K
Karen D. Tsuchiya
Researcher at University of Washington
Publications - 39
Citations - 2355
Karen D. Tsuchiya is an academic researcher from University of Washington. The author has contributed to research in topics: Cancer & Gene. The author has an hindex of 20, co-authored 37 publications receiving 2171 citations. Previous affiliations of Karen D. Tsuchiya include Boston Children's Hospital & Seattle Children's.
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Epigenetic silencing of the intronic microRNA hsa-miR-342 and its host gene EVL in colorectal cancer.
William M. Grady,Rachael K. Parkin,Patrick S. Mitchell,Jun Ho Lee,Young Ho Kim,Karen D. Tsuchiya,Mary Kay Washington,C Paraskeva,James K V Willson,Andrew M. Kaz,Evan M. Kroh,April Allen,Brian R. Fritz,Sanford D. Markowitz,Muneesh Tewari +14 more
TL;DR: Reconstitution of hsa-miR-342 in the colorectal cancer cell line HT-29 induced apoptosis, suggesting that this microRNA could function as a proapoptotic tumor suppressor and support a novel mechanism for silencing intronic microRNAs in cancer by epigenetic alterations of cognate host genes.
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Boundaries between chromosomal domains of X inactivation and escape bind CTCF and lack CpG methylation during early development.
Galina N. Filippova,Mimi K. Cheng,James M. Moore,Jean Pierre Truong,Ying J. Hu,Di Kim Nguyen,Karen D. Tsuchiya,Christine M. Disteche +7 more
TL;DR: The 5' end of Jarid1c, a mouse escape gene adjacent to an inactivated gene, binds CTCF, displays high levels of histone H3 acetylation, and functions as a C TCF-dependent chromatin insulator, suggesting a role in maintaining both X inactivation and escape domains.
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Enhanced expression of an insulin growth factor-like binding protein (mac25) in senescent human mammary epithelial cells and induced expression with retinoic acid
TL;DR: It is found that mac25 accumulates in senescent cells and is up-regulated in normal, growing mammary epithelial cells by all-trans-retinoic acid or the synthetic retinoid fenretinide, suggesting a tumor-suppressor role.
Journal Article
Gonadoblastoma: molecular definition of the susceptibility region on the Y chromosome.
TL;DR: Although the results do not directly implicate TSPY or YRRM in the etiology of the tumor, they raise the issue of whether there is one GBY gene in the critical region or possibly multiple GBY loci dispersed on the Y chromosome.
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The Smo/Smo Model: Hedgehog-Induced Medulloblastoma with 90% Incidence and Leptomeningeal Spread
Beryl A. Hatton,Elisabeth H. Villavicencio,Elisabeth H. Villavicencio,Karen D. Tsuchiya,Joel I. Pritchard,Sally Ditzler,Barbara Pullar,Stacey Hansen,Sue E. Knoblaugh,Dong-Hoon Lee,Charles G. Eberhart,Andrew R. Hallahan,James M. Olson,James M. Olson +13 more
TL;DR: The Smo/Smo model is the first mouse medulloblastoma model to show leptomeningeal spread and the adherence to human pathology, high incidence, and early onset of tumors thus make Smo-Smo mice an efficient model for preclinical studies.