P N Kelly

TL;DR: It is found that Bim is essential for ER stress-induced apoptosis in a diverse range of cell types both in culture and within the whole animal.

TL;DR: It is demonstrated that Bim and Bad account for most, perhaps all, imatinib-induced killing of Bcr/Abl+ leukemic cells and suggest previously undescribed drug combination strategies for cancer therapy.

TL;DR: It is demonstrated that the initiation, development, continued growth, and severity of Emu-myc lymphoma do not depend upon endogenous Bcl-2, nor upon the total number of B lymphoid cells driven by the EmU- myc transgene.

TL;DR: Findings identify Bcl-x(L) as a prerequisite for the emergence of c-Myc-driven pre-B/B lymphoma and suggest that BH3 mimetic drugs may provide a prophylactic strategy for c- MYC-driven tumors.

TL;DR: The absence of endogenous Bcl-2 in mice expressing an Emu-myc transgene reduced mature B-cell numbers and enhanced their apoptosis, but unexpectedly, lymphoma development was undiminished or even delayed, which suggests that these tumors originate in an earlier cell type, such as the pro-B or pre-B cell, and that the nascent neoplastic clones do not require BCl-2 but may instead be protected by a B cl-2 relative.