Adrenal myelolipoma: a mingle of progenitor cells?

Abstract

Adrenal myelolipoma (AML) is a rare benign tumour composed or mature haematopoietic tissue and fat. The tumour is functionally inert and is usually detected incidentally. Mainly introduced in case reports, the tumourigenesis of AML is poorly understood with 3 historical hypotheses seemingly unrelated to each other. Here we propose the tumourigenic pathway based on the novel findings on stem/progenitor cell and our preliminary data. We hypothesize the tumourigenesis as follows: the fat components are derived by the mesenchymal stem cells of stromal fat of adrenal cortex under certain stimuli. Mature adipocytes begin to accumulate and become inflammatory stimulating neighbouring adrenal cortex tissue to release possibly G-CSF to recruit circulating haematopoietic progenitors. During the tumour growth, haematopoietic cell in the central part acquire energy from burning the surrounding fat until they are fully differentiated and division stops. Lacking the ability to further grow, the central part undergoes necrosis and calcification whilst the peripheral part continues to slowly pile up newly derived adipocytes and haematopoietic progenitor cells. The necrosis or calcification of the tumour the inflammation persists and the tumour generates a self-growing signalling loop, entailing a continuous growth even without further stimuli. Our theory offers a logical explanation to the diverse phenomena identified on AML and unifies the historical theories. Future studies may focus on the stem/progenitor cell profiles of AML to confirm and supplement our hypothesis.