Noncanonical agonist PPARγ ligands modulate the response to DNA damage and sensitize cancer cells to cytotoxic chemotherapy.
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| Title: | Noncanonical agonist PPARγ ligands modulate the response to DNA damage and sensitize cancer cells to cytotoxic chemotherapy. |
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| Authors: | Khandekar MJ; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Radiation Oncology, Massachusetts General Hospital, Boston, MA 02114., Banks AS; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215., Laznik-Bogoslavski D; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215., White JP; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215., Choi JH; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215., Kazak L; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215., Lo JC; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215., Cohen P; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215., Wong KK; Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215., Kamenecka TM; Department of Molecular Therapeutics, The Scripps Research Institute, Jupiter, FL 33458., Griffin PR; Department of Molecular Therapeutics, The Scripps Research Institute, Jupiter, FL 33458., Spiegelman BM; Department of Cell Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215; Bruce_Spiegelman@dfci.harvard.edu.; Department of Cancer Biology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02215. |
| Source: | Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2018 Jan 16; Vol. 115 (3), pp. 561-566. Date of Electronic Publication: 2018 Jan 02. |
| Publication Type: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
| Journal Info: | Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE |
| Database: | MEDLINE Ultimate |
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