James M. Olson
作者: 转载 / 5687次阅读 时间: 2012年11月13日
标签: OLSON Olson

James M. Olson心理学空间6H2r)h;f2tA y


jolson@fhcrc.org 206-667-4286


2PK(ec:H0Assistant Member, Fred Hutchinson Cancer Research Center; Assistant Professor, Medicine Concurrent; Adjunct, Department of Pathology


%wEgh zN0Dr. Olson cares for pediatric cancer patients at Seattle Children's.

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Pediatric Hematology Oncology Specialist, Seattle Children's心理学空间x)^6q q+Fi6U|

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Member, Clinical Research Division, Fred Hutchinson Cancer Research Center心理学空间1j-r]'A BB#A


Professor, Hematology Oncology Division, University of Washington School of Medicine心理学空间"lwWvx^ f8Y1X/p


Clinical Expertise心理学空间+X}S/H&iT

q)BQ,xR0tZ0Pediatric brain tumors, tumor paint (intraoperative cancer detection and removal) and cancer drug discovery.心理学空间_'g!\jY$|


Education And Training心理学空间1cZ5X,z/R9}n;z

l!Hv9U c:CrM3Y0University of Michigan, Medicine, 1991


University of Michigan, Pharmacology, 1989心理学空间3\8dPQ}3~2f4N"O

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More Information

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For more information about Dr. James M. Olson's clinical and research expertise, click here.心理学空间A2_w:gZ:K/}UG|;?

1nm'XVYE"D6b6_0Dr. Olson's work, which uses scorpion venom to light up cancer cells, has been featured onKOMO News.心理学空间 H}X_*~sG


Lab Website

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Pediatric Brain Tumors:We are generating new mouse models of medulloblastoma (pediatric brain tumor) and testing candidate drugs that interfere with the aberrant signaling pathways. We demonstrated efficacy of two drug classes, retinoids and cyclopamine derivatives. Both induce apoptosis in medulloblastoma cells. We elucidated the mechanism by which retinoids induce apoptosis, providing a basis for understanding why some cells are sensitive to this agent and others are resistant. We are developing a national Phase III clinical trial to assess the efficacy of retinoids in children with medulloblastoma.心理学空间 Z9c)TnwiY*GH [$K#j


Brain Development:The neuroD family of transcription factors regulates expression of genes that are necessary for nerve cell development. We demonstrated that neuroD proteins were sufficient to convert rapidly dividing embryonal carcinoma cells into nonreplicating, mature neurons. We then assessed the role of neuroD2 by generating neuroD2-null mice. These mice experienced premature death preceded by ataxia, seizures, motor deficits, and weight loss. Cells that normally express neuroD2 underwent excessive apoptosis in the absence of neuroD2, establishing that this transcription factor is important for neuronal survival in addition to its established role in neuronal differentiation. Ongoing studies will determine how neuroD2 is regulated in developing brain and identify transcriptional targets of neuroD2.


Huntington's Disease:Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded polyglutamine repeat in the huntingtin protein. The mutant protein forms intracellular aggregates that incorporate many other proteins, including transcription factors. We hypothesize that the mutant huntingtin protein causes neuronal dysfunction, in part, by altering transcription of genes that are necessary for neurotransmission. We organized a consortium of 60 investigators that conducted microarray studies in neurodegenerative disease models. The results were reported in a special series in Human Molecular Genetics (issue 11(17). Based on this work, we have identified two classes of drugs that show promise in pre-clinical trials.

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