Publications by authors named "Marieke Burleson"

Breast cancer remains to be the second leading cause of cancer deaths worldwide thereby highlighting the critical need to find superior treatment strategies for this disease. In the current era of cancer treatment, personalized medicine is garnering much attention as this type of treatment is more selective thereby minimizing harmful side effects. Personalized medicine is dependent upon knowing the underlying genetic landscape of the initial tumor.

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Prostate cancer is a disease that depends on androgenic stimulation and is thus commonly treated with androgen deprivation therapy (ADT). ADT is highly successful initially; however, patients inevitably relapse at which point the cancer grows independently of androgens and is termed castration-resistant prostate cancer (CRPC). CRPC develops through various mechanisms, one of these being crosstalk of the androgen receptor (AR) signaling pathway with other signaling pathways.

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Mediator complex subunit 12 (MED12) is a subunit of Mediator, a large multi-subunit protein complex that acts an important regulator of transcription. Specifically, MED12 is an integral part of the kinase module of Mediator along with MED13, CyclinC (CycC) and CDK8. Structural studies have indicated that MED12 makes a direct connection to CycC through a specific interface and thereby functions to create a link between MED13 and CycC-CDK8.

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Although the Sonic hedgehog (SHH) signaling pathway has been implicated in promoting malignant phenotypes of prostate cancer, details on how it is activated and exerts its oncogenic role during prostate cancer development and progression is less clear. Here, we show that GLI3, a key SHH pathway effector, is transcriptionally upregulated during androgen deprivation and posttranslationally stabilized in prostate cancer cells by mutation of speckle-type POZ protein (SPOP). GLI3 is a substrate of SPOP-mediated proteasomal degradation in prostate cancer cells and prostate cancer driver mutations in SPOP abrogate GLI3 degradation.

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The initiation and progression of cancer is dependent on the acquisition of mutations in oncogenes or tumor suppressor genes that ultimately leads to the dysregulation of key regulatory pathways. Though these mutations often occur in direct regulators of such pathways, some may confer tumorigenic potential by indirectly targeting several pathways congruently thereby exerting pleiotropic effects. In recent years, the tumor suppressor gene Speckle Type POZ Protein (SPOP) has gained a lot of attention as it has been found to be altered in a variety of different cancers.

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