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  1. AU="Kannan, Sarmishta"
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  1. Article ; Online: Genetic drivers and cells of origin in sarcomagenesis.

    Kannan, Sarmishta / Lock, Ian / Ozenberger, Benjamin B / Jones, Kevin B

    The Journal of pathology

    2021  Volume 254, Issue 4, Page(s) 474–493

    Abstract: Sarcoma comprises a group of malignancies that includes over 100 individual disease entities. Type-specific genetic events initiate each tumor, occurring within a specific cellular context or circumstance. All sarcomas share a relationship with ... ...

    Abstract Sarcoma comprises a group of malignancies that includes over 100 individual disease entities. Type-specific genetic events initiate each tumor, occurring within a specific cellular context or circumstance. All sarcomas share a relationship with mesenchymal tissues of origin. Conceptual models for each specific route towards sarcomagenesis have developed over the years as clinical, cellular, and increasingly molecular observations have advanced hypotheses to be tested in the forward or reverse direction in experimental systems, often genetically engineered model organisms. This review considers the history of these discoveries in the context of technologies available at the time each was made and provides a comprehensive summary of the current knowledge of sarcoma genetics, including characteristic translocations, oncogene activation and loss of tumor suppressor gene events, and their putative cells of origin. Also considered are the interrelatedness of molecular clinical observations and genetic experiments in model systems to move this field of knowledge forward, as well as their implications for diagnostic and therapeutic paradigms for sarcoma. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    MeSH term(s) Animals ; Carcinogenesis/genetics ; Humans ; Sarcoma/genetics ; Sarcoma/pathology
    Language English
    Publishing date 2021-03-18
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.5617
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.12: Show issues Location:
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  2. Article ; Online: ASPSCR1-TFE3 reprograms transcription by organizing enhancer loops around hexameric VCP/p97.

    Pozner, Amir / Li, Li / Verma, Shiv Prakash / Wang, Shuxin / Barrott, Jared J / Nelson, Mary L / Yu, Jamie S E / Negri, Gian Luca / Colborne, Shane / Hughes, Christopher S / Zhu, Ju-Fen / Lambert, Sydney L / Carroll, Lara S / Smith-Fry, Kyllie / Stewart, Michael G / Kannan, Sarmishta / Jensen, Bodrie / John, Cini M / Sikdar, Saif /
    Liu, Hongrui / Dang, Ngoc Ha / Bourdage, Jennifer / Li, Jinxiu / Vahrenkamp, Jeffery M / Mortenson, Katelyn L / Groundland, John S / Wustrack, Rosanna / Senger, Donna L / Zemp, Franz J / Mahoney, Douglas J / Gertz, Jason / Zhang, Xiaoyang / Lazar, Alexander J / Hirst, Martin / Morin, Gregg B / Nielsen, Torsten O / Shen, Peter S / Jones, Kevin B

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 1165

    Abstract: The t(X,17) chromosomal translocation, generating the ASPSCR1::TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCCs), frustrating efforts to identify therapeutic ...

    Abstract The t(X,17) chromosomal translocation, generating the ASPSCR1::TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCCs), frustrating efforts to identify therapeutic targets for these rare cancers. Here, proteomic analysis identifies VCP/p97, an AAA+ ATPase with known segregase function, as strongly enriched in co-immunoprecipitated nuclear complexes with ASPSCR1::TFE3. We demonstrate that VCP is a likely obligate co-factor of ASPSCR1::TFE3, one of the only such fusion oncoprotein co-factors identified in cancer biology. Specifically, VCP co-distributes with ASPSCR1::TFE3 across chromatin in association with enhancers genome-wide. VCP presence, its hexameric assembly, and its enzymatic function orchestrate the oncogenic transcriptional signature of ASPSCR1::TFE3, by facilitating assembly of higher-order chromatin conformation structures demonstrated by HiChIP. Finally, ASPSCR1::TFE3 and VCP demonstrate co-dependence for cancer cell proliferation and tumorigenesis in vitro and in ASPS and RCC mouse models, underscoring VCP's potential as a novel therapeutic target.
    MeSH term(s) Animals ; Mice ; Humans ; Proteomics ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/pathology ; Translocation, Genetic ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Kidney Neoplasms/genetics ; Chromatin/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Chromosomes, Human, X/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Valosin Containing Protein/genetics
    Chemical Substances Oncogene Proteins, Fusion ; Chromatin ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; TFE3 protein, human ; ASPSCR1 protein, human ; Intracellular Signaling Peptides and Proteins ; VCP protein, human (EC 3.6.4.6) ; Valosin Containing Protein (EC 3.6.4.6)
    Language English
    Publishing date 2024-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-45280-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: ASPSCR1-TFE3 reprograms transcription by organizing enhancer loops around hexameric VCP/p97.

