Evidence map›Paper›PMID 33869030›Full record

ReviewFrontiers in oncology2021

Autophagy in Human T-Cell Leukemia Virus Type 1 (HTLV-1) Induced Leukemia.

Nicolás Ducasa, Daniel Grasso, Paula Benencio, Daniela L Papademetrio, Mirna Biglione, Fatah Kashanchi, Carolina Berini, Maria Noé Garcia

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Inflammasomes and autophagy in cancer: unlocking targeted therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  3. The helicase-like transcription factor redirects the autophagic flux and restricts human T cell leukemia virus type 1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Review
  5. Review
  6. Review
  7. 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

8 authors at 4 institutions in 2 countries.

Nicolás DucasaInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), CONICET- Universidad de Buenos Aires, Buenos Aires, Argentina.
Daniel GrassoCátedra de Fisiopatología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Paula BenencioInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), CONICET- Universidad de Buenos Aires, Buenos Aires, Argentina.
Daniela L PapademetrioConsejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Instituto de Estudios de la Inmunidad Humoral (IDEHU), Buenos Aires, Argentina.
Mirna BiglioneInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), CONICET- Universidad de Buenos Aires, Buenos Aires, Argentina.
Fatah KashanchiLaboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA, United States.
Carolina BeriniInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), CONICET- Universidad de Buenos Aires, Buenos Aires, Argentina.
Maria Noé GarciaConsejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Instituto de Estudios de la Inmunidad Humoral (IDEHU), Buenos Aires, Argentina.
University of Buenos Aires · ARConsejo Nacional de Investigaciones Científicas y Técnicas · ARGeorge Mason University · USInstituto de Investigaciones Biomédicas en Retrovirus y Sida · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viruses play an important role in the development of certain human cancers. They are estimated to contribute 16% to all human cancers. Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus to be discovered and is the etiological agent of adult T-cell leukemia/lymphoma (ATLL), an aggressive T-cell malignancy with poor prognosis. HTLV-1 viral proteins interact with mechanisms and proteins present in host cells for their own benefit, evading the immune system and promoting the establishment of disease. Several viruses manipulate the autophagy pathway to achieve their infective goals, and HTLV-1 is not the exception. HTLV-1 Tax viral protein engages NF-κB and autophagy pathways prone favoring viral replication and T cell transformation. In this review we focus on describing the relationship of HTLV-1 with the autophagy machinery and its implication in the development of ATLL.

Indexed as

autophagyHTLV-1NF-κBtaxT-cell leukemia

Identifiers

PMID33869030
PMCPMC8045967
OpenAlexW3152394894

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.