Evidence map›Paper›PMID 35583991›Full record

ArticleInternational journal of cancer2022

An induced pluripotent stem cell t(7;12)(q36;p13) acute myeloid leukemia model shows high expression of MNX1 and a block in differentiation of the erythroid and megakaryocytic lineages.

Tina Nilsson, Ahmed Waraky, Anders Östlund, Susann Li, Anna Staffas, Julia Asp, Linda Fogelstrand, Jonas Abrahamsson, Lars Palmqvist

Abstract read
In one paragraph

Article in International journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Acute Myeloid Leukemia WithCase reports in hematology · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. 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

9 authors.

Tina NilssonDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Ahmed WarakyDepartment of Laboratory Medicine, University of Gothenburg, Institute of Biomedicine, Gothenburg, Sweden.
Anders ÖstlundDepartment of Laboratory Medicine, University of Gothenburg, Institute of Biomedicine, Gothenburg, Sweden.
Susann LiDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Anna StaffasDepartment of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Julia AspDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Linda FogelstrandDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Jonas AbrahamssonDepartment of Pediatrics, Institute of Clinical Sciences, University of Gothenburg, Gothenburg, Sweden.
Lars PalmqvistDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.ORCID 0000-0001-9274-360X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) results from aberrant hematopoietic processes and these changes are frequently initiated by chromosomal translocations. One particular subtype, AML with translocation t(7;12)(q36;p13), is found in children diagnosed before 2 years of age. The mechanisms for leukemogenesis induced by t(7;12) is not understood, in part because of the lack of efficient methods to reconstruct the leukemia-associated genetic aberration with correct genomic architecture and regulatory elements. We therefore created induced pluripotent stem cell (iPSC) lines that carry the translocation t(7;12) using CRISPR/Cas9. These t(7;12) iPSC showed propensity to differentiate into all three germ layers, confirming retained stem cell properties. The potential for differentiation into hematopoietic stem and progenitor cells (HSPC) was shown by expression of CD34, CD43 and CD45. Compared with the parental iPSC line, a significant decrease in cells expressing CD235a and CD41a was seen in the t(7;12) iPSC-derived HSPC (iHSPC), suggesting a block in differentiation. Moreover, colony formation assay showed an accumulation of cells at the erythroid and myeloid progenitor stages. Gene expression analysis revealed significant down-regulation of genes associated with megakaryocyte differentiation and up-regulation of genes associated with myeloid pathways but also genes typically seen in AML cases with t(7;12). Thus, this iPSC t(7;12) leukemia model of the t(7;12) AML subtype constitutes a valuable tool for further studies of the mechanisms for leukemia development and to find new treatment options.

Indexed as

Cell DifferentiationHomeodomain ProteinsInduced Pluripotent Stem CellsLeukemia, Myeloid, AcuteMegakaryocyte-Erythroid Progenitor CellsTranscription FactorsChildGene ExpressionGene Expression ProfilingHematopoietic Stem CellsHumansMegakaryocytesTranslocation, GeneticHomeodomain ProteinsMNX1 protein, humanTranscription FactorsAMLchromosome translocationleukemiapluripotencystem cells

Identifiers

PMID35583991
PMCPMC9545334

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.