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Kathleen E. Richkind, PhD; Elena Boder, MD; Raymond L. Teplitz, MD

JAMA. 1982;248(11):1346-1347.

Abstract
Ataxia-telangiectasia (AT) is a genetic disorder of unknown pathogenesis, with primary effects on the immune and nervous systems. The presence of a fetal-like thymus and elevated a-fetoprotein (aFP) levels in patients with AT suggests that suppressed mesodermal development may be a factor in the development of this disease. We investigated this hypothesis by using electrophoretic and quantitative analyses to test for the presence of other fetal proteins in mesodermal tissues. With the exceptions of aFP and carcinoembryonic antigen, all other proteins assessed in these patients were present at levels or in isozymic patterns characteristic of a normal, nonfetal state.

(JAMA 1982;248:1346-1347)

Author Affiliations
From the Division of Cytogenetics and Cytology, City of Hope Medical Center, Duarte, Calif (Drs Richkind and Teplitz); and the Department of Pediatrics, UCLA Medical Center, Los Angeles (Dr Boder).

Footnotes
Presented in part at the Sixth International Congress of Human Genetics, Jerusalem, Israel, September 1981.

Reprint requests to Division of Cytogenetics and Cytology, City of Hope Medical Center, 1500 E Duarte Rd, Duarte, CA 91010 (Dr Teplitz).

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