Melinda A. Miller

TL;DR: It is shown that CSF1 is the gene at the chromosome 1p13 breakpoint and suggested a tumor-landscaping effect with aberrant CSF 1 expression in the neoplastic cells, leading to the abnormal accumulation of nonneoplastic Cells that form a tumorous mass.

TL;DR: The results suggest that MYC and PVT1 contribute independently to ovarian and breast pathogenesis when overexpressed because of genomic abnormalities, and suggest that PVT 1-mediated inhibition of apoptosis may explain why amplification of 8q24 is associated with reduced survival duration in patients treated with agents that act through apoptotic mechanisms.

TL;DR: Results suggest that PI3K inhibitors should target both p110alpha and p110beta catalytic subunits, whether wild-type or mutant, and be combined with endocrine therapy for maximal efficacy when treating ER(+) breast cancer.

TL;DR: This study indicates that TMPRSS2:ERG gene rearrangements in CaP may be used as a diagnostic tool to identify prognostically relevant sub-classifications of these cancers.

TL;DR: The consistent presence of CSF1 overexpression in all cases of PVNS/TGCT and reactive synovitides suggests both an important role for CSf1 in the spectrum of synovial pathologies and the possibility of targeting the CSF 1/CSF1R interaction therapeutically.