Evidence map›Paper›PMID 11420675›Full record

ArticleOncogene2001

Autocrine and paracrine effects of an ES-cell derived, BCR/ABL-transformed hematopoietic cell line that induces leukemia in mice.

D G Peters, K M Klucher, R C Perlingeiro, S K Dessain, E Y Koh, G Q Daley

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  3. Article
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  5. Article
  6. CREB in the pathophysiology of cancer: implications for targeting transcription factors for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  7. Article
  8. Review
  9. Article
  10. Article
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  12. IL-3 receptor signaling is dispensable for BCR-ABL-induced myeloproliferative disease.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  13. Article
  14. Review
  15. 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

6 authors at 2 institutions in 1 country.

D G PetersWhitehead Institute, 9 Cambridge Center, Cambridge, Massachusetts, MA 02142, USA.
K M Klucher
R C Perlingeiro
S K Dessain
E Y Koh
G Q Daley
Harvard University · USWhitehead Institute for Biomedical Research · US

Funding

Therapeutic Mechanisms in Chronic Myelogenous LeukemiaR01CA086991 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DALEY, GEORGE Q · 2001 to 2005
$1.5M
PROGRESSION OF CHRONIC MYELOGENOUS LEUKEMIAK08HL004463 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI DESSAIN, SCOTT KENDALL · 2000 to 2004
$649k
MOLECULAR PATHWAYS IN MYELOPROLIFERATIVE DISEASER29CA076418 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DALEY, GEORGE Q · 1998 to 2002
$261k
NCI NIH HHS CA76418-01NCI NIH HHS CA86991-01NHLBI NIH HHS K08 HL 04463
6 · The paper itself

Abstract

During differentiation in vitro, Embryonic Stem (ES) cells generate both primitive erythroid and definitive myeloid lineages in a process that mimics hematopoiesis in the mammalian yolk sac. To investigate leukemic transformation of these embryonic hematopoietic progenitors, we infected differentiating cultures of ES cells with the Chronic Myeloid Leukemia-specific BCR/ABL oncoprotein. Following a period of liquid culture, we isolated two transformed subclones, EB57 and EB67, that retained characteristics of embryonic hematopoietic progenitors and induced a fatal leukemia in mice characterized by massive splenomegaly and granulocytosis. Histopathology of the spleen revealed an abundance of undifferentiated blast-like cells. Investigation of the clonal origins of the granulocytes in the peripheral blood demonstrated that the injected donor cells contributed modestly to the granulocyte population while the majority were host-derived. EB57 secretes IL-3 and unidentified cytokines that can stimulate autocrine and paracrine cell proliferation, presumably accounting for the reactive granulocytosis in diseased mice. These BCR/ABL transformed hematopoietic derivatives of ES cells recapitulate the relationship of BCR/ABL expression to IL-3 production that has been described for primitive hematopoietic progenitors from human CML patients, and illustrates the potential for autocrine and paracrine effects of BCR/ABL-infected cells in murine models.

Indexed as

Genes, ablAnimalsAntigens, SurfaceCell DifferentiationCell Line, TransformedCell Transformation, ViralErythroid Precursor CellsFusion Proteins, bcr-ablGranulocytesHematopoietic Stem CellsInterleukin-3Leukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMice, Inbred BALB CRetroviridaeReverse Transcriptase Polymerase Chain ReactionAntigens, SurfaceFusion Proteins, bcr-ablInterleukin-3

Identifiers

PMID11420675
OpenAlexW2328341306

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.