Evidence map›Paper›PMID 16642049›Full record

ArticleLeukemia2006

Synergy between an IGF-1R antibody and Raf/MEK/ERK and PI3K/Akt/mTOR pathway inhibitors in suppressing IGF-1R-mediated growth in hematopoietic cells.

F E Bertrand, L S Steelman, W H Chappell, S L Abrams, J G Shelton, E R White, D L Ludwig, J A McCubrey

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Notch Partners in the Long Journey of T-ALL Pathogenesis.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Upregulation of IGF1R by mutant RAS in leukemia and potentiation of RAS signaling inhibitors by small-molecule inhibition of IGF1R.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  13. Review
  14. Article
  15. Overcoming IGF1R/IR resistance through inhibition of MEK signaling in colorectal cancer models.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  16. Rational combination of a MEK inhibitor, selumetinib, and the Wnt/calcium pathway modulator, cyclosporin A, in preclinical models of colorectal cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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 1 institution in 1 country.

F E BertrandDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27384, USA.
L S Steelman
W H Chappell
S L Abrams
J G Shelton
E R White
D L Ludwig
J A McCubrey
East Carolina University · US

Funding

Ras/Raf &PI3K/Akt Induced Breast Cancer Drug ResistanceR01CA098195 · NCI · EAST CAROLINA UNIVERSITY · PI MC CUBREY, JAMES A · 2003 to 2007
$1.5M
NCI NIH HHS R01 CA098195
6 · The paper itself

Abstract

The Insulin-like growth factor-1 receptor (IGF-1R) is overexpressed in a variety of tumors including breast, prostate and myeloma. Thus, IGF-1R and its downstream signaling effectors are good candidates for molecular-based targeted antitumor therapies. Indeed, protein inhibitors of IGF-1R signaling and IGF-1R blocking antibodies are undergoing clinical trials. Herein, the molecular basis for antibody-mediated IGF-1R signal inhibition has been investigated in a hematopoietic cell line model, FDC-P1, that has been rendered interleukin-3 independent in a ligand-dependent manner through retroviral-mediated expression of IGF-1R (FD/IGF-1R). Furthermore, the ability of an anti-IGF-1R antibody to synergize with signal-transduction pathway inhibitors and induce apoptosis was determined. The alphaIGF-1R antibody, A12, was capable of arresting IGF-1 or insulin-induced FD/IGF-1R cell proliferation in the G1 phase of the cell cycle and resulted in apoptotic induction. A12 effectiveness could be potentiated through combination treatment with small molecule inhibitors of the Ras/Raf/MEK/ERK or PI3K/Akt/mTOR pathways. These results validate the use of the FD/IGF-1R cells to evaluate the effectiveness and mechanisms of targeted IGF-1R therapeutic strategies.

Indexed as

AnimalsAntibodies, MonoclonalAntibody SpecificityApoptosisCell DivisionCell Line, TransformedEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesG1 PhaseHematopoietic Stem CellsImmunotherapyInsulin-Like Growth Factor ILeukemiaMiceMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesAntibodies, MonoclonalEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesInsulin-Like Growth Factor IMitogen-Activated Protein KinasesmTOR protein, mousePhosphatidylinositol 3-KinasesProtein KinasesProto-Oncogene Proteins c-aktraf KinasesReceptor, IGF Type 1TOR Serine-Threonine Kinases

Identifiers

PMID16642049
OpenAlexW2015673732

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.