Evidence map›Paper›PMID 15169904›Full record

ArticleMolecular and cellular biology2004

Role of pescadillo and upstream binding factor in the proliferation and differentiation of murine myeloid cells.

Marco Prisco, Arianna Maiorana, Clara Guerzoni, George Calin, Bruno Calabretta, Renate Voit, Ingrid Grummt, Renato Baserga

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.6field-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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Repression of PES1 expression inhibits growth of gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  5. Article
  6. Article
  7. MicroRNA-126-mediated control of cell fate in B-cell myeloid progenitors as a potential alternative to transcriptional factors.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  8. Article
  9. Targeting PES1 for restoring the ERα/ERβ ratio in breast cancer.The Journal of clinical investigation · 2012
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. 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 3 institutions in 2 countries.

Marco PriscoKimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Arianna Maiorana
Clara Guerzoni
George Calin
Bruno Calabretta
Renate Voit
Ingrid Grummt
Renato Baserga
Sidney Kimmel Cancer Center · USThomas Jefferson University · USGerman Cancer Research Center · DE

Funding

TRAIL Receptors in Apoptosis and CancerP01CA078890 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CALABRETTA, BRUNO · 1999 to 2007
$8.9M
REGULATION OF CELL PROLIFERATION BY GENES OF THE MYB FAMILYP01CA056309 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BASERGA, RENATO LUIGI · 1991 to 2001
$1.4M
NCI NIH HHS CA56309NCI NIH HHS CA78890NCI NIH HHS P01 CA078890
6 · The paper itself

Abstract

Pescadillo (PES1) and the upstream binding factor (UBF1) play a role in ribosome biogenesis, which regulates cell size, an important component of cell proliferation. We have investigated the effects of PES1 and UBF1 on the growth and differentiation of cell lines derived from 32D cells, an interleukin-3 (IL-3)-dependent murine myeloid cell line. Parental 32D cells and 32D IGF-IR cells (expressing increased levels of the type 1 insulin-like growth factor I [IGF-I] receptor [IGF-IR]) do not express insulin receptor substrate 1 (IRS-1) or IRS-2. 32D IGF-IR cells differentiate when the cells are shifted from IL-3 to IGF-I. Ectopic expression of IRS-1 inhibits differentiation and transforms 32D IGF-IR cells into a tumor-forming cell line. We found that PES1 and UBF1 increased cell size and/or altered the cell cycle distribution of 32D-derived cells but failed to make them IL-3 independent. PES1 and UBF1 also failed to inhibit the differentiation program initiated by the activation of the IGF-IR, which is blocked by IRS-1. 32D IGF-IR cells expressing PES1 or UBF1 differentiate into granulocytes like their parental cells. In contrast, PES1 and UBF1 can transform mouse embryo fibroblasts that have high levels of endogenous IRS-1 and are not prone to differentiation. Our results provide a model for one of the theories of myeloid leukemia, in which both a stimulus of proliferation and a block of differentiation are required for leukemia development.

Indexed as

AnimalsBase SequenceCell CycleCell Cycle ProteinsCell DifferentiationCell DivisionCell LineDNA, ComplementaryInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsLeukemia, MyeloidMiceModels, BiologicalMyeloid CellsPhosphoproteinsPol1 Transcription Initiation Complex ProteinsCell Cycle ProteinsDNA, ComplementaryInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsIrs1 protein, mousePes1 protein, mousePhosphoproteinsPol1 Transcription Initiation Complex ProteinsProteinsReceptor, IGF Type 1RNA-Binding Proteinstranscription factor UBF

Identifiers

PMID15169904
PMCPMC419857
OpenAlexW2169678275

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.