Publications by authors named "Megan Jibilian"
Article Synopsis
- Researchers created a new mouse model called EvoCaP to study how prostate cancer spreads to other parts of the body, including bones, liver, and lungs.
- They tracked tumor migration using a barcoding technique, finding that only a few aggressive clones are responsible for most of the cancer's spread, while the majority of cells stay localized.
- The study suggests that prostate cancer acts as a systemic disease driven by these aggressive clones, and understanding these patterns is crucial for developing new treatments.
Optogenetic effectors and sensors provide a novel real-time window into complex physiological processes, enabling determination of molecular signaling processes within functioning cellular networks. However, the combination of these optical tools in mice is made practical by construction of genetic lines that are optically compatible and genetically tractable. We present a new toolbox of 21 mouse lines with lineage-specific expression of optogenetic effectors and sensors for direct biallelic combination, avoiding the multiallelic requirement of Cre recombinase -mediated DNA recombination, focusing on models relevant for cardiovascular biology.
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- Metastatic prostate cancer typically shows bi-allelic mutations in key tumor suppressor genes, but often has large deletions of genes like PHLPP2 on chromosome 16q, which usually inhibits tumor growth.
- In a study using a mutant mouse model, researchers discovered that losing PHLPP2 can surprisingly hinder prostate cancer progression while supporting Myc, a critical driver of aggressive cancer.
- The researchers also found that inhibitors targeting PHLPP2 can effectively reduce Myc levels and eliminate mutant cancer cells, suggesting a potential treatment strategy by exploiting these frequent deletions as a therapeutic target.