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centimetres in diameter. One of the lumps contained another, smaller cyst, filled with hair intermixed with a greasy yellow substance and some fluid. The other lump was more surprising. Encased in a tortuous network of blood vessels, the doctors uncovered another, smaller growth. There were no muscles, ligaments, or organs inside the homunculus, but from the outside it looked eerily like a tiny, dismembered baby, lying face down, with only a hirsute head and part of its right arm formed. The head was partially split open, and from it spilled a herniated brain. X-rays revealed an imperfect but impressively well-crafted skull, shaped somewhat like a cross between a Spartan and a Samurai helmet. The skull bones included easily recognizable structures, including a cranium and a jawbone.

The following year, in 2003, Japanese doctors operating on a twenty-five-year-old virgin identified the most fully formed teratoma found to date. Once again the outer layer of the tumour was filled with a mixture of hair and fat. Cutting through this mess of cells, the woman’s doctors found a solid, hard lump. When the lump was cleaned up, the doctors could see that it was a small, ‘doll-like’ body, mostly complete. Like any normal foetus, the body was covered with fine, downy hair, but the homunculus was unmistakably deformed. It appeared to have spina bifida, a condition in which the ectoderm doesn’t quite finish rolling up into the spinal column (the name is Latin for ‘split spine’). Its head exhibited malformations normally seen in babies with holoprosencephalia, which occurs when the forebrain of the embryo fails to divide fully into two normal hemispheres. In the centre of the forehead was a single soft, spherical, fluid-filled ‘eye’ cloaked by thick, long eyelashes – a disorder named cyclopia, for the one-eyed Cyclops of Greek mythology. This strange foetus had one ear, all its limbs, a brain, a spinal nerve, intestines, bones, and blood vessels – even a jaw, already ruptured by several teeth, emerging from beneath the skin. Paradoxically, it also had what looked like a phallus, positioned neatly between its legs.

A complete human is built from the instructions spelled out on our forty-six chromosomes. Twenty-three of these we inherit from our mother’s egg, and twenty-three from our father’s sperm. The egg and the sperm, unlike every other cell in the human body (except red blood cells, which contain no chromosomal DNA), therefore each have only twenty-three chromosomes. When egg and sperm fuse during fertilization, these chromosomes are paired – say, chromosome 15 from your mother’s egg will be matched with chromosome 15 from your father’s sperm – and form a full double-helix set of forty-six chromosomes in the resulting cells.

If you were then to compare the genes on these two sets of chromosomes, you would find that they are either homozygous (encoding the same instructions) or heterozygous (encoding different instructions) for certain genes that lead to a child’s inheritance. Take EYCL3, one of the genes that spell out the colour of your eyes. EYCL3 is located on chromosome 15 and codes for either a blue or brown tint in the iris. The chromosomes 15 that you inherited from your mother and your father may both carry the blue variant of the gene, in which case you are homozygous for this gene and are likely to have been born with blue eyes. On the other hand, the chromosome 15 you inherited from your father may encode brown eye colour, and the one from your mother may encode blue eye colour, and in this case, you are heterozygous for the EYCL3 gene and will probably have brown eyes. (The inheritance of eye colour is quite a bit more complex than that, involving several genes and their interactions.)

By this logic, the DNA of ovarian teratomas, coming only from an egg, should be homozygous – it all comes from the mother, after all. But some genes in mature ovarian teratomas have been found to be heterozygous. And teratomas almost always contain forty-six chromosomes, with any outliers involving missing or extra chromosomes – a teratoma with forty-five, forty-seven or forty-eight chromosomes, not the twenty-three available in the egg. The missing or extra chromosomes do affect the development of the teratoma: having three copies of chromosome 13 has also been implicated in the fused brain and ‘cyclops’ eye features that appeared on the Japanese homunculus. But the teratomas seem to gain or lose chromosomes fairly randomly; some have lost chromosome 13; others have gained an extra copy of chromosome 21, which, in a fertilized embryo, sometimes causes Down syndrome. Not even the sex chromosomes are off-limits: though teratomas nearly always have the XX chromosome signature of a female, a few have been found to contain XXX (one extra X), XXXX (two extra Xs) or XO (a missing X). The one thing that seems to be true of all teratomas, however, is that they never have a Y chromosome, which makes sense, since eggs should never carry this genetic material. Even without a Y, these kinds of tumours have been known to grow prostate tissue, even more often than tumours of the male testis do.

The very fact that ovarian teratomas appear raises many intriguing questions. What makes an unfertilized egg start dividing? How does the teratoma end up with two or more sets of chromosomes, when no other source – say, a father – has contributed to the teratoma’s creation? How is it that the teratoma can have two different versions of the same gene if it started life as an egg, which would hold a copy of just one version? How does it grow prostate tissue or phallus-like organs when an egg has merely the X female sex chromosome at its disposal? And how does the egg get around the requirement for other, non-genetic components, such as the centriole, which