Evidence map›Paper›PMID 26338970›Full record

ArticleOncotarget2015

Stat5-deficient hematopoiesis is permissive for Myc-induced B-cell leukemogenesis.

Zhengqi Wang, Magdalena Medrzycki, Silvia T Bunting, Kevin D Bunting

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. 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
1.3field-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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. STAT5 as a Key Protein of Erythropoietin Signalization.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. PD-1 regulates KLRG1The Journal of experimental medicine · 2017
    Article
  12. Article
  13. 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

4 authors at 2 institutions in 1 country.

Zhengqi WangDepartment of Pediatrics, Division of Hematology-Oncology-BMT, Aflac Cancer and Blood Disorders Center of Children's Healthcare of Atlanta and Emory University, Atlanta GA, USA.
Magdalena MedrzyckiDepartment of Pediatrics, Division of Hematology-Oncology-BMT, Aflac Cancer and Blood Disorders Center of Children's Healthcare of Atlanta and Emory University, Atlanta GA, USA.
Silvia T BuntingDepartment of Pathology, Children's Healthcare of Atlanta, Atlanta GA, USA.
Kevin D BuntingDepartment of Pediatrics, Division of Hematology-Oncology-BMT, Aflac Cancer and Blood Disorders Center of Children's Healthcare of Atlanta and Emory University, Atlanta GA, USA.
Children's Healthcare of Atlanta · USEmory University · US

Funding

STAT5 Structure-Function in HematopoiesisR01DK059380 · NIDDK · EMORY UNIVERSITY · PI BUNTING, KEVIN D · 2002 to 2017
$4.2M
NIDDK NIH HHS NIH R01DK059380NIDDK NIH HHS R01 DK059380
6 · The paper itself

Abstract

Despite being an attractive molecular target for both lymphoid and myeloid leukemias characterized by activated tyrosine kinases, the molecular and physiological consequences of reduced signal transducer and activator of transcription-5 (Stat5) during leukemogenesis are not well known. Stat5 is a critical regulator of mouse hematopoietic stem cell (HSC) self-renewal and is essential for normal lymphocyte development. We report that pan-hematopoietic deletion in viable adult Vav1-Cre conditional knockout mice as well as Stat5ab(null/null) fetal liver transplant chimeras generated HSCs with reduced expression of quiescence regulating genes (Tie2, Mpl, Slamf1, Spi1, Cited2) and increased expression of B-cell development genes (Satb1, Dntt, Btla, Flk2). Using a classical murine B-cell acute lymphoblastic leukemia (B-ALL) model, we demonstrate that these HSCs were also poised to produce a burst of B-cell precursors upon expression of Bcl-2 combined with oncogenic Myc. This strong selective advantage for leukemic transformation in the background of Stat5 deficient hematopoiesis was permissive for faster initiation of Myc-induced transformation to B-ALL. However, once established, the B-ALL progression in secondary transplant recipients was Stat5-independent. Overall, these studies suggest that Stat5 can play multiple important roles that not only preserve the HSC compartment but can limit accumulation of potential pre-leukemic lymphoid populations.

Indexed as

HematopoiesisAnimalsBone Marrow TransplantationCell Transformation, NeoplasticDisease ProgressionGene Expression Regulation, LeukemicGenetic Predisposition to DiseaseHematopoietic Stem CellsLeukemia, B-CellLiverMice, Inbred C57BLMice, KnockoutPhenotypePrecursor Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mycBcl2 protein, mouseMyc protein, mouseProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mycStat5a protein, mouseStat5b protein, mouseSTAT5 Transcription FactorB-cell transformationhematopoiesisleukemogenesislymphoid-primed multipotent progenitortranscription factor

Identifiers

PMID26338970
PMCPMC4745704
OpenAlexW1949975475

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.