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Wu, Jennifer

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Wu

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Jennifer

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Wu, Jennifer
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    Development of Bag-1L as a therapeutic target in androgen receptor-dependent prostate cancer
    (eLife Sciences Publications, Ltd, 2017) Cato, Laura; Neeb, Antje; Sharp, Adam; Buzón, Victor; Ficarro, Scott B; Yang, Linxiao; Muhle-Goll, Claudia; Kuznik, Nane C; Riisnaes, Ruth; Nava Rodrigues, Daniel; Armant, Olivier; Gourain, Victor; Adelmant, Guillaume; Ntim, Emmanuel A; Westerling, Thomas; Dolling, David; Rescigno, Pasquale; Figueiredo, Ines; Fauser, Friedrich; Wu, Jennifer; Rottenberg, Jaice T; Shatkina, Liubov; Ester, Claudia; Luy, Burkhard; Puchta, Holger; Troppmair, Jakob; Jung, Nicole; Bräse, Stefan; Strähle, Uwe; Marto, Jarrod A; Nienhaus, Gerd Ulrich; Al-Lazikani, Bissan; Salvatella, Xavier; de Bono, Johann S; Cato, Andrew CB; Brown, Myles
    Targeting the activation function-1 (AF-1) domain located in the N-terminus of the androgen receptor (AR) is an attractive therapeutic alternative to the current approaches to inhibit AR action in prostate cancer (PCa). Here we show that the AR AF-1 is bound by the cochaperone Bag-1L. Mutations in the AR interaction domain or loss of Bag-1L abrogate AR signaling and reduce PCa growth. Clinically, Bag-1L protein levels increase with progression to castration-resistant PCa (CRPC) and high levels of Bag-1L in primary PCa associate with a reduced clinical benefit from abiraterone when these tumors progress. Intriguingly, residues in Bag-1L important for its interaction with the AR AF-1 are within a potentially druggable pocket, implicating Bag-1L as a potential therapeutic target in PCa.
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    SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation
    (2016) Wang, Xiaofeng; Lee, Ryan; Alver, Burak; Haswell, Jeffrey; Wang, Su; Mieczkowski, Jakub; Drier, Yotam; Gillespie, Shawn M.; Archer, Tenley; Wu, Jennifer; Tzvetkov, Evgeni P.; Troisi, Emma C.; Pomeroy, Scott; Biegel, Jaclyn A.; Tolstorukov, Michael; Bernstein, Bradley; Park, Peter; Roberts, Charles W. M.
    SMARCB1 (SNF5/INI1/BAF47), a core subunit of the SWI/SNF (BAF) chromatin remodeling complex1,2, is inactivated in nearly all pediatric rhabdoid tumors3–5. These aggressive cancers are among the most genomically stable6–8, suggesting an epigenetic mechanism by which SMARCB1 loss drives transformation. Here, we show that despite indistinguishable mutational landscapes, human rhabdoid tumors show distinct enhancer H3K27ac signatures, which reveal remnants of differentiation programs. We show that SMARCB1 is required for the integrity of SWI/SNF complexes and that its loss alters enhancer targeting – markedly impairing SWI/SNF binding to typical enhancers, particularly those required for differentiation, while maintaining SWI/SNF binding at super-enhancers. We show that these retained super-enhancers are essential for rhabdoid tumor survival, including some that are shared across all subtypes, such as SPRY1, and other lineage-specific super-enhancers, like SOX2 in brain-derived rhabdoid tumors. Taken together, our findings reveal a novel chromatin-based epigenetic mechanism underlying the tumor suppressive activity of SMARCB1.
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    Case Report of a Child after Hematopoietic Cell Transplantation with Acute Aspergillus Tracheobronchitis as a Cause for Respiratory Failure
    (Hindawi Publishing Corporation, 2016) Gauguet, Stefanie; Madden, Kate; Wu, Jennifer; Duncan, Christine; Lee, Gi Soo; Miller, Tonya; Klingensmith, William C.; Burchett, Sandra; van der Velden, Meredith
    Rapid respiratory failure due to invasive mycosis of the airways is an uncommon presentation of Aspergillus infection, even in immunocompromised patients, and very few pediatric cases have been reported. Patients with Aspergillus tracheobronchitis present with nonspecific symptoms, and radiologic studies are often noninformative, leading to a delay in diagnosis. Prompt initiation of adequate antifungal therapies is of utmost importance to improve outcome. We report the case of a 9-year-old girl with chronic myelogenous leukemia who developed respiratory distress 41 days after hematopoietic cell transplantation and rapidly deteriorated despite multiple interventions and treatment modalities.