Evidence map›Paper›PMID 34022967›Full record

ReviewCell & bioscience2021

Research models and mesenchymal/epithelial plasticity of osteosarcoma.

Xiaobin Yu, Jason T Yustein, Jianming Xu

Open access · goldAbstract readReview
In one paragraph

Review in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
12.5field-weighted citation impact, top 1% 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

39 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Choosing the right animal model for sarcoma research.Cellular and molecular life sciences : CMLS · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Osteosarcoma: current insights and advances.Exploration of targeted anti-tumor therapy · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Targeted therapy for osteosarcoma: a review.Journal of cancer research and clinical oncology · 2023
    Review
  20. 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

3 authors at 1 institution in 1 country.

Xiaobin YuDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Jason T YusteinDepartment of Pediatrics, Texas Children's Cancer and Hematology Center, and The Faris D. Virani Ewing Sarcoma Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA.
Jianming XuDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030, USA. jxu@bcm.edu.ORCID http://orcid.org/0000-0002-8208-9162
Baylor College of Medicine · US

Funding

NCOA6, A Novel Tumor Suppressor of Endometrial CancerR01CA193455 · NCI · BAYLOR COLLEGE OF MEDICINE · PI XU, JIANMING · 2016 to 2021
$1.9M
NCI NIH HHS R01 CA193455NIH HHS R01 CA193455
6 · The paper itself

Abstract

Most osteosarcomas (OSs) develop from mesenchymal cells at the bone with abnormal growth in young patients. OS has an annual incidence of 3.4 per million people and a 60-70% 5-year surviving rate. About 20% of OS patients have metastasis at diagnosis, and only 27% of patients with metastatic OS survive longer than 5 years. Mutation of tumor suppressors RB1, TP53, REQL4 and INK4a and/or deregulation of PI3K/mTOR, TGFβ, RANKL/NF-κB and IGF pathways have been linked to OS development. However, the agents targeting these pathways have yielded disappointing clinical outcomes. Surgery and chemotherapy remain the main treatments of OS. Recurrent and metastatic OSs are commonly resistant to these therapies. Spontaneous canine models, carcinogen-induced rodent models, transgenic mouse models, human patient-derived xenograft models, and cell lines from animal and human OSs have been developed for studying the initiation, growth and progression of OS and testing candidate drugs of OS. The cell plasticity regulated by epithelial-to-mesenchymal transition transcription factors (EMT-TFs) such as TWIST1, SNAIL, SLUG, ZEB1 and ZEB2 plays an important role in maintenance of the mesenchymal status and promotion of cell invasion and metastasis of OS cells. Multiple microRNAs including miR-30/9/23b/29c/194/200, proteins including SYT-SSX1/2 fusion proteins and OVOL2, and other factors that inhibit AMF/PGI and LRP5 can suppress either the expression or activity of EMT-TFs to increase epithelial features and inhibit OS metastasis. Further understanding of the molecular mechanisms that regulate OS cell plasticity should provide potential targets and therapeutic strategies for improving OS treatment.

Indexed as

EMT/MET-related processEMT-TFsExperimental modelMetastasisOsteosarcoma

Identifiers

PMID34022967
PMCPMC8141200
OpenAlexW3165668011

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.