Evidence map›Paper›PMID 37780210›Full record

ArticleFrontiers in molecular biosciences2023

The p53 tumor suppressor regulates AKR1B1 expression, a metastasis-promoting gene in breast cancer.

Carolina Di Benedetto, Carla Borini Etichetti, Nabila Cocordano, Alejo Cantoia, Evelyn Arel Zalazar, Silvio Bicciato, Mauricio Menacho-Márquez, Germán Leandro Rosano, Javier Girardini

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular biosciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Potential Role ofClinical Medicine Insights. Oncology · 2024
    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

9 authors at 4 institutions in 3 countries.

Carolina Di BenedettoDepartment of Radiation Oncology, University of California San Francisco, San Francisco, CA, United States.
Carla Borini EtichettiInstituto de Fisiología Experimental de Rosario (IFISE), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
Nabila CocordanoInstituto de Inmunología Clínica y Experimental de Rosario (IDICER), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
Alejo CantoiaUnidad de Espectrometría de Masa, Instituto de Biología Molecular y Celular de Rosario (IBR), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
Evelyn Arel ZalazarInstituto de Inmunología Clínica y Experimental de Rosario (IDICER), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
Silvio BicciatoDepartment of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
Mauricio Menacho-MárquezInstituto de Inmunología Clínica y Experimental de Rosario (IDICER), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
Germán Leandro RosanoUnidad de Espectrometría de Masa, Instituto de Biología Molecular y Celular de Rosario (IBR), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
Javier GirardiniInstituto de Inmunología Clínica y Experimental de Rosario (IDICER), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional de Rosario, Rosario, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARNational University of Rosario · ARUniversity of California, San Francisco · USUniversity of Modena and Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alteration of metabolism in cancer cells is a central aspect of the mechanisms that sustain aggressive traits. Aldo-keto reductase 1 B1 (AKR1B1) catalyzes the reduction of several aldehydes to alcohols consuming NADPH. Nevertheless, the ability of AKR1B1 to reduce different substrates renders difficult to comprehensively ascertain its biological role. Recent evidence has implicated AKR1B1 in cancer; however, the mechanisms underlying its pro-oncogenic function remain largely unknown. In this work, we report that AKR1B1 expression is controlled by the p53 tumor suppressor. We found that breast cancer patients bearing wild-type

Indexed as

aldo–keto reductase 1 B1aldo–keto reductasesbreast cancerelectron transport chainmetastasismitochondriap53proteomics

Identifiers

PMID37780210
PMCPMC10538543
OpenAlexW4386736753

What Socratic 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 Socratic graph.