C
Christopher J. Ormandy
Researcher at Garvan Institute of Medical Research
Publications - 136
Citations - 9544
Christopher J. Ormandy is an academic researcher from Garvan Institute of Medical Research. The author has contributed to research in topics: Prolactin & Breast cancer. The author has an hindex of 54, co-authored 131 publications receiving 8757 citations. Previous affiliations of Christopher J. Ormandy include St. Vincent's Health System & French Institute of Health and Medical Research.
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Journal ArticleDOI
Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse.
Christopher J. Ormandy,A Camus,J. Barra,Diane Damotte,B. Lucas,Hélène Buteau,Marc Edery,Nicole Brousse,Charles Babinet,Nadine Binart,Paul A. Kelly +10 more
TL;DR: This work establishes the prolactin receptor as a key regulator of mammalian reproduction, and provides the first total ablation model to further study the role of the prolACTin receptor and its ligands.
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Osteoclast differentiation factor RANKL controls development of progestin-driven mammary cancer.
Daniel Schramek,Andreas Leibbrandt,Verena Sigl,Lukas Kenner,John A. Pospisilik,Heather J. Lee,Reiko Hanada,Purna A. Joshi,Antonios O. Aliprantis,Laurie H. Glimcher,Manolis Pasparakis,Rama Khokha,Christopher J. Ormandy,Martin Widschwendter,Georg Schett,Josef M. Penninger +15 more
TL;DR: It is shown that the in vivo administration of MPA triggers massive induction of the key osteoclast differentiation factor RANKL (receptor activator of NF-κB ligand) in mammary-gland epithelial cells and controls the incidence and onset of progestin-driven breast cancer.
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Prolactin controls mammary gland development via direct and indirect mechanisms
Cathrin Brisken,Sarabjeet Kaur,Tony E. Chavarria,Nadine Binart,Robert L. Sutherland,Robert A. Weinberg,Paul A. Kelly,Christopher J. Ormandy +7 more
TL;DR: Prolactin affects mammary morphogenesis in two different ways: it controls ductal side branching and terminal end bud regression in virgin animals via indirect mechanisms, but acts directly on the mammary epithelium to produce lobuloalveolar development during pregnancy.
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Null mutation of the prolactin receptor gene produces a defect in maternal behavior.
TL;DR: The PRLR is established as a regulator of maternal behavior in mice carrying a germ line null mutation of the PRL receptor (PRLR) gene, and eating, locomotor activity, sexual behavior, and exploration are normal in PRLR mutant mice.
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Cyclin D1, EMS1 and 11q13 amplification in breast cancer.
TL;DR: Although the region harbors several genes with known or suspected oncogenic potential, the complex structure of the amplicons and the fact that 11q13 is gene-rich have made definitive identification of specific genes that contribute to the genesis and progression of breast cancer a difficult and continuing process.