Publications by authors named "Shaishavi Jansari"
Article Synopsis
- Cancer cells adapt to various stresses, including those from treatments, through metabolic adaptability, focusing on the energy sensor AMP-activated protein kinase (AMPK).
- In pancreatic ductal adenocarcinoma (PDAC), high levels of AMPK expression and activity were observed, leading to the identification of PF-3758309 as a potential AMPK inhibitor through drug repurposing.
- PF-3758309 not only demonstrates pre-clinical effectiveness in PDAC models but also helps sensitizes cancer cells to ferroptosis inducers, paving the way for AMPK-targeted therapies in combination treatments for this type of cancer.
Background: Breast cancer (BC) is the most frequent tumor entity in women worldwide with a high chance of therapeutic response in early- and non-metastatic disease stages. Among all BC subtypes, triple-negative BC (TNBC) is the most challenging cancer subtype lacking effective molecular targets due to the particular enrichment of cancer stem cells (CSCs), frequently leading to a chemoresistant phenotype and metastasis. The Ubiquitin Specific Peptidase 22 (USP22) is a deubiquitinase that has been frequently associated with a CSC-promoting function and intimately implicated in resistance to conventional therapies, tumor relapse, metastasis and overall poor survival in a broad range of cancer entities, including BC.
View Article and Find Full Text PDFTriple-negative breast cancer (TNBC) is the most difficult breast cancer subtype to treat due to the lack of targeted therapies. Cancer stem cells (CSCs) are strongly enriched in TNBC lesions and are responsible for the rapid development of chemotherapy resistance and metastasis. Ubiquitin-based epigenetic circuits are heavily exploited by CSCs to regulate gene transcription and ultimately sustain their aggressive behavior.
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