Evidence map›Paper›PMID 18559972›Full record

ArticleBlood2008

Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells.

Winnie F Tam, Ting-Lei Gu, Jing Chen, Benjamin H Lee, Lars Bullinger, Stefan Fröhling, Andrew Wang, Stefano Monti, Todd R Golub, D Gary Gilliland

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy.International journal of medical sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. ID proteins regulate diverse aspects of cancer progression and provide novel therapeutic opportunities.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Review
  18. Review
  19. Article
  20. 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

10 authors at 5 institutions in 2 countries.

Winnie F TamHematology Division, Brigham and Women's Hospital, Boston, MA 02115, USA.
Ting-Lei Gu
Jing Chen
Benjamin H Lee
Lars Bullinger
Stefan Fröhling
Andrew Wang
Stefano Monti
Todd R Golub
D Gary Gilliland
Brigham and Women's Hospital · USHarvard University · USHoward Hughes Medical Institute · USMassachusetts Institute of Technology · USUniversity Hospital Ulm · DE

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
SIGNAL TRANSDUCTION PATHWAYS IN STABLE PHASE CHRONIC MYELOID LEUKEMIA CELLSP01DK050654 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN DAVID · 1996 to 2006
$10.3M
NCI NIH HHS P01 CA066996NIDDK NIH HHS P01 DK050654
6 · The paper itself

Abstract

Oncogenic tyrosine kinases, such as BCR-ABL, TEL-ABL, TEL-PDGFbetaR, and FLT3-ITD, play a major role in the development of hematopoietic malignancy. They activate many of the same signal transduction pathways. To identify the critical target genes required for transformation in hematopoietic cells, we used a comparative gene expression strategy in which selective small molecules were applied to 32Dcl3 cells that had been transformed to factor-independent growth by these respective oncogenic alleles. We identified inhibitor of DNA binding 1 (Id1), a gene involved in development, cell cycle, and tumorigenesis, as a common target of these oncogenic kinases. These findings were prospectively confirmed in cell lines and primary bone marrow cells engineered to express the respective tyrosine kinase alleles and were also confirmed in vivo in murine models of disease. Moreover, human AML cell lines Molm-14 and K562, which express the FLT3-ITD and BCR-ABL tyrosine kinases, respectively, showed high levels of Id1 expression. Antisense and siRNA based knockdown of Id1-inhibited growth of these cells associated with increased p27(Kip1) expression and increased sensitivity to Trail-induced apoptosis. These findings indicate that Id1 is an important target of constitutively activated tyrosine kinases and may be a therapeutic target for leukemias associated with oncogenic tyrosine kinases.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBenzamidesCell Line, TumorCell Transformation, NeoplasticGene ExpressionHL-60 CellsHumansImatinib MesylateInhibitor of Differentiation Protein 1K562 CellsLeukemiaLeukemia, ExperimentalMiceOncogenesAntineoplastic AgentsBenzamidesID1 protein, humanIdb1 protein, mouseImatinib MesylateInhibitor of Differentiation Protein 1PiperazinesProtein Kinase InhibitorsProtein-Tyrosine KinasesPyrimidinesQuinazolinesRNA, Small Interferingtandutinib

Identifiers

PMID18559972
PMCPMC2518899
OpenAlexW2072601028

What Socratic 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 Socratic graph.