A cellular and molecular portrait of endometriosis subtypes
Fonseca, M. A. S.; Wright, K. N.; Lin, X.; Abbasi, F.; Haro, M.; Sun, J.; Hernandez, L.; Orr, N. L.; Hong, J.; Choi-Kuaea, Y.; Maluf, H. M.; Balzer, B. L.; Cass, I.; Truong, M.; Wang, Y.; Pisarska, M. D.; Dinh, H.; EL-Naggar, A.; Huntsman, D.; Anglesio, M. S.; Goodman, M. T.; Medeiros, F.; Siedhoff, M.; Lawrenson, K.
Show abstract
Endometriosis is a common, benign condition characterized by extensive heterogeneity in lesion appearance and patient symptoms. We profiled transcriptomes of 207,949 individual cells from endometriomata (n=7), extra-ovarian endometriosis (n=19), eutopic endometrium (n=4), unaffected ovary (n=1) and endometriosis-free peritoneum (n=4) to create a cellular atlas of endometrial-type epithelial cells, endometrial-type stromal cells and microenvironmental cell populations across tissue sites. Signatures of endometrial-type epithelium and stroma differed markedly across eutopic endometrium, endometrioma, superficial extra-ovarian disease and deep infiltrating endometriosis, suggesting that extensive transcriptional reprogramming is a core component of the disease process. Endometriomas were notable for the dysregulation of pro-inflammatory pathways and upregulation of complement proteins C3 and C7. Somatic ARID1A mutation in epithelial cells was associated with upregulation of pro-angiogenic factor SOX17 and remodeling of the endothelial cell compartment. Finally, signatures of endometriosis-associated endometrial-type epithelial clusters were enriched in ovarian cancers, reinforcing the epidemiologic associations between these two diseases.
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