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In particular, to recapitulate the proliferative phase, organoids are exposed to an estrogen receptor (ER) agonist (typically E2), while a combination of E2 with a progesterone receptor (PGR) agonist (typically P4 or medroxyprogesterone acetate (MPA)) and decidualization-promoting cyclic adenosine monophosphate (cAMP) is employed to replicate the transition to the secretory phase [53, 54, 63]

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Studies consistently show a 2-4 fold increase in neural tube defects with low B12 status (3)

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