A rare form of CHM, the familial biparental CHM, is not androgenetic but rather is related to mutations in maternal effect genes NLRP7 (NALP7; chromosome 19) and KHDC3L (C6orf221; chromosome 6), which result in global imprinting alteration leading to preferential expression of paternally imprinted genes in villous trophoblast.
Mutations in NALP7 cause recurrent hydatidiform moles and reproductive wastage in humans.
Some of the other genes that we identified as being regulated by [E.sub.2] and [T.sub.3] are directly involved in cell proliferation, such as EMP1, IFNAR2, VMP, FLJ20073, MYC, and AREG, and some are involved in nucleotide binding and/or protein binding, such as PFKFB3, APPBP2, SSFA2, and NALP7
. Other genes, such as CSTA, show altered expression in the tissue invasion process during breast carcinogenesis .