Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2009 Mar 10;28(1):35.
doi: 10.1186/1756-9966-28-35.

Reduction of serum IGF-I levels in patients affected with Monoclonal Gammopathies of undetermined significance or Multiple Myeloma. Comparison with bFGF, VEGF and K-ras gene mutation

Claudia Greco  1 , Gaetano Vitelli, Giuseppe Vercillo, Rosa Vona, Diana Giannarelli, Isabella Sperduti, Francesco Pisani, Ettore Capoluongo, Maria Concetta Petti, Franco Ameglio
Affiliations

Reduction of serum IGF-I levels in patients affected with Monoclonal Gammopathies of undetermined significance or Multiple Myeloma. Comparison with bFGF, VEGF and K-ras gene mutation

Claudia Greco et al. J Exp Clin Cancer Res. .

Abstract

Background: Serum levels of IGF-I in patients affected with multiple myeloma (MM) have been scarcely studied. The present study is aimed to explore this point comparing 55 healthy subjects, 71 monoclonal gammopaties of uncertain significance (MGUS) and 77 overt MM patients. In the same subjects, basic FGF and VEGF, have been detected. All three mediators were analyzed in function of K-ras mutation and melphalan response. Concerning IGF-I, two representative monitoring examples have also been added.

Methods: Cytokine determinations were performed by commercially available ELISA kits, while K12-ras mutation was investigated on genomic DNA isolated from bone marrow cell specimens by RFLP-PCR assay.

Results: Significant reductions of IGF-I levels were observed in MGUS and MM as compared with healthy controls. In addition, MM subjects showed significantly decreased serum IGF-I levels than MGUS. Conversely, increasing levels were observed for bFGF and VEGF, molecules significantly correlated. A multivariate analysis corrected for age and gender confirmed the significant difference only for IGF-I values (P = 0.01). K12-ras mutation was significantly associated with malignancy, response to therapy and with significantly increased serum bFGF levels.

Conclusion: IGF-I reduction in the transition: Controls-->MGUS-->MM and changes observed over time suggest that IGF-I should be furtherly studied in future clinical trials as a possible monitoring marker for MM.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Serial measurements of IGF-1 and serum M-Protein (s-MP) from diagnosis (0) to last follow-up before death in two MM patients. Serum MP concentrations were derived from medical records. The first arrow indicates when MP treatment started, according to the protocol described in "Methods; the others two arrows indicate the repetition of new cycles of therapy due to disease progression. [symbols: cube = IGF-I; diamond = s-M protein].
See this image and copyright information in PMC

References

    1. Berenson JR, Ed . Humana Press. New Jersey, USA; 2004. Biology and management of multiple myeloma.
    1. Zhong H, Bowen JP. Antiangiogenesis drug design: multiple pathways targeting tumour vasculature. Curr Med Chem. 2006;13:849–862. doi: 10.2174/092986706776361085. - DOI - PubMed
    1. Shih T, Lindley C. Bevacizumab: an angiogenesis inhibitor for the treatment of solid malignancies. Clin Ther. 2006;28:1779–1802. doi: 10.1016/j.clinthera.2006.11.015. - DOI - PubMed
    1. Rosinol L, Cibeira MT, Segarra M, Cid MC, Filella X, Aymerich M, Rozman M, Arenillas L, Esteve J, Blade J, Montserrat E. Response to Thalidomide in multiple myeloma: impact of angiogenic factors. Cytokine. 2004;26:145–148. doi: 10.1016/j.cyto.2004.02.002. - DOI - PubMed
    1. Ribatti D, Nico B, Vacca A. Importance of the bone marrow microenvironment in inducine the angiogenic response in multiple myeloma. Oncogene. 2006;25:4257–4266. doi: 10.1038/sj.onc.1209456. - DOI - PubMed

MeSH terms

Substances