IGF-1 receptor antibody – a T-ALL order for lymphoblastic leukemia?

IGF1 is a member of the somatomedin, or insulin-like growth factor family. We at Novus Biologicals have an extensive range of IGF1 antibodies on our antibody database. An essential mediator of growth hormone function, IGF1is also linked to many types of cancer.

The association between raised IGF1 levels and increased risk of cancer has been well documented. Although IGF1production is at its highest in puberty, acting as an important mediator between growth hormone and childhood development, IGF-1 is continually expressed throughout adult life. IGF-1 antibody studies have shown the protein binds to both the insulin receptor and the IGF-1 receptor (IGF1R), being modulated by at least six IGF binding proteins.

As well as regulating cellular growth, development and proliferation, IGF-1 is thought to play a role in DNA synthesis, and to be a potent inhibitor of apoptosis. IGF-1 receptor binding is also known to be one of the most potent activators of the AKT intracellular signaling pathway.

A recent IGF1 antibody study suggested a strong link between IGF1 receptor populations, and T-cell acute lymphoblastic leukemia (T-ALL), a rare and aggressive form of cancer in adolescents. It is often defined by aberrations of the Notch1 and PI3K–Akt pathways, although the role of growth factor-dependent activation remains unclear. Now, antibody research published by A. Trumpp et al. has demonstrated that T-ALL is characterized by overexpression of IGF1R. When IGF1R was blocked or genetically deleted, the growth and viability of T-ALL cells was halted.

Furthermore, in murine transplantation experiments, partial blocking of IGF1R compromised leukemia-initiating cell (LIC) activity. Studies with IGF1R and Notch 1 antibodies revealed IGF1R to be a target for the Notch1 ligand, with Notch1 signaling necessary to maintain high levels of IGF1R expression in T-ALL cells. These results suggest Notch signalling effects on LIC activity could be regulated by amplifying T-ALL responsiveness to ambient growth factors, with IGF1R inhibitors possibly being of future therapeutic use to T-ALL sufferers.

Many of the antibodies used in this study can be found in our antibody catalog.

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