Evidence map›Paper›PMID 30564554›Full record

ReviewFrontiers in oncology2018

Metabolic Reprogramming of Non-Hodgkin's B-Cell Lymphomas and Potential Therapeutic Strategies.

Jean-Ehrland Ricci, Johanna Chiche

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The effect of metabolic syndrome on prognosis of diffuse large B-cell lymphoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. 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

2 authors.

Jean-Ehrland RicciINSERM U1065, C3M, Team Metabolism, Cancer and Immune Responses, Universiteé Côte d'Azur, Nice, France.
Johanna ChicheINSERM U1065, C3M, Team Metabolism, Cancer and Immune Responses, Universiteé Côte d'Azur, Nice, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolism is a wide and general term that refers to any intracellular pathways the cell utilizes in order to satisfy its energetic demand and to support cell viability and/or division. Along with phenotypic changes, all mammalian cells including immune cells modulate their metabolic program in order to reach their effector functions. Exacerbated metabolism and metabolic flexibility are also hallmarks of tumor initiation and of tumor cell progression in a complex tumor microenvironment. Metabolic reprogramming is mainly directed by the serine/threonine kinase mTOR (mammalian target of rapamycin). mTOR exists in two structurally and functionally distinct complexes, mTORC1 and mTORC2 that coordinate environmental signals and metabolic/anabolic pathways to provide macromolecules and energy needed for survival and growth. Activation of mTORC1 is required during development, differentiation and activation of immune cells. Aberrant and persistent activation of mTORC1 is often observed in malignant B cells such as Non-Hodgkin's (NH) B-cell lymphomas. Here, we review recent insights on cell metabolism and on basic mechanisms of mTORC1 regulation and metabolic functions. We highlight the distinct mechanisms driving mTORC1 activation in the three most-common types of NH B-cell lymphomas (Diffuse Large B Cell Lymphomas, Follicular Lymphomas, and Mantle Cell Lymphomas), for which the first generation of mTORC1 inhibitors (rapalogs) have been extensively evaluated in preclinical and clinical settings. Finally, we discuss the reasons for limited clinical success of this therapy and focus on potential therapeutic strategies targeting metabolic pathways, upstream and downstream of mTORC1, that can be combined to rapalogs in order to improve patient's outcome.

Indexed as

DLBCL–Diffuse large B cell lymphomafolicular lymphomamammalian target of rapamycin complexmantel cell lymphomametabolismmTORCNon-Hodgekins lymphomatherapeutic strategies

Identifiers

PMID30564554
PMCPMC6288288

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.