Evidence map›Paper›PMID 35181743›Full record

ReviewCancer gene therapy2022

Mitochondrial Fus1/Tusc2 and cellular Ca2

Roman Uzhachenko, Akiko Shimamoto, Sanika S Chirwa, Sergey V Ivanov, Alla V Ivanova, Anil Shanker

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. 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

6 authors at 2 institutions in 1 country.

Roman UzhachenkoDepartment of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA.
Akiko ShimamotoDepartment of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA.
Sanika S ChirwaDepartment of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA.
Sergey V IvanovDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA.
Alla V IvanovaSchool of Graduate Studies and Research, Meharry Medical College, Nashville, TN, USA. aivanova@mmc.edu.ORCID http://orcid.org/0000-0002-4149-5105
Anil ShankerDepartment of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, School of Medicine, Meharry Medical College, Nashville, TN, USA. ashanker@mmc.edu.ORCID http://orcid.org/0000-0001-6372-3669
Meharry Medical College · USVanderbilt University · US

Funding

Technologies and Resources CoreU54MD007593 · NIMHD · MEHARRY MEDICAL COLLEGE · PI ADUNYAH, SAMUEL EVANS · 2012 to 2018
$24.7M
Translational Pathology CoreU54CA163069 · NCI · MEHARRY MEDICAL COLLEGE · PI ADUNYAH, SAMUEL EVANS · 2011 to 2025
$18.8M
Role of Fus1-mediated antitumor CD8T-NK crosstalk in Alzheimer's disease pathologySC1CA182843 · NCI · MEHARRY MEDICAL COLLEGE · PI SHANKER, ANIL · 2013 to 2020
$3.1M
NCI NIH HHS SC1 CA182843NCI NIH HHS U54 CA163069NIMHD NIH HHS U54 MD007593
6 · The paper itself

Abstract

FUS1/TUSC2 (FUSion1/TUmor Suppressor Candidate 2) is a tumor suppressor gene (TSG) originally described as a member of the TSG cluster from human 3p21.3 chromosomal region frequently deleted in lung cancer. Its role as a TSG in lung, breast, bone, and other cancers was demonstrated by several groups, but molecular mechanisms of its activities are starting to unveil lately. They suggest that Fus1-dependent mechanisms are relevant in etiologies of diseases beyond cancer, such as chronic inflammation, bacterial and viral infections, premature aging, and geriatric diseases. Here, we revisit the discovery of FUS1 gene in the context of tumor initiation and progression, and review 20 years of research into FUS1 functions and its molecular, structural, and biological aspects that have led to its use in clinical trials and gene therapy. We present a data-driven view on how interactions of Fus1 with the mitochondrial Ca

Indexed as

Lung NeoplasmsTumor Suppressor ProteinsAgedAgingAnti-Inflammatory AgentsGenes, Tumor SuppressorHomeostasisHumansAnti-Inflammatory AgentsTumor Suppressor ProteinsTUSC2 protein, human

Identifiers

PMID35181743
PMCPMC9576590
OpenAlexW4213090973

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.