Evidence map›Paper›PMID 27913602›Full record

ArticleGenes & development2016

Clonal conversion of B lymphoid leukemia reveals cross-lineage transfer of malignant states.

Rajesh Somasundaram, Josefine Åhsberg, Kazuki Okuyama, Jonas Ungerbäck, Henrik Lilljebjörn, Thoas Fioretos, Tobias Strid, Mikael Sigvardsson

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Molecular Regulation of Differentiation in Early B-Lymphocyte Development.International journal of molecular sciences · 2018
    Review
  11. Cellular plasticity in B-cell leukemia.Cell cycle (Georgetown, Tex.) · 2017
    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

8 authors at 2 institutions in 1 country.

Rajesh SomasundaramDepartment of Clinical and Experimental Medicine, Experimental Hematopoiesis Unit, Faculty of Health Sciences, Linköping University, 58183 Linkoping, Sweden.
Josefine ÅhsbergDepartment of Clinical and Experimental Medicine, Experimental Hematopoiesis Unit, Faculty of Health Sciences, Linköping University, 58183 Linkoping, Sweden.
Kazuki OkuyamaDepartment of Clinical and Experimental Medicine, Experimental Hematopoiesis Unit, Faculty of Health Sciences, Linköping University, 58183 Linkoping, Sweden.
Jonas UngerbäckDepartment of Clinical and Experimental Medicine, Experimental Hematopoiesis Unit, Faculty of Health Sciences, Linköping University, 58183 Linkoping, Sweden.
Henrik LilljebjörnDepartment of Laboratory Medicine, Division of Clinical Genetics, Lund University, 22184 Lund, Sweden.
Thoas FioretosDepartment of Laboratory Medicine, Division of Clinical Genetics, Lund University, 22184 Lund, Sweden.
Tobias StridDepartment of Clinical and Experimental Medicine, Experimental Hematopoiesis Unit, Faculty of Health Sciences, Linköping University, 58183 Linkoping, Sweden.
Mikael SigvardssonDepartment of Clinical and Experimental Medicine, Experimental Hematopoiesis Unit, Faculty of Health Sciences, Linköping University, 58183 Linkoping, Sweden.
Linköping University · SELund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Even though leukemia is considered to be confined to one specific hematopoietic cell type, cases of acute leukemia of ambiguous lineage and patients relapsing in phenotypically altered disease suggest that a malignant state may be transferred between lineages. Because B-cell leukemia is associated with mutations in transcription factors of importance for stable preservation of lineage identity, we here investigated the potential lineage plasticity of leukemic cells. We report that primary pro-B leukemia cells from mice carrying heterozygous mutations in either or both the Pax5 and Ebf1 genes, commonly mutated in human leukemia, can be converted into T lineage leukemia cells. Even though the conversion process involved global changes in gene expression and lineage-restricted epigenetic reconfiguration, the malignant phenotype of the cells was preserved, enabling them to expand as T lineage leukemia cells in vivo. Furthermore, while the transformed pro-B cells displayed plasticity toward myeloid lineages, the converted cells failed to cause myeloid leukemia after transplantation. These data provide evidence that a malignant phenotype can be transferred between hematopoietic lineages. This has important implications for modern cancer medicine because lineage targeted treatment of leukemia patients can be predicted to provoke the emergence of phenotypically altered subclones, causing clinical relapse.

Indexed as

AnimalsB-LymphocytesCell LineCell LineageCell Line, TumorCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansLeukemia, LymphoidLeukemia, T-CellMiceMice, Inbred C57BLMutationMyeloid CellsPrecursor Cells, B-LymphoidReceptors, NotchB-ALLlineage conversiontranscription factors

Identifiers

PMID27913602
PMCPMC5159664
OpenAlexW2557550751

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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.