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Peptide Growth Factors: The Parallel Between Fetal Development and Malignant Transformation
Author(s) -
MYERS CHARLES
Publication year - 1991
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.1991.tb01081.x
Subject(s) - autocrine signalling , growth factor , epidermal growth factor , growth factor receptor inhibitor , fibroblast growth factor , biology , microbiology and biotechnology , growth factor receptor , receptor , transforming growth factor , fibroblast growth factor receptor 3 , fibroblast growth factor receptor , malignant transformation , suramin , cell growth , paracrine signalling , epidermal growth factor receptor , cancer research , signal transduction , biochemistry
Normal embryonic development and tissue homeostasis depend upon cell‐to‐cell and tissue‐to‐tissue communication. Much of this depends upon the production and release of peptide growth regulators such as fibroblast growth factor, epidermal growth factor, etc. As the molecular basis of malignant transformation has been documented, it is apparent that a common means by which a tumor becomes autonomous of external control is by becoming independent of the need for external growth factor stimulation. This can occur through the cell producing and releasing the growth factors needed for its own growth. A similar end result can occur with growth factor receptor mutants in which the receptor gives a positive signal even when no growth factor is bound to the receptor. One potential therapeutic strategy is to interfere with this autocrine loop. Suramin is presented as an example of a drug capable of blocking such autocrine loops. This drug also reverses malignant transformation due to Platelet Derived Growth Factor and K‐fgf/hst oncogenes on this basis. Another potential mechanism to accomplish the same end is through the use of monoclonal antibodies to either the growth factor or its receptor. Examples of this are available for TGF‐alpha. We have discussed a range of practical issues involved in developing monoclonal antibodies as therapeutic agents.