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  1. Article: Chemical Biology Screening Identifies a Vulnerability to Checkpoint Kinase Inhibitors in TSC2-Deficient Renal Angiomyolipomas.

    Vaughan, Robert M / Kordich, Jennifer J / Chan, Chun-Yuan / Sasi, Nanda K / Celano, Stephanie L / Sisson, Kellie A / Van Baren, Megan / Kortus, Matthew G / Aguiar, Dean J / Martin, Katie R / MacKeigan, Jeffrey P

    Frontiers in oncology

    2022  Volume 12, Page(s) 852859

    Abstract: The tuberous sclerosis complex (TSC) is a rare genetic syndrome and multisystem disease resulting in tumor formation in major organs. A molecular hallmark of TSC is a dysregulation of the mammalian target of rapamycin (mTOR) through loss-of-function ... ...

    Abstract The tuberous sclerosis complex (TSC) is a rare genetic syndrome and multisystem disease resulting in tumor formation in major organs. A molecular hallmark of TSC is a dysregulation of the mammalian target of rapamycin (mTOR) through loss-of-function mutations in either tumor suppressor
    Language English
    Publishing date 2022-03-10
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.852859
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Interrogating the aged striatum: robust survival of grafted dopamine neurons in aging rats produces inferior behavioral recovery and evidence of impaired integration.

    Collier, Timothy J / O'Malley, Jennifer / Rademacher, David J / Stancati, Jennifer A / Sisson, Kellie A / Sortwell, Caryl E / Paumier, Katrina L / Gebremedhin, Kibrom G / Steece-Collier, Kathy

    Neurobiology of disease

    2015  Volume 77, Page(s) 191–203

    Abstract: Advanced age is the primary risk factor for Parkinson's disease (PD). In PD patients and rodent models of PD, advanced age is associated with inferior symptomatic benefit following intrastriatal grafting of embryonic dopamine (DA) neurons, a pattern ... ...

    Abstract Advanced age is the primary risk factor for Parkinson's disease (PD). In PD patients and rodent models of PD, advanced age is associated with inferior symptomatic benefit following intrastriatal grafting of embryonic dopamine (DA) neurons, a pattern believed to result from decreased survival and reinnervation provided by grafted neurons in the aged host. To help understand the capacity of the aged, parkinsonian striatum to be remodeled with new DA terminals, we used a grafting model and examined whether increasing the number of grafted DA neurons in aged rats would translate to enhanced behavioral recovery. Young (3months), middle-aged (15months), and aged (22months) parkinsonian rats were grafted with proportionately increasing numbers of embryonic ventral mesencephalic (VM) cells to evaluate whether the limitations of the graft environment in subjects of advancing age can be offset by increased numbers of transplanted neurons. Despite robust survival of grafted neurons in aged rats, reinnervation of striatal neurons remained inferior and amelioration of levodopa-induced dyskinesias (LID) was delayed or absent. This study demonstrates that: 1) counter to previous evidence, under certain conditions the aged striatum can support robust survival of grafted DA neurons; and 2) unknown factors associated with the aged striatum result in inferior integration of graft and host, and continue to present obstacles to full therapeutic efficacy of DA cell-based therapy in this model of aging.
    MeSH term(s) Aging ; Amphetamine/pharmacology ; Animals ; Corpus Striatum/physiology ; Corpus Striatum/surgery ; Disease Models, Animal ; Dopamine and cAMP-Regulated Phosphoprotein 32/metabolism ; Dopaminergic Neurons/physiology ; Dyskinesia, Drug-Induced/physiopathology ; Embryo, Mammalian ; Functional Laterality ; Levodopa/adverse effects ; Neurites/physiology ; Oxidopamine/toxicity ; Parkinson Disease/drug therapy ; Parkinson Disease/etiology ; Parkinson Disease/surgery ; Proto-Oncogene Proteins c-fos/metabolism ; Rats ; Rats, Inbred F344 ; Recovery of Function/physiology ; Stem Cell Transplantation/methods ; Substance P/metabolism
    Chemical Substances Dopamine and cAMP-Regulated Phosphoprotein 32 ; Fosb protein, rat ; Proto-Oncogene Proteins c-fos ; Substance P (33507-63-0) ; Levodopa (46627O600J) ; Oxidopamine (8HW4YBZ748) ; Amphetamine (CK833KGX7E)
    Language English
    Publishing date 2015-03-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2015.03.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The genomic landscape of tuberous sclerosis complex.

    Martin, Katie R / Zhou, Wanding / Bowman, Megan J / Shih, Juliann / Au, Kit Sing / Dittenhafer-Reed, Kristin E / Sisson, Kellie A / Koeman, Julie / Weisenberger, Daniel J / Cottingham, Sandra L / DeRoos, Steven T / Devinsky, Orrin / Winn, Mary E / Cherniack, Andrew D / Shen, Hui / Northrup, Hope / Krueger, Darcy A / MacKeigan, Jeffrey P

    Nature communications

    2017  Volume 8, Page(s) 15816

    Abstract: Tuberous sclerosis complex (TSC) is a rare genetic disease causing multisystem growth of benign tumours and other hamartomatous lesions, which leads to diverse and debilitating clinical symptoms. Patients are born with TSC1 or TSC2 mutations, and somatic ...

    Abstract Tuberous sclerosis complex (TSC) is a rare genetic disease causing multisystem growth of benign tumours and other hamartomatous lesions, which leads to diverse and debilitating clinical symptoms. Patients are born with TSC1 or TSC2 mutations, and somatic inactivation of wild-type alleles drives MTOR activation; however, second hits to TSC1/TSC2 are not always observed. Here, we present the genomic landscape of TSC hamartomas. We determine that TSC lesions contain a low somatic mutational burden relative to carcinomas, a subset feature large-scale chromosomal aberrations, and highly conserved molecular signatures for each type exist. Analysis of the molecular signatures coupled with computational approaches reveals unique aspects of cellular heterogeneity and cell origin. Using immune data sets, we identify significant neuroinflammation in TSC-associated brain tumours. Taken together, this molecular catalogue of TSC serves as a resource into the origin of these hamartomas and provides a framework that unifies genomic and transcriptomic dimensions for complex tumours.
    MeSH term(s) Carcinoma/genetics ; Carcinoma/metabolism ; Genomics ; Humans ; Mutation ; Tuberous Sclerosis/genetics ; Tuberous Sclerosis/metabolism ; Tuberous Sclerosis Complex 1 Protein/genetics ; Tuberous Sclerosis Complex 1 Protein/metabolism ; Tuberous Sclerosis Complex 2 Protein/genetics ; Tuberous Sclerosis Complex 2 Protein/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
    Chemical Substances TSC1 protein, human ; TSC2 protein, human ; Tuberous Sclerosis Complex 1 Protein ; Tuberous Sclerosis Complex 2 Protein ; Tumor Suppressor Proteins
    Language English
    Publishing date 2017-06-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/ncomms15816
    Database MEDical Literature Analysis and Retrieval System OnLINE

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