Evidence map›Paper›PMID 35053485›Full record

ReviewCancers2022

Pathophysiological Integration of Metabolic Reprogramming in Breast Cancer.

Roberto Corchado-Cobos, Natalia García-Sancha, Marina Mendiburu-Eliçabe, Aurora Gómez-Vecino, Alejandro Jiménez-Navas, Manuel Jesús Pérez-Baena, Marina Holgado-Madruga, Jian-Hua Mao, Javier Cañueto, Sonia Castillo-Lluva and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Endothelial metabolic zonation in the vascular network: a spatiotemporal blueprint for angiogenesis.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Breast cancers as ecosystems: a metabolic perspective.Cellular and molecular life sciences : CMLS · 2023
    Review
  16. Article
  17. Evolutionary Origins of Metabolic Reprogramming in Cancer.International journal of molecular sciences · 2022
    Review
  18. Review
  19. Targeting Energy Metabolism in Cancer Treatment.International journal of molecular sciences · 2022
    Review
  20. 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

11 authors at 3 institutions in 2 countries.

Roberto Corchado-CobosInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0002-3452-2486
Natalia García-SanchaInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0001-7731-7020
Marina Mendiburu-EliçabeInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.
Aurora Gómez-VecinoInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.
Alejandro Jiménez-NavasInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0001-7621-576X
Manuel Jesús Pérez-BaenaInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0001-6820-215X
Marina Holgado-MadrugaInstituto de Investigación Biosanitaria de Salamanca (IBSAL), 37007 Salamanca, Spain.
Jian-Hua MaoBiological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.ORCID 0000-0001-9320-6021
Javier CañuetoInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0003-0037-7353
Sonia Castillo-LluvaDepartamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas, Universidad Complutense, 28040 Madrid, Spain.ORCID 0000-0001-5357-7178
Jesús Pérez-LosadaInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Universidad de Salamanca/CSIC, 37007 Salamanca, Spain.ORCID 0000-0003-2400-624X
Universidad de Salamanca · ESLawrence Berkeley National Laboratory · USUniversidad Complutense de Madrid · ES

Funding

Carlos III Health Institute PIE14/00066Gerencia Regional de Salud de Castilla y León GRS2139/A/20Instituto de Salud Carlos III PI18/00587Instituto de Salud Carlos III PI21/01207Ministerio de Ciencia e Innovación PDC2021-121735-I00Ministerio de Ciencia e Innovación PID2020-118527RB-I00Ministerio de Ciencia e Innovación RTI2018-094130-B-100Ministerio de Economía, Industria y Competitividad SAF2014-56989-RMinisterio de Economía, Industria y Competitividad SAF2017-88854RRegional Government of Castile and León CSI144P20Regional Government of Castile and León CSI234P18
6 · The paper itself

Abstract

Metabolic changes that facilitate tumor growth are one of the hallmarks of cancer. The triggers of these metabolic changes are located in the tumor parenchymal cells, where oncogenic mutations induce an imperative need to proliferate and cause tumor initiation and progression. Cancer cells undergo significant metabolic reorganization during disease progression that is tailored to their energy demands and fluctuating environmental conditions. Oxidative stress plays an essential role as a trigger under such conditions. These metabolic changes are the consequence of the interaction between tumor cells and stromal myofibroblasts. The metabolic changes in tumor cells include protein anabolism and the synthesis of cell membranes and nucleic acids, which all facilitate cell proliferation. They are linked to catabolism and autophagy in stromal myofibroblasts, causing the release of nutrients for the cells of the tumor parenchyma. Metabolic changes lead to an interstitium deficient in nutrients, such as glucose and amino acids, and acidification by lactic acid. Together with hypoxia, they produce functional changes in other cells of the tumor stroma, such as many immune subpopulations and endothelial cells, which lead to tumor growth. Thus, immune cells favor tissue growth through changes in immunosuppression. This review considers some of the metabolic changes described in breast cancer.

Indexed as

cancer-associated fibroblastsglucosehypoxiainterstitiumlactatemacrophagesmetabolism

Identifiers

PMID35053485
PMCPMC8773662
OpenAlexW4206255038

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.