Evidence map›Paper›PMID 35029792›Full record

ReviewCancer metastasis reviews2021

The role of metabolic ecosystem in cancer progression - metabolic plasticity and mTOR hyperactivity in tumor tissues.

Anna Sebestyén, Titanilla Dankó, Dániel Sztankovics, Dorottya Moldvai, Regina Raffay, Catherine Cervi, Ildikó Krencz, Viktória Zsiros, András Jeney, Gábor Petővári

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Heme-glycolysis interplay in oral squamous cell carcinoma: insights into SLC48A1 and GLUT1 expression across histological grades.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Lipid Metabolism and Oncogenesis.Cancer treatment and research · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Cancer metabolism and carcinogenesis.Experimental hematology & oncology · 2024
    Review
  19. Review
  20. mTOR hyperactivity andPathology oncology research : POR · 2024
    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

10 authors at 1 institution in 1 country.

Anna Sebestyén1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary. sebestyen.anna@med.semmelweis-univ.hu.
Titanilla Dankó1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Dániel Sztankovics1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Dorottya Moldvai1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Regina Raffay1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Catherine Cervi1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Ildikó Krencz1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Viktória ZsirosDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó utca 58, 1094, Budapest, Hungary.
András Jeney1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Gábor Petővári1St Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, 1085, Budapest, Hungary.
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite advancements in cancer management, tumor relapse and metastasis are associated with poor outcomes in many cancers. Over the past decade, oncogene-driven carcinogenesis, dysregulated cellular signaling networks, dynamic changes in the tissue microenvironment, epithelial-mesenchymal transitions, protein expression within regulatory pathways, and their part in tumor progression are described in several studies. However, the complexity of metabolic enzyme expression is considerably under evaluated. Alterations in cellular metabolism determine the individual phenotype and behavior of cells, which is a well-recognized hallmark of cancer progression, especially in the adaptation mechanisms underlying therapy resistance. In metabolic symbiosis, cells compete, communicate, and even feed each other, supervised by tumor cells. Metabolic reprogramming forms a unique fingerprint for each tumor tissue, depending on the cellular content and genetic, epigenetic, and microenvironmental alterations of the developing cancer. Based on its sensing and effector functions, the mechanistic target of rapamycin (mTOR) kinase is considered the master regulator of metabolic adaptation. Moreover, mTOR kinase hyperactivity is associated with poor prognosis in various tumor types. In situ metabolic phenotyping in recent studies highlights the importance of metabolic plasticity, mTOR hyperactivity, and their role in tumor progression. In this review, we update recent developments in metabolic phenotyping of the cancer ecosystem, metabolic symbiosis, and plasticity which could provide new research directions in tumor biology. In addition, we suggest pathomorphological and analytical studies relating to metabolic alterations, mTOR activity, and their associations which are necessary to improve understanding of tumor heterogeneity and expand the therapeutic management of cancer.

Indexed as

EcosystemNeoplasmsCarcinogenesisHumansSignal TransductionTOR Serine-Threonine KinasesTumor MicroenvironmentMTOR protein, humanTOR Serine-Threonine KinasesCancerMetabolic heterogeneityMetabolic phenotypesMetabolic plasticitymTOR hyperactivity

Identifiers

PMID35029792
PMCPMC8825419
OpenAlexW4205974265

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.