Full Text Journal Articles by
Author Sander B Frank


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Notch3 promotes prostate cancer-induced bone lesion development via MMP-3.

Sourik S Ganguly, Galen Hostetter, Lin Tang, Sander B Frank, Kathylynn Saboda, Rohit Mehra, Lisha Wang, Xiaohong Li, Evan T Keller, Cindy K Miranti,

Prostate cancer metastases primarily localize in the bone where they induce a unique osteoblastic response. Elevated Notch activity is associated with high-grade disease and metastasis. To address how Notch affects prostate cancer bone lesions, we manipulated Notch expression in mouse tibia xenografts and monitored tumor growth, lesion phenotype, and the ... Read more >>

Oncogene (Oncogene)
[2020, 39(1):204-218]

Cited: 2 times

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Supraphysiological androgens suppress prostate cancer growth through androgen receptor-mediated DNA damage.

Payel Chatterjee, Michael T Schweizer, Jared M Lucas, Ilsa Coleman, Michael D Nyquist, Sander B Frank, Robin Tharakan, Elahe Mostaghel, Jun Luo, Colin C Pritchard, Hung-Ming Lam, Eva Corey, Emmanuel S Antonarakis, Samuel R Denmeade, Peter S Nelson,

Prostate cancer (PC) is initially dependent on androgen receptor (AR) signaling for survival and growth. Therapeutics designed to suppress AR activity serve as the primary intervention for advanced disease. However, supraphysiological androgen (SPA) concentrations can produce paradoxical responses leading to PC growth inhibition. We sought to discern the mechanisms by ... Read more >>

J. Clin. Invest. (The Journal of clinical investigation)
[2019, 129(10):4245-4260]

Cited: 5 times

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Human prostate luminal cell differentiation requires NOTCH3 induction by p38-MAPK and MYC.

Sander B Frank, Penny L Berger, Mats Ljungman, Cindy K Miranti,

Many pathways dysregulated in prostate cancer are also involved in epithelial differentiation. To better understand prostate tumor initiation, we sought to investigate specific genes and mechanisms required for normal basal to luminal cell differentiation. Utilizing human prostate basal epithelial cells and an in vitro differentiation model, we tested the hypothesis ... Read more >>

J. Cell. Sci. (Journal of cell science)
[2017, 130(11):1952-1964]

Cited: 8 times

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Receptor tyrosine kinase Met promotes cell survival via kinase-independent maintenance of integrin α3β1.

Lia Tesfay, Veronique V Schulz, Sander B Frank, Laura E Lamb, Cindy K Miranti,

Matrix adhesion via integrins is required for cell survival. Adhesion of epithelial cells to laminin via integrin α3β1 was previously shown to activate at least two independent survival pathways. First, integrin α3β1 is required for autophagy-induced cell survival after growth factor deprivation. Second, integrin α3β1 independently activates two receptor tyrosine ... Read more >>

Mol. Biol. Cell (Molecular biology of the cell)
[2016, 27(15):2493-2504]

Cited: 6 times

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Transient induction of ING4 by Myc drives prostate epithelial cell differentiation and its disruption drives prostate tumorigenesis.

Penny L Berger, Sander B Frank, Veronique V Schulz, Eric A Nollet, Mathew J Edick, Brittany Holly, Ting-Tung A Chang, Galen Hostetter, Suwon Kim, Cindy K Miranti,

The mechanisms by which Myc overexpression or Pten loss promotes prostate cancer development are poorly understood. We identified the chromatin remodeling protein, ING4, as a crucial switch downstream of Myc and Pten that is required for human prostate epithelial differentiation. Myc-induced transient expression of ING4 is required for the differentiation ... Read more >>

Cancer Res. (Cancer research)
[2014, 74(12):3357-3368]

Cited: 17 times

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Disruption of prostate epithelial differentiation pathways and prostate cancer development.

Sander B Frank, Cindy K Miranti,

One of the foremost problems in the prostate cancer (PCa) field is the inability to distinguish aggressive from indolent disease, which leads to difficult prognoses and thousands of unnecessary surgeries. This limitation stems from the fact that the mechanisms of tumorigenesis in the prostate are poorly understood. Some genetic alterations ... Read more >>

Front Oncol (Frontiers in Oncology)
[2013, 3:273]

Cited: 20 times

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