Browsing by Author "Panka, David"
Now showing items 1-4 of 4
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Clinical Profiling of BCL-2 Family Members in the Setting of BRAF Inhibition Offers a Rationale for Targeting De Novo Resistance Using BH3 Mimetics
Frederick, Dennie T.; Salas Fragomeni, Roberto A.; Schalck, Aislyn; Ferreiro-Neira, Isabel; Hoff, Taylor; Cooper, Zachary A.; Haq, Rizwan; Panka, David J.; Kwong, Lawrence N.; Davies, Michael A.; Cusack, James C.; Flaherty, Keith T.; Fisher, David E.; Mier, James W.; Wargo, Jennifer A.; Sullivan, Ryan J. (Public Library of Science, 2014)While response rates to BRAF inhibitiors (BRAFi) are high, disease progression emerges quickly. One strategy to delay the onset of resistance is to target anti-apoptotic proteins such as BCL-2, known to be associated with ... -
Effects of HDM2 antagonism on sunitinib resistance, p53 activation, SDF-1 induction, and tumor infiltration by CD11b+/Gr-1+ myeloid derived suppressor cells
Panka, David Joel; Liu, Qingjun; Geissler, Andrew K; Mier, James W. (BioMed Central, 2013)Background: The studies reported herein were undertaken to determine if the angiostatic function of p53 could be exploited as an adjunct to VEGF-targeted therapy in the treatment of renal cell carcinoma (RCC). Methods: ... -
Novel drugs that target the metabolic reprogramming in renal cell cancer
van der Mijn, Johannes C.; Panka, David J.; Geissler, Andrew K.; Verheul, Henk. M.; Mier, James W. (BioMed Central, 2016)Molecular profiling studies of tumor tissue from patients with clear cell renal cell cancer (ccRCC) have revealed extensive metabolic reprogramming in this disease. Associations were found between metabolic reprogramming, ... -
Resistance of Renal Cell Carcinoma to Sorafenib Is Mediated by Potentially Reversible Gene Expression
Bhasin, Manoj; Schor-Bardach, Rachel; Collins, Michael P.; Zhang, Liang; Wang, Xiaoen; Panka, David Joel; Putheti, Prabhakar; Signoretti, Sabina; Alsop, David C.; Libermann, Towia Aron; Atkins, Michael B.; Mier, James W.; Goldberg, S. Nahum; Bhatt, Rupal Satish (Public Library of Science, 2011)Purpose: Resistance to antiangiogenic therapy is an important clinical problem. We examined whether resistance occurs at least in part via reversible, physiologic changes in the tumor, or results solely from stable genetic ...