Exome sequencing of bilateral XXXX suggests independent development lineages.

@entity1 @entity675 @entity71596 @entity4637 @entity2971 @entity5 @entity2969 @entity50601
@entity2971 , the precursor of @entity2969 ( @entity2969 ), is hypothesized to arise during embryogenesis from developmentally arrested primordial germ cells (PGCs) or gonocytes. In early embryonal life, the PGCs migrate from the yolk sac to the dorsal body wall where the cell population separates before colonizing the genital ridges. However, whether the malignant transformation takes place before or after this separation is controversial. We have explored the somatic exome-wide mutational spectra of bilateral @entity2969 to provide novel insight into the in utero critical time frame of malignant transformation and @entity2969 pathogenesis. Exome sequencing was performed in five @entity1 with bilateral @entity2969 ( @entity5 ), of these three @entity1 in whom both @entity5 were available (six @entity5 ) and two @entity1 each with only one available @entity5 (two @entity5 ). Selected loci were explored by Sanger sequencing in 71 @entity1 with bilateral @entity2969 . From the exome-wide mutational spectra, no identical mutations in any of the three bilateral @entity5 pairs were identified. Exome sequencing of all @entity5 revealed 87 somatic non-synonymous mutations (median 10 per @entity5 ; range 5-21), some in already known @entity5 genes such as @entity4637 , NEB, @entity675 ( @entity675 ), and @entity50601 . @entity71596 was found recurrently mutated in two @entity5 . We suggest independent development lineages of bilateral @entity2969 . Thus, malignant transformation into intratubular germ cell @entity5 is likely to occur after the migration of PGCs. We reveal possible drivers of @entity2969 pathogenesis, such as mutated @entity675 , potentially with therapeutic implications for @entity2969 @entity1 .
