3 results match your criteria: "Louisiana State University Health Sciences Center and the Feist-Weiller Cancer Center[Affiliation]"
Laryngoscope
October 2011
Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center and the Feist-Weiller Cancer Center, Shreveport, Louisiana 71130, USA.
Objectives/hypothesis: The eukaryotic translation initiation factor 4E (eIF4E) in conjunction with its binding protein, 4EBP1, regulates the translation of cap-dependent mRNAs. An aberrant increase in eIF4E shifts the balance in favor of translation of transcripts that promote cell proliferation and malignancy. eIF4E protein is commonly elevated in head and neck squamous cell carcinomas (HNSCC), and its overexpression is associated with increased recurrence.
View Article and Find Full Text PDFCancer Prev Res (Phila)
October 2009
Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center and the Feist-Weiller Cancer Center, 1501 Kings Highway, Shreveport, LA 71130, USA.
Squamous cell carcinoma (SCC) of the skin is the most clinically aggressive form of nonmelanoma skin cancer. We have determined the effects of all-trans retinoic acid (ATRA), a naturally occurring chemopreventive retinoid, on signal transducer and activator of transcription 3 (Stat3) signaling during the development of skin SCC. Stat3 is a transcription factor that plays a critical role in cell proliferation and survival, and it is constitutively active in several malignant cell types.
View Article and Find Full Text PDFOncogene
April 2008
Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center and The Feist-Weiller Cancer Center, Shreveport, LA 71130-3932, USA.
Sequence-specific transcriptional regulators function by stably binding cognate DNA sequences followed by recruitment of both general and specialized factors to target gene promoters. The tumor suppressor p53 mediates its anti-oncogenic effect on cells by functioning as a sequence-specific regulator. p53 employs a secondary mechanism to suppress tumor formation by permeabilizing the outer mitochondrial membrane, thereby releasing pro-apoptotic factors.
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