IGF-1: An Important Myeloma Growth Factor
A study published in the journal Blood suggests that certain myeloma growth factors may one day serve as a target for therapies. This particular study found significant results pertaining to insulin-like growth factor type 1, or IGF-1.
IGF-1 is a molecule produced in bone marrow that binds to the IGF-1 receptor (IGF-1R), if present. Binding sets off a cascade of molecular events that ultimately stimulates cell growth. Many myeloma growth factors exist, and this study investigated five.
Using cell lines derived from human myeloma cells, the researchers found that of the five growth factors studied, IGF-1 significantly stimulated the growth of myeloma cells, as did interleuken-6 (IL-6).
The finding supports several other studies, and the researchers suggest that a therapy that inhibits IGF-1R could be useful in patients whose cells express the receptor. Normal immune system cells do not express the IGF-1R gene, but it is found in 30 to 50 percent of untreated myeloma patients.
In the second part of the study, the researchers found that the presence of IGF-1R correlated with poor prognosis in myeloma patients. Patients without IGF-1R had a longer median event-free survival and overall survival than patients with IGF-1R.
The researchers emphasize that the study does not suggest that presence of IGF-1R can be useful in defining new classifications for prognosis. Instead, they maintain that because the presence of IGF-1R in myeloma cells is correlated with poor prognosis, targeting IGF-1R could be promising for the treatment of myeloma patients.
For further details, see the article in the journal Blood (subscription required for full article; abstract available for free).
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What do you mean by "target" IGF-1r? Would it be suppressed or would there be attempts to increase the production of it? A little confused here, sorry.
Hi Tony,
Thanks for your question.
Since binding of IGF-1 to its receptor IGF-1R causes cell growth, the goal would be to inhibit IGF-1 from binding to IGF-1R. This is often done by creating a molecule that would mimic IGF-1. The mimic would bind to and block IGF-1R so that IGF-1 cannot bind. By preventing them from binding, the drug would therefore block uncontrolled cell growth.
Hopefully that helps clarify the issue. If you have any more questions, feel free to ask.
My father had non-hodgins lymphoma, which became leukemia. He passed away in 2006, I have been diagnosed with smoldering myeloma (2008). Would you like his records, to see if you can find any connection in genetics?