K
Kirsteen J. Campbell
Researcher at University of Glasgow
Publications - 42
Citations - 2937
Kirsteen J. Campbell is an academic researcher from University of Glasgow. The author has contributed to research in topics: Programmed cell death & Cancer. The author has an hindex of 20, co-authored 38 publications receiving 2416 citations. Previous affiliations of Kirsteen J. Campbell include University of Melbourne & University of Dundee.
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Journal ArticleDOI
Modulating the therapeutic response of tumours to dietary serine and glycine starvation
Oliver D. K. Maddocks,Dimitris Athineos,Eric C. Cheung,Pearl Lee,Tong Zhang,Niels J. F. van den Broek,Gillian M. Mackay,Christiaan F. Labuschagne,Flore Kruiswijk,Julianna Blagih,David F. Vincent,Kirsteen J. Campbell,Fatih Ceteci,Owen J. Sansom,Karen Blyth,Karen H. Vousden +15 more
TL;DR: The authors showed that restricting dietary serine and glycine can reduce tumour growth in xenograft and allograft models, and this observation translates into more clinically relevant autochthonous tumours in genetically engineered mouse models of intestinal cancer or lymphoma.
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Active Repression of Antiapoptotic Gene Expression by RelA(p65) NF-κB
TL;DR: It is demonstrated that NF-kappa B induced by cytotoxic stimuli, such as ultraviolet light and the chemotherapeutic drugs daunorubicin/doxorubsicin, is functionally distinct to that seen with the inflammatory cytokine TNF and is an active repressor of antiapoptotic gene expression.
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Targeting BCL-2 regulated apoptosis in cancer
TL;DR: The BCL-2 family, their deregulation in cancer and recent pharmaceutical developments to target specific members of this family as cancer therapy are discussed.
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p53- and Mdm2-Independent Repression of NF-κB Transactivation by the ARF Tumor Suppressor
TL;DR: It is found that ARF inhibits NF-kappa B function and its antiapoptotic activity independent of Mdm2 and p53, and shows that the response of NF- kappa B to the oncogene Bcr-Abl is determined by the ARF status of the cell.
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Bcl-2, Bcl-x(L), and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells.
Delphine Merino,Delphine Merino,Seong Lin Khaw,Stephan P. Glaser,Stephan P. Glaser,Daniel Anderson,Lisa D. Belmont,Chihunt Wong,Peng Yue,Mikara Robati,Belinda Phipson,Belinda Phipson,W.D. Fairlie,W.D. Fairlie,Erinna F. Lee,Erinna F. Lee,Kirsteen J. Campbell,Cassandra J. Vandenberg,Cassandra J. Vandenberg,Suzanne Cory,Suzanne Cory,Andrew W. Roberts,Andrew W. Roberts,Andrew W. Roberts,Mary J. C. Ludlam,David C.S. Huang,David C.S. Huang,Philippe Bouillet,Philippe Bouillet +28 more
TL;DR: It is found that Bcl-2 is the critical target in vivo for antitumor efficacy in vivo, suggesting that patients with tumors overexpressing B cl-2 will probably benefit and the use of these compounds can be optimized for treating lymphoid malignancies.