Loss of BAP1 function is associated with increased sensitivity to TRAIL and other death receptor agonists in malignant mesothelioma, where this is a frequent event, with immediate and actionable therapeutic implications.
Inhibition of ITGA2-mediated cancer cell-collagen interaction or targeting focal adhesion kinase activity may present an opportunity for therapeutic intervention of metastatic spread in ovarian cancer.
Expression of the transcription factor Wt1 is required in a lateral mesoderm domain to develop the mesenchymal population required for the closure of the pleural cavities and the formation of the diaphragm.
Genetic inactivation of the transcription factor, Zfp423, in visceral white adipocyte precursors leads to the formation of thermogenic adipocytes in visceral fat depots and improves insulin sensitivity in obese mice.
FLT3-ITD/STAT5A signaling is more sensitive to Dot1L inhibition than the canonical MLL-fusion activated drivers of leukemogenesis, providing a potential therapeutic avenue for one of the most frequent lesions in leukemia.