Evidence map›Paper›PMID 28655536›Full record

ReviewExperimental hematology2017

B-cell identity as a metabolic barrier against malignant transformation.

Lai N Chan, Markus Müschen

Open access · bronzeAbstract readReview
In one paragraph

Review in Experimental hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. PON2 subverts metabolic gatekeeper functions in B cells to promote leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Review
  12. Review
  13. Article
  14. Regulation of Energy Metabolism during Early B Lymphocyte Development.International journal of molecular sciences · 2018
    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

2 authors at 2 institutions in 1 country.

Lai N ChanDepartment of Systems Biology, Beckman Research Institute and City of Hope Comprehensive Cancer Center, Pasadena, CA. Electronic address: lachan@coh.org.
Markus MüschenDepartment of Systems Biology, Beckman Research Institute and City of Hope Comprehensive Cancer Center, Pasadena, CA.
Beckman Research InstituteCity of Hope · US

Funding

Metabolic gatekeepers in B-cell malignanciesR35CA197628 · NCI · YALE UNIVERSITY · PI Markus Müschen · 2016 to 2026
$11.7M
Targeted activation of autoimmune checkpoints in B cell malignanciesR01CA157644 · NCI · YALE UNIVERSITY · PI Markus Müschen · 2011 to 2026
$5.7M
PRE-B CELL RECEPTOR SIGNALING IN ACUTE LYMPHOBLASTIC LEUKEMIAR01CA137060 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2009 to 2016
$2.7M
CD25-mediated feedback control of BCR-signaling and its oncogenic mimicsR01CA213138 · NCI · YALE UNIVERSITY · PI MÜSCHEN, MARKUS · 2017 to 2022
$1.9M
Negative feedback signaling in tyrosine kinase-driven leukemiaR01CA172558 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MÜSCHEN, MARKUS · 2013 to 2015
$972k
NCI NIH HHS R01 CA137060NCI NIH HHS R01 CA157644NCI NIH HHS R01 CA172558NCI NIH HHS R01 CA213138NCI NIH HHS R35 CA197628Wellcome Trust
6 · The paper itself

Abstract

B-lineage and myeloid leukemia cells are often transformed by the same oncogenes, but have different biological and clinical characteristics. Although B-lineage acute lymphoblastic leukemia (B-ALL) cells are characterized by a state of chronic energy deficit, myeloid leukemia cells show abundant energy reserve. Interestingly, fasting has been demonstrated to inhibit selectively the development of B-ALL but not myeloid leukemia, further suggesting that lineage identity may be linked to divergent metabolic states in hematopoietic malignancies. The B-lymphoid transcription factors IKZF1, EBF1, and PAX5 are essential for early B-cell development and commitment to B-cell identity. However, in >80% of human pre-B-ALL cases, the leukemic clones harbor genetic lesions of these transcription factors. The significance of these defects has only recently been investigated. Here, we discuss the unexpected function of a B-lymphoid transcriptional program as a metabolic barrier against malignant transformation of B-cell precursor cells. The metabolic gatekeeper function of B-lymphoid transcription factors may force silent preleukemic clones carrying potentially oncogenic lesions to remain in a latent state. In addition, this program sets the threshold for responses to glucocorticoids in pre-B-ALL. Finally, the link between the tumor-suppressor and metabolic functions of B-lymphoid transcription factors is matched by observations in clinical trials: obesity and hyperglycemia are associated with poor clinical outcome in patients with pre-B-ALL.

Indexed as

Cell Transformation, NeoplasticAnimalsB-LymphocytesCell LineageEnergy MetabolismForkhead Box Protein O1HumansIkaros Transcription FactorMiceObesityPAX5 Transcription FactorPhosphatidylinositol 3-KinasesPrecursor B-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-aktReceptors, LeptinForkhead Box Protein O1Ikaros Transcription FactorIKZF1 protein, humanPAX5 Transcription FactorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Leptin

Identifiers

PMID28655536
PMCPMC5568490
OpenAlexW2639976476

What OpenQuestion holds

Textmetadata
LicenceTDM
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.