Evidence map›Paper›PMID 28715648›Full record

ReviewDiscovery medicine2017

Tumor suppressor candidate 2 (TUSC2, FUS-1) and human cancers.

Tadas Rimkus, Sherona Sirkisoon, Alexandra Harrison, Hui-Wen Lo

Abstract readReview
In one paragraph

Review in Discovery medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
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  4. Lipid-based nucleic acid therapeutics with in vivo efficacy.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Identification of High-Risk Multiple Myeloma With a Plasma Cell Leukemia-Like Transcriptomic Profile.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Nano Approaches to Nucleic Acid Delivery: Barriers, Solutions, and Current Landscape.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology
    Review
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

4 authors at 1 institution in 1 country.

Tadas RimkusDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Sherona SirkisoonDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Alexandra HarrisonDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Hui-Wen LoDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Wake Forest University · US

Funding

Truncated GLI1 In GlioblastomaR01NS087169 · NINDS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LO, HUI-WEN · 2014 to 2018
$2.1M
NINDS NIH HHS R01 NS087169
6 · The paper itself

Abstract

Tumor suppressor candidate 2 (TUSC2, also known as FUS1) was identified in 2000 as a candidate tumor suppressor gene located in a region on chromosome 3p21.3 that is homozygously deleted in some lung and breast cancers. The deletion is rare in lung and breast cancers, but is frequent in malignant pleural mesothelioma. Evidence to date indicates that TUSC2 behaves as a tumor suppressor in lung cancer; however, its role as a tumor suppressor for other tumor types has not been fully established. Loss of TUSC2 expression at the mRNA and protein levels has been reported in various cancers. While the mechanisms underlying the loss are still not well understood, several microRNAs have been reported to downregulate TUSC2 expression. TUSC2 elicits its anti-tumor effects through regulating G1 cell cycle progression, apoptosis, calcium homeostasis, gene expression, and the activity of various protein tyrosine kinases and Ser/Thr kinases, albeit the precise mechanisms that TUSC2 utilizes to regulate these cellular processes and signaling molecules are still elusive. TUSC2 restoration has been exploited as an anti-cancer therapy in various cancers in preclinical models, and clinically in patients with lung cancer. The first-in-human phase I trial demonstrated desirable safety outcomes. Phase I/II trials are being conducted to evaluate the efficacy of combining TUSC2-nanoparticles with erlotinib, an FDA-approved EGFR inhibitor. This review summarizes recent findings that advanced our understanding of TUSC2 as a novel tumor suppressor and a therapeutic opportunity for treating TUSC2-deficient cancers.

Indexed as

Genes, Tumor SuppressorGene Expression Regulation, NeoplasticHumansMicroRNAsModels, BiologicalNeoplasmsMicroRNAs

Identifiers

PMID28715648
PMCPMC5808457
OpenAlexW2988602026

What OpenQuestion holds

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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.