Evidence map›Paper›PMID 35215499›Full record

ReviewNutrients2022

Lipid Metabolism and Epigenetics Crosstalk in Prostate Cancer.

Juan C Pardo, Vicenç Ruiz de Porras, Joan Gil, Albert Font, Manel Puig-Domingo, Mireia Jordà

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Metabolic convergence of diabetes and prostate cancer: from dysglycemia to tumor microenvironment reprogramming.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  3. Article
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  8. Review
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  13. Review
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  15. Article
  16. Review
  17. Article
  18. Metabolic adaptations in prostate cancer.British journal of cancer · 2024
    Review
  19. Epigenetics and environmental health.Frontiers of medicine · 2024
    Review
  20. 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 3 institutions in 1 country.

Juan C PardoDepartment of Medical Oncology, Catalan Institute of Oncology, University Hospital Germans Trias i Pujol, Ctra. Can Ruti-Camí de les Escoles s/n, 08916 Badalona, Spain.
Vicenç Ruiz de PorrasCatalan Institute of Oncology, Badalona Applied Research Group in Oncology (B·ARGO), Ctra. Can Ruti-Camí de les Escoles s/n, 08916 Badalona, Spain.ORCID 0000-0002-4352-1784
Joan GilGermans Trias i Pujol Research Institute (IGTP), Ctra. Can Ruti-Camí de les Escoles s/n, 08916 Badalona, Spain.ORCID 0000-0003-1030-9119
Albert FontDepartment of Medical Oncology, Catalan Institute of Oncology, University Hospital Germans Trias i Pujol, Ctra. Can Ruti-Camí de les Escoles s/n, 08916 Badalona, Spain.
Manel Puig-DomingoGermans Trias i Pujol Research Institute (IGTP), Ctra. Can Ruti-Camí de les Escoles s/n, 08916 Badalona, Spain.
Mireia JordàGermans Trias i Pujol Research Institute (IGTP), Ctra. Can Ruti-Camí de les Escoles s/n, 08916 Badalona, Spain.
Institut Català d'Oncologia · ESUniversitat Autònoma de Barcelona · ESInstitut d'Investigació en Ciències de la Salut Germans Trias i Pujol · ES

Funding

Instituto de Salud Carlos III CM20/00028Instituto de Salud Carlos III PI18/00654Spanish Society of Medical Oncology 2021 D. Jesús Angel Sánchez Castillo for Research Projects
6 · The paper itself

Abstract

Prostate cancer (PCa) is the most commonly diagnosed malignant neoplasm in men in the Western world. Localized low-risk PCa has an excellent prognosis thanks to effective local treatments; however, despite the incorporation of new therapeutic strategies, metastatic PCa remains incurable mainly due to disease heterogeneity and the development of resistance to therapy. The mechanisms underlying PCa progression and therapy resistance are multiple and include metabolic reprogramming, especially in relation to lipid metabolism, as well as epigenetic remodelling, both of which enable cancer cells to adapt to dynamic changes in the tumour. Interestingly, metabolism and epigenetics are interconnected. Metabolism can regulate epigenetics through the direct influence of metabolites on epigenetic processes, while epigenetics can control metabolism by directly or indirectly regulating the expression of metabolic genes. Moreover, epidemiological studies suggest an association between a high-fat diet, which can alter the availability of metabolites, and PCa progression. Here, we review the alterations of lipid metabolism and epigenetics in PCa, before focusing on the mechanisms that connect them. We also discuss the influence of diet in this scenario. This information may help to identify prognostic and predictive biomarkers as well as targetable vulnerabilities.

Indexed as

Lipid MetabolismProstatic NeoplasmsEpigenesis, GeneticEpigenomicsHumansMalePrognosischolesteroldietDNA methylationepigeneticsfatty acidhistone modificationslipid metabolismpredictive biomarkersprostate cancertherapeutic vulnerabilities

Identifiers

PMID35215499
PMCPMC8874497
OpenAlexW4214583658

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.