Evidence map›Paper›PMID 32502465›Full record

ArticleStem cell reports2020

Driver Mutations in Leukemia Promote Disease Pathogenesis through a Combination of Cell-Autonomous and Niche Modulation.

Baskar Ramdas, Raghuveer Singh Mali, Lakshmi Reddy Palam, Ruchi Pandey, Zhigang Cai, Santhosh Kumar Pasupuleti, Sarah S Burns, Reuben Kapur

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Role of TET dioxygenases in the regulation of both normal and pathological hematopoiesis.Journal of experimental & clinical cancer research : CR · 2022
    Review
  9. Article
  10. Article
  11. Cancer stem cells: a major culprit of intra-tumor heterogeneity.American journal of cancer research · 2021
    Review
  12. Review
  13. 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

8 authors at 2 institutions in 1 country.

Baskar RamdasDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA. Electronic address: ramdasb@iupui.edu.
Raghuveer Singh MaliDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA.
Lakshmi Reddy PalamDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA.
Ruchi PandeyDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA.
Zhigang CaiDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA.
Santhosh Kumar PasupuletiDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA.
Sarah S BurnsDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA.
Reuben KapurDepartment of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, R4, 1044 West Walnut Street, Indianapolis, IN 46202, USA; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA; Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA; Department of Molecular Biology and Biochemistry, Indiana University School of Medicine, Indianapolis, IN 46202, USA. Electronic address: rkapur@iupui.edu.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

Role of p21 activated kinase in LeukemogenesisR01CA173852 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2014 to 2025
$3.4M
Role of Shp2 in FLT3-ITD-Induced LeukemogenesisR01CA134777 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2011 to 2023
$3.4M
Hyperglycemia mediated myeloproliferative diseaseR01HL140961 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2019 to 2022
$2.3M
Targeting Novel Pathways in JMMLR01HL146137 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2019 to 2022
$2.2M
NCI NIH HHS R01 CA134777NCI NIH HHS R01 CA173852NHLBI NIH HHS R01 HL140961NHLBI NIH HHS R01 HL146137
6 · The paper itself

Abstract

Studies of patients with acute myeloid leukemia (AML) have led to the identification of mutations that affect different cellular pathways. Some of these have been classified as preleukemic, and a stepwise evolution program whereby cells acquire additional mutations has been proposed in the development of AML. How the timing of acquisition of these mutations and their impact on transformation and the bone marrow (BM) microenvironment occurs has only recently begun to be investigated. We show that constitutive and early loss of the epigenetic regulator, TET2, when combined with constitutive activation of FLT3, results in transformation of chronic myelomonocytic leukemia-like or myeloproliferative neoplasm-like phenotype to AML, which is more pronounced in double-mutant mice relative to mice carrying mutations in single genes. Furthermore, we show that in preleukemic and leukemic mice there are alterations in the BM niche and secreted cytokines, which creates a permissive environment for the growth of mutation-bearing cells relative to normal cells.

Indexed as

AnimalsBone Marrow CellsCell DifferentiationCell ProliferationCytokinesDioxygenasesDNA-Binding Proteinsfms-Like Tyrosine Kinase 3HeterozygoteHomozygoteHumansInflammation MediatorsLeukemia, Myeloid, AcuteMice, Inbred C57BLMutationNeoplastic Stem CellsCytokinesDioxygenasesDNA-Binding ProteinsFlt3 protein, mousefms-Like Tyrosine Kinase 3Inflammation MediatorsProto-Oncogene ProteinsTet2 protein, mouseAMLbone marrow microenvironmentCMMLcytokinesFlt3ITD/ITDMPNTET2

Identifiers

PMID32502465
PMCPMC7363747
OpenAlexW3033481409

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.