Instructor in Medicine
Harvard Medical School, Brigham and Women's Hospital
Benjamin Freedman, PhD, studies the role of PKD and ciliopathy disease genes in pluripotent stem cells and their somatic descendant cells. He has many years of first-hand experience with iPSC derivation and culture, differentiation of human pluripotent stem cells, teratoma formation assays, and genome modification. Dr. Freedman’s laboratory is funded from young investigator grants from NIH (NIDDK) and NKF. Dr. Freedman has unique experience generating iPSCs from PKD patients and performing disease modeling experiments with these cells in the kidney lineage. He has identified a specific and disease-relevant phenotype in ADPKD iPSCs, and has also published techniques to differentiate iPSCs into kidney progenitor cells.
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Lam AQ, Freedman BS, Bonventre JV (2014). Directed differentiation of pluripotent stem cells to kidney cells. Semin Nephrol 34(4): 445-461 (review). A summary of recent progress and remaining challenges in using human pluripotent stem cells for kidney regeneration and disease modeling.
Lam AQ*, Freedman BS*, Morizane R*, Valerius MT, Bonventre JV (2014). Rapid and efficient differentiation of human pluripotent stem cells into intermediate mesoderm which forms tubules expressing kidney proximal tubular markers. J Am Soc Nephrol 25(6): 1211-1225. This paper introduces a new protocol for rapidly converting ES and iPS cells into mesoderm and subsequently kidney progenitor cells.
Freedman BS,* Lam AQ,* Sundsbak JL, Iatrino R, Su X, Koon SJ, Wu M, Daheron L, Harris PC, Zhou J, Bonventre JV (2013). Reduced ciliary polycystin-2 in iPS cells from PKD patients with PKD1 mutations. J Am Soc Nephrol 24: 1571-1586. In this paper, we generated iPS cells from patients with autosomal dominant and recessive PKD, and used them to identify a possible therapeutic approach.