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Human iPSC-derived fallopian tube organoids with BRCA1 mutation recapitulate early-stage carcinogenesis.

Authors :
Yucer, Nur
Yucer, Nur
Ahdoot, Rodney
Workman, Michael J
Laperle, Alexander H
Recouvreux, Maria S
Kurowski, Kathleen
Naboulsi, Diana J
Liang, Victoria
Qu, Ying
Plummer, Jasmine T
Gayther, Simon A
Orsulic, Sandra
Karlan, Beth Y
Svendsen, Clive N
Yucer, Nur
Yucer, Nur
Ahdoot, Rodney
Workman, Michael J
Laperle, Alexander H
Recouvreux, Maria S
Kurowski, Kathleen
Naboulsi, Diana J
Liang, Victoria
Qu, Ying
Plummer, Jasmine T
Gayther, Simon A
Orsulic, Sandra
Karlan, Beth Y
Svendsen, Clive N
Source :
Cell reports; vol 37, iss 13, 110146; 2211-1247
Publication Year :
2021

Abstract

Germline pathogenic mutations in BReast CAncer (BRCA1) genes are thought to drive normal fallopian tube epithelial (FTE) cell transformation to high-grade serous ovarian cancer. No human models capture the sequence of events for disease initiation and progression. Here, we generate induced pluripotent stem cells (iPSCs) from healthy individuals and young ovarian cancer patients with germline pathogenic BRCA1 mutations (BRCA1mut). Following differentiation into FTE organoids, BRCA1mut lines exhibit cellular abnormalities consistent with neoplastic transformation compared to controls. BRCA1mut organoids show an increased production of cancer-specific proteins and survival following transplantation into mice. Organoids from women with the most aggressive ovarian cancer show the greatest pathology, indicating the potential value to predict clinical severity prior to disease onset. These human FTE organoids from BRCA1mut carriers provide a faithful physiological in vitro model of FTE lesion generation and early carcinogenesis. This platform can be used for personalized mechanistic and drug screening studies.

Details

Database :
OAIster
Journal :
Cell reports; vol 37, iss 13, 110146; 2211-1247
Notes :
application/pdf, Cell reports vol 37, iss 13, 110146 2211-1247
Publication Type :
Electronic Resource
Accession number :
edsoai.on1341877350
Document Type :
Electronic Resource