    Pozner, Amir / Verma, Shiv Prakash / Li, Li / Wang, Shuxin / Barrott, Jared J / Nelson, Mary L / Yu, Jamie S E / Negri, Gian Luca / Colborne, Shane / Hughes, Christopher S / Zhu, Ju-Fen / Lambert, Sydney L / Carroll, Lara S / Smith-Fry, Kyllie / Stewart, Michael G / Kannan, Sarmishta / Jensen, Bodrie / Mortenson, Katelyn L / John, Cini /
    Sikdar, Saif / Liu, Hongrui / Dang, Ngoc Ha / Bourdage, Jennifer / Li, Jinxiu / Vahrenkamp, Jeffery M / Groundland, John S / Wustrack, Rosanna / Senger, Donna L / Zemp, Franz J / Mahoney, Douglas J / Gertz, Jason / Zhang, Xiaoyang / Lazar, Alexander J / Hirst, Martin / Morin, Gregg B / Nielsen, Torsten O / Shen, Peter S / Jones, Kevin B

    bioRxiv : the preprint server for biology

    2023  

    Abstract: The t(X,17) chromosomal translocation, generating the ASPSCR1-TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCC), frustrating efforts to identify therapeutic ... ...

    Abstract The t(X,17) chromosomal translocation, generating the ASPSCR1-TFE3 fusion oncoprotein, is the singular genetic driver of alveolar soft part sarcoma (ASPS) and some Xp11-rearranged renal cell carcinomas (RCC), frustrating efforts to identify therapeutic targets for these rare cancers. Proteomic analysis showed that VCP/p97, an AAA+ ATPase with known segregase function, was strongly enriched in co-immunoprecipitated nuclear complexes with ASPSCR1-TFE3. We demonstrate that VCP is a likely obligate co-factor of ASPSCR1-TFE3, one of the only such fusion oncoprotein co-factors identified in cancer biology. Specifically, VCP co-distributed with ASPSCR1-TFE3 across chromatin in association with enhancers genome-wide. VCP presence, its hexameric assembly, and its enzymatic function orchestrated the oncogenic transcriptional signature of ASPSCR1-TFE3, by facilitating assembly of higher-order chromatin conformation structures as demonstrated by HiChIP. Finally, ASPSCR1-TFE3 and VCP demonstrated co-dependence for cancer cell proliferation and tumorigenesis
    Language English
    Publishing date 2023-10-02
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.09.29.560242
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Modeling synovial sarcoma metastasis in the mouse: PI3'-lipid signaling and inflammation.

    Barrott, Jared J / Kafchinski, Lisa A / Jin, Huifeng / Potter, Jared W / Kannan, Sarmishta D / Kennedy, Robert / Mosbruger, Tim / Wang, Wei-Lien / Tsai, Jen-Wei / Araujo, Dejka M / Liu, Ting / Capecchi, Mario R / Lazar, Alexander J / Jones, Kevin B

    The Journal of experimental medicine

    2016  Volume 213, Issue 13, Page(s) 2989–3005

    Abstract: Solid tumor metastasis is a complex biology, impinged upon by a variety of dysregulated signaling pathways. PI3'-lipid signaling has been associated with metastasis and inflammation in many cancers, but the relationship between tumor cell-intrinsic PI3'- ... ...

    Abstract Solid tumor metastasis is a complex biology, impinged upon by a variety of dysregulated signaling pathways. PI3'-lipid signaling has been associated with metastasis and inflammation in many cancers, but the relationship between tumor cell-intrinsic PI3'-lipid signaling and inflammatory cell recruitment has remained enigmatic. Elevated PI3'-lipid signaling associates with progression of synovial sarcoma, a deadly soft tissue malignancy initiated by a t(X;18) chromosomal translocation that generates an SS18-SSX fusion oncoprotein. Here, we show in genetically engineered mouse models of locally induced expression of SS18-SSX1 or SS18-SSX2 that Pten silencing dramatically accelerated and enhanced sarcomagenesis without compromising synovial sarcoma characteristics. PTEN deficiency increased tumor angiogenesis, promoted inflammatory gene expression, and enabled highly penetrant spontaneous pulmonary metastasis. PTEN-deficient sarcomas revealed infiltrating myeloid-derived hematopoietic cells, particularly macrophages and neutrophils, recruited via PI3'-lipid-induced CSF1 expression in tumor cells. Moreover, in a large panel of human synovial sarcomas, enhanced PI3'-lipid signaling also correlated with increased inflammatory cell recruitment and CSF1R signal transduction in both macrophages and endothelial cells. Thus, both in the mouse model and in human synovial sarcomas, PI3'-lipid signaling drives CSF1 expression and associates with increased infiltration of the monocyte/macrophage lineage as well as neutrophils.
    MeSH term(s) Animals ; Macrophage Colony-Stimulating Factor/genetics ; Macrophage Colony-Stimulating Factor/metabolism ; Mice ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Sarcoma, Synovial/genetics ; Sarcoma, Synovial/metabolism ; Sarcoma, Synovial/pathology ; Signal Transduction
    Chemical Substances Oncogene Proteins, Fusion ; Proto-Oncogene Proteins ; Repressor Proteins ; Ss18 protein, mouse ; Macrophage Colony-Stimulating Factor (81627-83-0) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
    Language English
    Publishing date 2016--12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20160817
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.107: Show issues Location:
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