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Shonnie Medina was a happy 
girl who felt she would die young.

Her physical beauty, when she was a young woman in Culebra and a young wife in Alamosa, was the primary thing that people mentioned about her. Photographs and snatches of videotape don’t quite capture it because fundamentally what people were talking about was charisma. It came through her looks when she was in front of you, tossing her full head of dark hair and giving you her full attention. Then her beauty acted like a mooring for her other outward qualities, undulating from that holdfast like fronds of kelp on the sea. Then Shonnie was magnetic, vain, kind to others, religious without reservation, funny, a little goofy, and headstrong.

Being headstrong or unreasonable was the quality that the doctors in Alamosa and Denver blamed for her death—for Shonnie was right about dying young. She carried in her cells a dangerous genetic mutation and died when she was 28, after refusing surgery for her aggressive, inherited breast cancer. Jealous of her body, oblivious to the gene, she insisted on 
another style of care.


Shonnie Medina grew up in the San Luis Valley of Colorado. Her family is Hispano, a mix of Spanish and Indian people. Older than other Hispanics in North America, the Hispanos claim a 400-year history in northern New Mexico and southern Colorado. Their villages, dotting the northern reach of the Rio Grande, were once as lively and insular as the shtetls of Eastern Europe.

The gene Shonnie inherited, known as BRCA1.185delAG, also has a long pedigree. Its discovery in the Hispano community confirmed events of half a millennium before in Spain that are echoing still. Most likely the mutation arrived by way of Sephardic Jews who converted to Catholicism under pressure from the Spanish Inquisition. From Spain they traveled to the New World, where eventually they seeded the modern Hispano population. Indian blood and new terrain erased part of the history those emigrants carried, assuming they were even aware of their Jewish legacy. For the Hispano Catholic people of northern New Mexico and southern Colorado, Jewish ancestry was a will-o’-the-wisp of memory and culture, which many people had heard about without knowing if it was true. Shonnie’s mutation shows that it is.

The breast-cancer mutation 185delAG entered the gene pool of Jews some 2,500 years ago, around the time they were exiled to Babylon. Random and unbidden, the mutation appeared on the chromosome of a single person, who is known as the founder. In the same sense that Abraham is said to have founded the Jewish people, scientists call the person at the top of a genetic pyramid a founder. This particular founder was born missing the letters A (for adenine) and G (guanine) from the DNA chain at the 185 site on one copy of his or her BRCA1 gene. BRCA1 is a tumor-suppressor gene; the deletion of the two letters disabled its protective function. But the mutation wasn’t immediately harmful to the founder because he or she had another copy of the gene that worked.

Researchers have no idea who the founder was, but they can deduce from historical evidence when he or she lived. When Jews were permitted to return to Jerusalem after their captivity in Babylon, not all the exiles went home. The ones who stayed behind are the ancestors of Iraqi Jews, whose numbers are today much reduced but who for centuries constituted a venerable center of the faith. In addition to the Jews living in Mesopotamia and Jerusalem, satellite immigrant communities sprang up elsewhere in the Middle East. A decentralization of the gene pool had begun, and the distances between groups acted as barriers to the exchange of DNA, barriers that have persisted into the modern day. When scientists in Israel tested BRCA1 carriers from the dispersed Jewish populations, they discovered that all shared the same basic spelling in the genetic region of 185delAG. But some of the matches between Jewish groups were off by a letter or two, which indicated minor changes since the groups had split. Rolling back the demographic clock, the scientists inferred that its founder must have lived before the groups divided—that is, prior to the Babylonian watershed.

Given that the 185delAG mutation originated among Jews, scientists think that when the mutation shows up in another ethnic or racial group—like Shonnie Medina’s Hispanos—it is because a Jew or a descendant of a Jew has married in. Beyond the bounds of Jewry, sightings of 185delAG are few. There are scattershot reports in the medical literature of gentile carriers in Spain, Chile, Slovakia, the Netherlands, Pakistan, India, even Africa, but most of these areas have or used to have Jewish enclaves. There are many American carriers who are not Jewish, but these people, like the Medinas, very likely have at least some Jewish ancestry.

So the gene that had followed Shonnie from Palestine to the Iberian Peninsula, and then to Mexico after Jews were expelled from Spain, and then from Mexico up the winding aisle of the Rio Grande, caught up with her at last in the remote, mountain-rimmed San Luis Valley. In 1998, hospitalized and close to the end of her life, Shonnie was advised to have a BRCA test. Her parents, Joseph and Marianne, went into their depleted savings and paid $2,800 for the analysis, which was not covered by her insurance. “Hmm,” said the genetic counselor, “your daughter is a carrier of 185delAG . . . but that’s the Ashkenazi mutation.” This was before the mutation’s link to Spanish or Sephardic Jews was known.

Given all that was going on with Shonnie, the Medinas put it out of their minds. The test was of no use to the patient anyway—it was a cancer alert to female relatives, but either the information wasn’t delivered properly to the family or else it didn’t sink in.

The Ashkenazim, who are originally from central and Eastern Europe, are the world’s most numerous population of Jews. Five and a half to six million Americans have Ashkenazi ancestry. Before they had to deal with heritable breast cancer and its lead agent, the BRCA1.185delAG mutation, a previous generation of Ashkenazim had confronted Tay-Sachs, another genetic disease. Tay-Sachs was (and is) a very grim neurological condition. Affected infants start life healthy but begin to lose muscular control at six months. Their heads loll helplessly and their vision dims; after a period of convulsions, they slide into coma and death.