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A developmental model for thalidomide defects

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Abstract

Thalidomide was prescribed as a mild sedative until it was demonstrated in 1961 that it was responsible for inducing congenital malformations in children whose mothers took the drug during pregnancy. Perhaps the most striking aspect of this syndrome is phocomelia (a severe shortening of the limbs). The long bones are shorter than normal and more proximal elements are lost, such that in extreme cases the hand or fingers are attached directly to the shoulder, a condition described as resembling the flipper of a seal1,2. Here I show how these defects can be understood in the context of current models for limb patterning.

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Figure 1: Progress-zone model for thalidomide teratology.

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Authors and Affiliations

  1. Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, 02115, Massachusetts, USA

    Clifford J. Tabin

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  1. Clifford J. Tabin
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Tabin, C. A developmental model for thalidomide defects. Nature 396, 322–323 (1998). https://doi.org/10.1038/24516

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