang.lee@uth.tmc.edu christoph.schaniel@mssm.edu.
Ihor R LemischkaDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Christoph SchanielDepartment of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029; dung-fang.lee@uth.tmc.edu christoph.schaniel@mssm.edu.ORCID 0000-0002-1343-4858
The Graduate Center, CUNY · USIcahn School of Medicine at Mount Sinai · USThe University of Texas MD Anderson Cancer Center · USLaboratoire d’immunologie intégrative du cancer · FRMount Sinai Hospital · CAUniversity of Coimbra · PT

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Global & Systems Level Analyses of Cell Fate RegulationR01GM078465 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEMISCHKA, IHOR R · 2007 to 2015
$3.7M
Modeling p53 Mutant-Associated Cancer With LFS Patient-Derived iPSCsR00CA181496 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LEE, DUNG-FANG · 2016 to 2018
$729k
System analysis of p53 mutant associated cancer development with LFS patient- specific iPSCsK00CA212489 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI KIM, HUENSUK · 2018 to 2019
$168k
System analysis of p53 mutant associated cancer development with LFS patient- specific iPSCsF99CA212489 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KIM, HUENSUK · 2016 to 2017
$87k
NCI NIH HHS F99 CA212489NCI NIH HHS K00 CA212489NCI NIH HHS P30 CA008748NCI NIH HHS R00 CA181496NIGMS NIH HHS R01 GM078465
6 · The paper itself

Abstract

Osteosarcoma (OS), the most common primary bone tumor, is highly metastatic with high chemotherapeutic resistance and poor survival rates. Using induced pluripotent stem cells (iPSCs) generated from Li-Fraumeni syndrome (LFS) patients, we investigate an oncogenic role of secreted frizzled-related protein 2 (SFRP2) in p53 mutation-associated OS development. Interestingly, we find that high SFRP2 expression in OS patient samples correlates with poor survival. Systems-level analyses identified that expression of SFRP2 increases during LFS OS development and can induce angiogenesis. Ectopic SFRP2 overexpression in normal osteoblast precursors is sufficient to suppress normal osteoblast differentiation and to promote OS phenotypes through induction of oncogenic molecules such as

Indexed as

AnimalsBone NeoplasmsCarcinogenesisCell Line, TumorCysteine-Rich Protein 61Forkhead Box Protein M1HumansInduced Pluripotent Stem CellsLi-Fraumeni SyndromeMaleMembrane ProteinsMiceMice, NudeNeovascularization, PathologicOsteoblastsOsteosarcomaCCN1 protein, humanCysteine-Rich Protein 61Forkhead Box Protein M1FOXM1 protein, humanMembrane ProteinsSecreted Frizzled-Related ProteinsSFRP2 protein, humanTumor Suppressor Protein p53autocrineosteosarcomap53paracrineSFRP2

Identifiers

PMID30385632
PMCPMC6255152
OpenAlexW2950489885

What OpenQuestion holds

Textmetadata
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.