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ShareApr. 28, 2009 — Several forms of cancer, including bladder cancer and multiple myeloma caused by the t(4;14) genetic abnormality, are associated with either overexpression or perpetual activation of the protein FGFR3.
A team of researchers, at Genentech Inc., South San Francisco, has now generated evidence that FGFR3 might be a good therapeutic target for these diseases and developed an FGFR3-targeted antibody that had potent antitumor activity in mice transplanted with either human bladder cancer cells or t(4;14)-positive multiple myeloma cells.
Additional in vivo and in vitro analysis indicated that the antibody was active against normal FGFR3 and mutated forms of the protein that are associated with cancer. The authors therefore suggest that antibody targeting of FGFR3 might be a viable therapeutic approach to treating cancers associated with aberrant expression or activation of FGFR3.
In an accompanying commentary, Yaron Hadari and Joseph Schlessinger, highlight the importance of these data and suggest that they might be relevant to other diseases, as similar FGFR3 mutations have been found to cause some skeletal dysplasias, disorders that cause abnormal shape and size of the skeleton.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Qing et al. Antibody-based targeting of FGFR3 in bladder carcinoma and t(4;14)-positive multiple myeloma in mice. Journal of Clinical Investigation, 2009; DOI: 10.1172/JCI38017
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