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. 2013 Apr 15;126(8):1845–1857. doi: 10.1242/jcs.119347

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© 2013. Published by The Company of Biologists Ltd

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Fig. 7. — Possible mechanisms of gonadotropin-independent and/or gonadotropin-dependent (LH) induction of adrenocortical neoplasia in conjunction with transgenically expressed GATA-4 in C57Bl/6N murine adrenals. In the adrenal cortex of intact TG mice (A), sparse stem/progenitor cells (differentiating into normal CYP21 positive adrenocortical cells) under transgene 21-OH-Gata4 influence transform into steroidogenically inactive neoplastic A cells. After gonadectomy (GDX) (B), chronically elevated serum LH might induce LHCGR expression to facilitate the stem/progenitor cells transformation to steroidogenically active neoplastic B cells. The population of LHCGR-negative stem/progenitor cells in GDX TG adrenals, analogous to intact TG adrenals, transforms into A cells. LH-dependent transformation of stem/progenitor cells into B cells is possibly modulated by activin B signalling.