Chitra Venugopal

TL;DR: The sequence of events and defining mechanisms that take place during EMT are described, and how these interactions drive cancer cell progression into metastasis are described.

TL;DR: This review details the emerging data that explores the extensive genetic, cellular and functional ITH present in glioblastoma and suggests harnessing new technologies to delineate GBM ITH and identify treatment-refractory cell populations, thus opening new therapeutic windows.

TL;DR: Findings implicate Bmi1 and Hh as mutually indispensable pathways in medulloblastoma BTIC maintenance and propose that the BTIC marker CD133 may segregate a cell population with a Hh-receptor phenotype, thus demonstrating a cell–cell interaction between the CD133+ Hh receptor cells and theCD133− HH-secreting cells.

TL;DR: CART133 cells may be a therapeutically tractable strategy to target CD133+ CSCs in human GBM or other treatment-resistant primary cancers.

TL;DR: It is concluded that patients with medulloblastoma expressing high levels of PLK1 are at elevated risk and screened a library of 129 compounds in clinical trials using a model of pediatric medullOBlastoma and determined thatPLK1 inhibitors were the most promising class of agents against the growth of medulloplastoma.