Evidence map›Paper›PMID 34535653›Full record

ArticleNature communications2021

Adipocytes disrupt the translational programme of acute lymphoblastic leukaemia to favour tumour survival and persistence.

Q Heydt, C Xintaropoulou, A Clear, M Austin, I Pislariu, F Miraki-Moud, P Cutillas, K Korfi, M Calaminici, W Cawthorn and 14 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-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

31 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Co-culture shock.Cell death discovery · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  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

24 authors at 7 institutions in 1 country.

Q HeydtCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
C XintaropoulouCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
A ClearCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
M AustinCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
I PislariuCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
F Miraki-MoudCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
P CutillasCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.ORCID 0000-0002-3426-2274
K KorfiCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
M CalaminiciCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
W CawthornBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, Edinburgh BioQuarter, University of Edinburgh, Edinburgh, Scotland, UK.ORCID 0000-0001-7832-5057
K SuchackiBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, Edinburgh BioQuarter, University of Edinburgh, Edinburgh, Scotland, UK.ORCID 0000-0002-4688-4126
A NaganoCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.
J G GribbenCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.ORCID 0000-0002-8505-7430
M SmithDepartment of Haemato-Oncology, St Bartholomew's Hospital, West Smithfield, London, UK.
J D CavenaghDepartment of Haemato-Oncology, St Bartholomew's Hospital, West Smithfield, London, UK.
H OakerveeDepartment of Haemato-Oncology, St Bartholomew's Hospital, West Smithfield, London, UK.
A CastletonChristie NHS Foundation Trust, Manchester, UK.
D TaussigHaemato-oncology Unit, The Royal Marsden Hospital, Sutton, UK.
B PeckCentre for Tumour Biology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.ORCID 0000-0002-6687-8495
A WilczynskaCRUK Beatson Institute, Glasgow, UK.ORCID 0000-0003-4548-9367
L McNaughtonHaematopoietic Stem Cell Laboratory, The Francis Crick Institute, London, UK.
D BonnetHaematopoietic Stem Cell Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-4735-5226
F MardakhehCentre for Molecular Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK.ORCID 0000-0003-3896-0827
B PatelCentre for Haemato-Oncology, Barts Cancer Institute, John Vane Science Centre, Charterhouse Square, Queen Mary University of London, London, UK. b.wrench@qmul.ac.uk.ORCID 0000-0002-1875-8974
Queen Mary University of London · GBSt Bartholomew's Hospital · GBThe Francis Crick Institute · GBThe Queen's Medical Research Institute · GBCancer Research UK Scotland Institute · GBRoyal Marsden Hospital · GBThe Christie NHS Foundation Trust · GB

Funding

Cancer Research UK 21019Cancer Research UK C16420/A18066Cancer Research UK CRUK A21019Medical Research Council MR/M021394/1
6 · The paper itself

Abstract

The specific niche adaptations that facilitate primary disease and Acute Lymphoblastic Leukaemia (ALL) survival after induction chemotherapy remain unclear. Here, we show that Bone Marrow (BM) adipocytes dynamically evolve during ALL pathogenesis and therapy, transitioning from cellular depletion in the primary leukaemia niche to a fully reconstituted state upon remission induction. Functionally, adipocyte niches elicit a fate switch in ALL cells towards slow-proliferation and cellular quiescence, highlighting the critical contribution of the adipocyte dynamic to disease establishment and chemotherapy resistance. Mechanistically, adipocyte niche interaction targets posttranscriptional networks and suppresses protein biosynthesis in ALL cells. Treatment with general control nonderepressible 2 inhibitor (GCN2ib) alleviates adipocyte-mediated translational repression and rescues ALL cell quiescence thereby significantly reducing the cytoprotective effect of adipocytes against chemotherapy and other extrinsic stressors. These data establish how adipocyte driven restrictions of the ALL proteome benefit ALL tumours, preventing their elimination, and suggest ways to manipulate adipocyte-mediated ALL resistance.

Indexed as

3T3-L1 CellsAdipocytesAdultAnimalsBiopsyBone MarrowCell LineageCell SurvivalHumansMiceMiddle AgedPrecursor Cell Lymphoblastic Leukemia-LymphomaProteomeStress, PhysiologicalSurvival AnalysisYoung AdultProteome

Identifiers

PMID34535653
PMCPMC8448863
OpenAlexW3200313697

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.