ic researchers and conducted a review of genetic and historical literature on the Ashkenazi Jewish population. The interviews revealed how geneticists came to substitute ethnicity for family history as the most relevant indicator of risk. Serendipity played a vital role. Researchers had previously found a high prevalence of a mutation causing Tay-Sachs disease in Ashkenazi Jews. Within 20 years, one-million Jews around the world had been tested for the mutation, and scientific institutions had created large repositories of genetic samples that could then be screened for the genetic mutations associated with breast cancer--but only in Ashkenazi Jews.

"The science of breast cancer genetics has been marked by methodological inconsistency in how researchers defined 'Ashkenazi Jew,'" said study coauthor Sherry Brandt-Rauf, JD, Associate Research Scholar at the Center. Most scientists relied on study participants' self-identification. Ashkenazi Jews are descended from Jews who lived in central and Eastern Europe, but a complex history of migrations, and multiple cultural and religious meanings of Ashkenazi, makes self-identification problematic.

The study also illuminates how geneticists interpreted Jewish history to support the theory of Ashkenazi genetic uniqueness. This interpretation views the historic Ashkenazi Jewish population as isolated, and as having undergone extreme expansions and contractions. It attributes Ashkenazi Jewish genetic uniqueness to "founder effects," the idea that genetic mutations can take hold and spread within small, geographically isolated populations, such as a group living alone on an island.

Although Ashkenazi Jews were never geographically isolated, Rothman said that "researchers made persecution--the pogroms and massacres in Jewish history--the equivalent of geographic isolation."

The study noted that a number of recent genetic surveys--including among Spanish, German, Dutch, Polish
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Contact: Janet Firshein
301-652-1558
Burness Communications
26-Oct-2006

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