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Cleavage of poly(ADP-ribose) polymerase by a proteinase with properties like ICE
TLDR
A novel protease resembling ICE (prICE) that is active in a cell-free system that reproduces the morphological and biochemical events of apoptosis in the extracts including morphological changes, cleavage of PARP and production of an oligonucleosomal ladder. Expand
Mammalian caspases: structure, activation, substrates, and functions during apoptosis.
TLDR
This work has shown that apoptotic cell death is a genetically programmed, morphologically distinct form of cell death that can be triggered by a variety of physiological and pathological stimuli, and that proteases play critical roles in initiation and execution of this process. Expand
PARP inhibition: PARP1 and beyond
TLDR
What is known about the structures and functions of the family ofPARP enzymes are reviewed, and a series of questions that should be addressed are outlined to guide the rational development of PARP inhibitors as anticancer agents. Expand
Specific proteolytic cleavage of poly(ADP-ribose) polymerase: an early marker of chemotherapy-induced apoptosis.
TLDR
The results suggest that proteolytic cleavage of pADPRp, in addition to being an early marker of chemotherapy-induced apoptosis, might reflect more widespread proteolysis that is a critical biochemical event early during the process of physiological cell death. Expand
Phase II trial of single-agent temsirolimus (CCI-779) for relapsed mantle cell lymphoma.
TLDR
It is demonstrated that agents that selectively target cellular pathways dysregulated in MCL cells can produce therapeutic benefit and single-agent temsirolimus has substantial antitumor activity in relapsed MCL. Expand
Induction of apoptosis by cancer chemotherapy.
TLDR
The two prototypic death pathways are described, current understanding of the role of the two pathways in chemotherapy-induced apoptosis is summarized, and the implications of these studies for mechanisms of resistance to chemotherapeutic agents are discussed. Expand
Rucaparib in relapsed, platinum-sensitive high-grade ovarian carcinoma (ARIEL2 Part 1): an international, multicentre, open-label, phase 2 trial.
TLDR
The ability of tumour genomic LOH, quantified with a next-generation sequencing assay, to predict response to rucaparib, an oral PARP inhibitor, was assessed in ARIEL2, an international, multicentre, two-part, phase 2, open-label study. Expand
Nonhomologous end joining drives poly(ADP-ribose) polymerase (PARP) inhibitor lethality in homologous recombination-deficient cells
TLDR
It is shown that PARP inhibitor treatment induces phosphorylation of DNA-dependent protein kinase substrates and stimulates error-prone nonhomologous end joining (NHEJ) selectively in HR-deficient cells, and it is indicated that deregulated NHEJ plays a major role in generating the genomic instability and cytotoxicity in HRs treated with PARP inhibitors. Expand
Loss of HSulf-1 Up-regulates Heparin-binding Growth Factor Signaling in Cancer*
TLDR
Observations provide evidence that HSulf-1 modulates signaling by heparin-binding growth factors, and HS sulfur-1 down-regulation represents a novel mechanism by which cancer cells can enhance growth factor signaling. Expand
Programmed cell death: alive and well in the new millennium.
TLDR
Current understanding of apoptotic events is summarized, recent advances in this field are noted and questions that might help guide research in the coming years are identified. Expand
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