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Brooke D. Paradise

Researcher at Mayo Clinic

Publications -  9
Citations -  205

Brooke D. Paradise is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Medicine & Smoothened. The author has an hindex of 4, co-authored 6 publications receiving 67 citations.

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Hedgehog/GLI Signaling Pathway: Transduction, Regulation, and Implications for Disease

TL;DR: The Hh/GLI pathway was originally discovered in Drosophila as a major regulator of segment patterning in development as mentioned in this paper, and it is observed in many types of cancer including basal cell carcinoma, medulloblastoma, colorectal, prostate, pancreatic, and many more.
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Recent Advances in the Clinical Targeting of Hedgehog/GLI Signaling in Cancer.

TL;DR: Pre-clinical evidence supporting the suitability of targeting this signaling pathway in cancers is summarized, and published and ongoing clinical trial data on single agent or combination therapeutic strategies, targeting Hedgehog/GLI signaling pathway, in both advanced solid tumors and hematologic malignancies are provided.
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ST3GAL1 is a target of the SOX2-GLI1 transcriptional complex and promotes melanoma metastasis through AXL.

TL;DR: A mechanism regulated by the oncogenic SOX2-GLI1 transcriptional complex driving melanoma invasion through the induction of the sialyltransferase ST3GAL1 is reported, supporting a key role of the ST3 GAL1-AXL axis as driver of melanoma metastasis and highlighting the therapeutic potential of targeting this axis to treat metastatic melanoma.
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Targeting Epigenetic Aberrations in Pancreatic Cancer, a New Path to Improve Patient Outcomes?

TL;DR: The potential to “reprogram” cancer cells to revert them to a healthy state presents great promise and merits further investigation.
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Targeting non-canonical activation of GLI1 by the SOX2-BRD4 transcriptional complex improves the efficacy of HEDGEHOG pathway inhibition in melanoma.

TL;DR: In this paper, a novel SOX2-BRD4-GLI1 complex was identified to drive the expression of GLI1, the final effector of the hedgehog/GLI pathway, providing a novel mechanism of non-canonical SMO-independent activation of HH and GLI signaling in melanoma.