Nathan Moore

TL;DR: The evidence for quiescent CSC populations is reviewed and potential cell cycle regulators that may serve as future targets for elimination of these cells are explored.

TL;DR: The results identify the ARRCD3-ITGβ4 pathway as a new therapeutic target in breast cancer and show the importance of connecting genetic arrays with mechanistic studies in the search for new treatments.

TL;DR: Using a novel application for the proliferation marker carboxyfluorescein diacetate, succinimidyl ester, this work identifies a population of slow-cycling, label-retaining tumor cells and demonstrates a multifold increase in ability to survive traditional forms of chemotherapy and reenter the cell cycle.

TL;DR: In this article, the diaminopyrimidine TAE684 and its derivative ceritinib (LDK378), which are structurally distinct from crizotinib-resistant ALKF1174L mutation arises de novo in neuroblastoma (NB) and is acquired in ALK translocation driven cancers, lending impetus to the development of novel anaplastic lymphoma kinase (ALK) inhibitors with different modes of action.

TL;DR: It is shown that in ALK-mutated, MYCN-amplified neuroblastoma cells, crizotinib alone does not affect mTORC1 activity as indicated by persistent RPS6 phosphorylation, and an inhibitor with potency against both mTOR and PI3K was more effective in promoting cytotoxicity when combined with crizotineib.