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Lisa J. Crawford

Researcher at Queen's University Belfast

Publications -  26
Citations -  851

Lisa J. Crawford is an academic researcher from Queen's University Belfast. The author has contributed to research in topics: Proteasome & Bortezomib. The author has an hindex of 12, co-authored 23 publications receiving 736 citations. Previous affiliations of Lisa J. Crawford include Belfast Health and Social Care Trust & Queen's University.

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Proteasome inhibitors in cancer therapy

TL;DR: This review summarises the main mechanisms of action of proteasome inhibitors in cancer, the development of prote asome inhibitors as therapeutic agents and the properties and progress of next generation proteasom inhibitors in the clinic.
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Comparative selectivity and specificity of the proteasome inhibitors BzLLLCOCHO, PS-341, and MG-132.

TL;DR: Multiple myeloma cells were more sensitive to induction of apoptosis by PS-341 and MG-132 than BzLLLCOCHO, emphasizing the need for further investigation of the effects of these compounds on gene and protein expression in the cell to allow for the development of more specific and targeted inhibitors.
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Targeting the ubiquitin proteasome system in haematological malignancies.

TL;DR: An overview of the ubiquitin proteasome system is provided and current and novel therapies targeting the UPS are discussed, which represent an attractive target for the development of anti-cancer therapies.
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Bortezomib induces apoptosis in primitive chronic myeloid leukemia cells including LTC-IC and NOD/SCID repopulating cells

TL;DR: Bortezomib is antiproliferative and induces apoptosis in chronic phase (CP) CD34+ CML cells at clinically achievable concentrations and is also effective in inhibiting proteasome activity and inducing apoptotic in cell lines expressing BCR-ABL mutations, including T315I.
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Adiponectin is produced by lymphocytes and is a negative regulator of granulopoiesis.

TL;DR: It is shown that although the adiponectin expression is low in lymphocytes, it is sufficient to induce a significant inhibitory effect on GM precursors (CFU‐GM) and activate the AMPK pathway in these cells.