Research ArticleCancer

Blockade of Nonhormonal Fibroblast Growth Factors by FP-1039 Inhibits Growth of Multiple Types of Cancer

See allHide authors and affiliations

Science Translational Medicine  27 Mar 2013:
Vol. 5, Issue 178, pp. 178ra39
DOI: 10.1126/scitranslmed.3005414

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Treating Cancer by Design

The Renaissance man (or woman) is held up as an ideal of someone with diverse knowledge. Yet, today, it is increasingly difficult to both be broad and have sufficient depth of knowledge to be successful in any one field. Unfortunately, this is also the case for cancer therapies. The most obvious outward signs of some cancers—severe weight loss, tiredness, hair loss, nausea—are actually caused by the nonspecific breadth of the treatments. One pathway that has proved particularly intractable is the fibroblast growth factor (FGF) pathway, which promotes tumor growth and angiogenesis but also contributes key metabolic hormones. Now, Harding et al. have designed a soluble FGF receptor Fc fusion protein (FP-1039) to overcome these difficulties.

The authors tested the specificity of FP-1039 both in vitro and in vivo across a wide swath of cancer types. FP-1039 binds to mitogenic FGF ligands, blocking angiogenesis and inhibiting growth of tumors of many different types. Tumors with amplified expression of, or mutations in, FGF receptors (such as certain lung and endometrial cancers) were especially well targeted by this drug. In contrast, FP-1039 did not bind tightly to the hormonal FGFs, and treatment in animal models had minimal toxicity. Although this drug has only been tested in early-stage clinical trial in humans, these data support a specialized inhibition of mitogenic FGFs. Cancer drug design is truly entering the Age of Reason.