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While mTORC1 activation is involved in its growth, mTORC1 inhibitors fail to eradicate AML, highlighting the need for new therapies. Moreover, the identity of the AML cell of origin is obscure. AML research, however, is hampered by the lack of\n                    <jats:italic>in\u00a0vivo<\/jats:italic>\n                    models. Here, we establish a human AML\u2010xenograft (Xn) model in mice, recapitulating AML at the histological and molecular levels. Microarray analysis demonstrated tumor growth\n                    <jats:italic>in\u00a0vivo<\/jats:italic>\n                    to involve robust PPAR\u03b3\u2010pathway activation. Similarly, immunostaining revealed strong PPAR\u03b3 expression in human AML specimens. Accordingly, we demonstrate that while PPAR\u03b3 agonism accelerates AML growth, PPAR\u03b3 antagonism is inhibitory, strongly suppressing AML proliferation and tumor\u2010initiating capacity, via a TGFB\u2010mediated inhibition of PDGFB and CTGF. Finally, we show striking similarity between AML cell lines and mesenchymal stem cells (MSCs) in terms of antigen and gene expression and differentiation potential. Altogether, we establish the first\n                    <jats:italic>in\u00a0vivo<\/jats:italic>\n                    human AML model, which provides evidence that AML may originate in a PPAR\u03b3\u2010activated renal MSC lineage that is\u00a0skewed\u00a0toward adipocytes and smooth muscle and away from osteoblasts, and uncover PPAR\u03b3 as a regulator of AML growth, which could serve as an attractive therapeutic target.\n                    <jats:sup>\u00a7<\/jats:sup>\n                  <\/jats:p>","DOI":"10.15252\/emmm.201506111","type":"journal-article","created":{"date-parts":[[2017,3,8]],"date-time":"2017-03-08T20:10:46Z","timestamp":1489003846000},"page":"508-530","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Peroxisome proliferator\u2010activated receptor gamma (PPAR\u03b3) is central to the initiation and propagation of human angiomyolipoma, suggesting its potential as a therapeutic target"],"prefix":"10.1038","volume":"9","author":[{"given":"Oren","family":"Pleniceanu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Racheli","family":"Shukrun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dorit","family":"Omer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Einav","family":"Vax","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Itamar","family":"Kanter","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Klaudyna","family":"Dziedzic","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naomi","family":"Pode\u2010Shakked","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michal","family":"Mark\u2010Daniei","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sara","family":"Pri\u2010Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yehudit","family":"Gnatek","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hadas","family":"Alfandary","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nira","family":"Varda\u2010Bloom","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dekel D","family":"Bar\u2010Lev","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naomi","family":"Bollag","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rachel","family":"Shtainfeld","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leah","family":"Armon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Achia","family":"Urbach","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomer","family":"Kalisky","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arnon","family":"Nagler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Orit","family":"Harari\u2010Steinberg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jack L","family":"Arbiser","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3784-8238","authenticated-orcid":false,"given":"Benjamin","family":"Dekel","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2017,3,8]]},"reference":[{"key":"BFEMMM201506111_CR1","doi-asserted-by":"crossref","first-page":"1142","DOI":"10.1172\/JCI200318549","volume":"112","author":"A Abramsson","year":"2003","unstructured":"Abramsson A, Lindblom P, Betsholtz C (2003) Endothelial and nonendothelial sources of PDGF\u2010B regulate pericyte recruitment and influence vascular pattern formation in tumors. 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