Evidence map›Paper›PMID 18246120›Full record

ArticleOncogene2008

Bcr-Abl induces autocrine IGF-1 signaling.

A Lakshmikuttyamma, E Pastural, N Takahashi, K Sawada, D P Sheridan, J F DeCoteau, C R Geyer

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. 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
3.5field-weighted citation impact, top 7% 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, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Impact of metformin on tyrosine kinase inhibitor response in chronic myeloid leukemia.Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners · 2022
    Observational
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. IGF1 stimulates crypt expansion via differential activation of 2 intestinal stem cell populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  12. IGF-IR determines the fates of BCR/ABL leukemia.Journal of hematology & oncology · 2015
    Article
  13. Association of preoperative serum IGF- I concentration with clinicopathological parameters in patients with non-small cell lung cancer.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

7 authors at 2 institutions in 2 countries.

A LakshmikuttyammaGenomic Medicine and Pathobiology Research Group, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
E Pastural
N Takahashi
K Sawada
D P Sheridan
J F DeCoteau
C R Geyer
University of Saskatchewan · CAAkita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bcr-Abl oncogene is responsible for the initial phase of chronic myelogenous leukemia (CML), which is effectively treated by the Bcr-Abl inhibitor imatinib. Over time patients become resistant to treatment and progress to blast crisis, an event that is driven by additional genetic and epigenetic aberrations. Recently, we showed that Riz1 expression decreases in blast crisis and that re-expression of Riz1 inhibits IGF-1 expression. IGF-1 signaling is required in many stages of hematopoiesis and inappropriate activation of autocrine IGF-1 signaling may facilitate transformation to blast crisis. We observed that in 8 out of 11 matched CML patient biopsies the IGF-1 expression is elevated in blast crisis. We examined mechanisms used by CML blast crisis cell lines to activate IGF-1 expression. We found that Bcr-Abl activates autocrine IGF-1 signaling using Hck and Stat5b. Inhibition of these signaling components using small molecule drugs or shRNA decreases proliferation and enhances apoptosis. Together, our study suggests that aberrant IGF-1 signaling is an important event in blast crisis transformation and it provides a mechanism to explain the activity of IGF-1R and Hck inhibitors in blocking CML blast crisis phenotypes.

Indexed as

Antineoplastic AgentsBenzamidesBlast CrisisFusion Proteins, bcr-ablGene Expression Regulation, NeoplasticHumansImatinib MesylateInsulin-Like Growth Factor ILeukemia, Myelogenous, Chronic, BCR-ABL PositivePiperazinesProto-Oncogene Proteins c-hckPyrimidinesRNA, MessengerSignal TransductionSTAT5 Transcription FactorAntineoplastic AgentsBenzamidesFusion Proteins, bcr-ablHCK protein, humanImatinib MesylateInsulin-Like Growth Factor IPiperazinesProto-Oncogene Proteins c-hckPyrimidinesRNA, MessengerSTAT5B protein, humanSTAT5 Transcription Factor

Identifiers

PMID18246120
OpenAlexW2091998318

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.