Publications by authors named "Rachel Fogley"
Identifying Novel Cancer Therapies Using Chemical Genetics and Zebrafish.
Adv Exp Med Biol
September 2016
Chemical genetics is the use of small molecules to perturb biological pathways. This technique is a powerful tool for implicating genes and pathways in developmental programs and disease, and simultaneously provides a platform for the discovery of novel therapeutics. The zebrafish is an advantageous model for in vivo high-throughput small molecule screening due to translational appeal, high fecundity, and a unique set of developmental characteristics that support genetic manipulation, chemical treatment, and phenotype detection.
View Article and Find Full Text PDFArticle Synopsis
- Studying cancer metabolism can reveal survival strategies and vulnerabilities of tumors, particularly in melanoma.
- HEXIM1 is identified as a key melanoma tumor suppressor that is usually underexpressed; increasing its levels can inhibit tumor formation in zebrafish models.
- Under low nucleotide conditions, HEXIM1 interacts with P-TEFb to block transcription elongation of oncogenes, while also promoting the stability of anti-tumorigenic RNAs, highlighting its dual role in regulating gene expression related to cancer.
Article Synopsis
- - The "cancerized field" theory explains that in tissues with cancer-prone cells, only certain clones have the ability to start tumors, often involving oncogenic mutations like BRAF(V600E) found in benign nevi that usually do not progress to melanoma.
- - Research using transgenic zebrafish shows that a single abnormal melanocyte can switch back to an embryonic neural crest progenitor state, which is critical for the onset of melanoma in a specific genetic context (BRAF(V600E) mutation combined with p53 deficiency).
- - The transcription factor sox10 is implicated in this process, as its overexpression speeds up melanoma development by activating genes related to the neural crest state, signaling that the re
In mammalian embryonic stem cells, the acquisition of pluripotency is dependent on Nanog, but the in vivo analysis of Nanog has been hampered by its requirement for early mouse development. In an effort to examine the role of Nanog in vivo, we identified a zebrafish Nanog ortholog and found that its knockdown impaired endoderm formation. Genome-wide transcription analysis revealed that nanog-like morphants fail to develop the extraembryonic yolk syncytial layer (YSL), which produces Nodal, required for endoderm induction.
View Article and Find Full Text PDF