We observed suggestive culture adaptation and growth advantages in these lines, as well as gains of known oncogenes and the possible deletion or loss of putative yet unrecognized tumor suppressor genes. The SNP arrays also revealed 10-Deacetylbaccatin III potentially tumorigenic changes in the karyotypically normal hESC lines. The hESC line CH-ES1 showed many characteristics typical of a teratocarcinoma-derived EC cell line. Spontaneous teratocarcinomas generally arise from primordial germ cells, typically in the testis, but also occasionally in the ovary or at non-gonad sites. Experimental teratocarcinomas may also be derived from ectopically transplanted embryos. A single blastomere of a four-cell stage human embryo could therefore also form a teratocarcinoma. It is likely that the blastomere cell that gave rise to the CH-ES1 line had an abnormal genetic constitution, which is very common in human pre-implantation embryos. Human EC cells commonly have nearly triploid genomes and DNA content with gross chromosomal changes and a large number of variations. It has been suggested that such tumor cells originate from a tetraploid derivative of primordial germ cells. These cells subsequently lose and rearrange their chromosomes to first generate a seminoma and then the more malignant and pluripotent EC cells, which stabilize at an approximately 3n DNA content. It is thus tempting to speculate that the blastomere that gave rise to CH-ES1 may have been tetraploid and that subsequent chromosomal loss resulted in an EC-like phenotype by a mechanism comparable to that by which EC cells arise. Our results emphasize the importance of not only cytogenetic testing but also more detailed genetic testing of hESC lines by microarray methods before their clinical application in regener ative medicine. A large proportion of early human HS-173 embryos are chromosomally abnormal, particularly those with poor morphology or developmental delays. The embryos donated for research are often of poor quality, but reported chromosomal abnormalities in hESC lines are not common, at least in early passages. For instance, all 30 hESC lines derived in our laboratory at Karolinska Institutet display karyotypically normal G-banding patterns.