Evidence map›Paper›PMID 14961028›Full record

ArticleLeukemia2004

p210BCR/ABL-induced alteration of pre-mRNA splicing in primary human CD34+ hematopoietic progenitor cells.

S Salesse, S J Dylla, C M Verfaillie

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Role of Pyk2 in Human Cancers.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Chronic myeloid leukemia stem cell biology.Current hematologic malignancy reports · 2012
    Article
  15. Article
  16. Review
  17. Chronic myeloid leukemia: mechanisms of blastic transformation.The Journal of clinical investigation · 2010
    Review
  18. Hematopoietic Pyk2 regulates migration of differentiated HL-60 cells.Journal of inflammation (London, England) · 2010
    Article
  19. Article
  20. Glycogen synthase kinase 3beta missplicing contributes to leukemia stem cell generation.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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

3 authors at 1 institution in 1 country.

S SalesseStem Cell Institute, University of Minnesota, Minneapolis, MN 55455, USA.
S J Dylla
C M Verfaillie
University of Minnesota · US

Funding

TRAINING GRANT IN MICROBIOLOGY/CANCER RESEARCHT32CA009138 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Scott M. Dehm · 1985 to 2026
$11.3M
NEGATIVE REGULATORY EFFECTS OF STROMA/PROGENITOR CONTACTR01HL049930 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI VERFAILLIE, CATHERINE M · 1994 to 2003
$1.1M
BETA-1 INTEGRINS &HEMATOPOIETIC PROGENITORS ENGRAFTMENTR01DK053673 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI VERFAILLIE, CATHERINE M · 1997 to 2000
$250k
NCI NIH HHS CA09138NHLBI NIH HHS R01 HL-49930NIDDK NIH HHS R01 DK-53673
6 · The paper itself

Abstract

Chronic myelogenous leukemia (CML) is a malignancy of the human hematopoietic stem cell (HSC) caused by the p210BCR/ABL oncoprotein. Although alternative splicing of pre-mRNA is a critical determinant of a cell's protein repertoire, it has not been associated with CML pathogenesis. We identified a BCR/ABL-dependent increase in expression of multiple genes involved in pre-mRNA splicing (eg SRPK1, RNA Helicase II/Gu, and hnRNPA2/B1) by subtractive hybridization of cDNA from p210BCR/ABL-eGFP vs eGFP-transduced umbilical cord blood CD34+ cells. beta1-integrin signaling is important to HSC maintenance and proliferation/differentiation, and is abnormal in CML. As an example of how changes in pre-mRNA processing might contribute to CML pathogenesis, we observed alternative splicing of a gene for a beta1-integrin-responsive nonreceptor tyrosine kinase (PYK2), resulting in increased expression of full-length Pyk2 in BCR/ABL-containing cells. Treatment of p210BCR/ABL-positive cells with the Abl-specific tyrosine kinase inhibitor STI571 reverted PYK2 splicing to a configuration more consistent with normal cells, and correlated with decreased expression of BCR/ABL-induced proteins involved in pre-mRNA processing. Whether altered PYK2 splicing contributes to CML pathogenesis remains undetermined; however, we propose that generic changes in pre-mRNA splicing as a result of p210BCR/ABL kinase activity may contribute to CML pathogenesis.

Indexed as

RNA SplicingAntigens, CD34Focal Adhesion Kinase 2Fusion Proteins, bcr-ablHematopoietic Stem CellsHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, Myeloid, Chronic-PhaseNeoplastic Stem CellsProtein-Tyrosine KinasesRNA PrecursorsAntigens, CD34Focal Adhesion Kinase 2Fusion Proteins, bcr-ablProtein-Tyrosine KinasesRNA Precursors

Identifiers

PMID14961028
OpenAlexW1997500900

What OpenQuestion holds

Textmetadata
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.