Customizing the Targeting of IGF-1 Receptor

Renato Baserga

Disclosures

Future Oncol. 2009;5(1):43-50. 

In This Article

Conclusion & Future Perspective

A list of suggestions for customizing IGF-IR targeting is provided in the Executive summary. One has to seriously consider the hypothesis that cancer cells can acquire the ability of using one growth factor rather than another, depending on circumstances, and that the response to a growth factor is an acquired taste. In some cases, this is due to a change in the signaling pathways, such as when IRS-1 transforms the IGF-IR from a receptor that causes differentiation to a mitogenic receptor. In other cases, it may be due to the ready availability of a given growth factor, such as in metastases from colon cancer or uveal melanomas, where the cancer cells find themselves awash in IGF-1. The hypothesis of some investigators that cancer cells may become 'oncogene-addicted' should perhaps be modified to cancer cells becoming oncogene- and/or growth factor-addicted. Addiction to IGFs should be considered a requirement for a successful therapy based on IGF-IR antibodies (and eventually small molecules). Nuclear translocation of IRS-1 is not an artifact of cell cultures. Nuclear IRS-1 has been found repeatedly in human breast cancers, in human medulloblastoma, and even in normal rat liver (reviewed in[7]). Expression of IRS-1, especially nuclear IRS-1, is, in my opinion, the second requirement and a biomarker for sensitivity to IGF-IR targeting.

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