Evidence map›Paper›PMID 14997210›Full record

ArticleBritish journal of cancer2004

Specific roles for the PI3K and the MEK-ERK pathway in IGF-1-stimulated chemotaxis, VEGF secretion and proliferation of multiple myeloma cells: study in the 5T33MM model.

E Menu, R Kooijman, E Van Valckenborgh, K Asosingh, M Bakkus, B Van Camp, K Vanderkerken

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 113 citations in OpenAlex.

  1. A Phase II Trial of AZD6244 (Selumetinib, ARRY-142886), an Oral MEK1/2 Inhibitor, in Relapsed/Refractory Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Trial
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  14. Immunological Prognostic Factors in Multiple Myeloma.International journal of molecular sciences · 2021
    Review
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  17. Article
  18. Article
  19. Review
  20. Role of Galectins in Multiple Myeloma.International journal of molecular sciences · 2017
    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

7 authors at 2 institutions in 1 country.

E MenuDepartment of Hematology and Immunology, Vrije Universiteit Brussel - VUB, 1090 Brussels, Belgium.
R Kooijman
E Van Valckenborgh
K Asosingh
M Bakkus
B Van Camp
K Vanderkerken
Vrije Universiteit Brussel · BEUniversitair Ziekenhuis Brussel · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-like growth factor-1 (IGF-1) has been described as an important factor in proliferation, cell survival and migration of multiple myeloma (MM) cells. Angiogenesis correlates with development and prognosis of the MM disease. Vascular endothelial growth factor (VEGF) is one of the prominent factors involved in this process. The different functions of IGF-1 were investigated in the 5TMM mouse model with emphasis on proliferation, migration and VEGF secretion, and the signalling pathways involved. Western Blot analysis revealed that ERK1/2 and Akt (PKB) were activated after IGF-1 stimulation. The activation of ERK1/2 was reduced by the PI3K inhibitor Wortmannin, implying that the PI3K pathway is involved in its activation. Insulin-like growth factor-1 induced an increase in DNA synthesis in MM cells, which was mediated by a PI3K/Akt-MEK/ERK pathway. Insulin-like growth factor-1 enhanced F-actin assembly and this process was only PI3K mediated. Stimulation by IGF-1 of VEGF production was reduced by PD98059, indicating that only the MEK-ERK pathway is involved in IGF-1-stimulated VEGF production. In conclusion, IGF-1 mediates its multiple effects on MM cells through different signal transduction pathways. In the future, we can study the potential in vivo effects of IGF-1 inhibition on tumour growth and angiogenesis in MM.

Indexed as

Protein Serine-Threonine KinasesAnimalsCell DivisionCell MovementChemotaxisDisease Models, AnimalDown-RegulationFlavonoidsHumansInsulin-Like Growth Factor IMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinases2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneAKT1 protein, humanFlavonoidsInsulin-Like Growth Factor IMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor A

Identifiers

PMID14997210
PMCPMC2409634
OpenAlexW2049101520

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.