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Gemma L. Kelly

Researcher at Walter and Eliza Hall Institute of Medical Research

Publications -  70
Citations -  4855

Gemma L. Kelly is an academic researcher from Walter and Eliza Hall Institute of Medical Research. The author has contributed to research in topics: Apoptosis & Epstein–Barr virus. The author has an hindex of 26, co-authored 55 publications receiving 3582 citations. Previous affiliations of Gemma L. Kelly include University of Birmingham & University of Melbourne.

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The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models

TL;DR: It is demonstrated that S63845 potently kills MCL1-dependent cancer cells, including multiple myeloma, leukaemia and lymphoma cells, by activating the BAX/BAK-dependent mitochondrial apoptotic pathway.
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How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression?

TL;DR: Current understanding of the mechanisms by which p53 induces cell death is discussed and how this affects p53-mediated tumour suppression and the response of malignant cells to anticancer therapy is discussed.
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An Inducible Lentiviral Guide RNA Platform Enables the Identification of Tumor-Essential Genes and Tumor-Promoting Mutations In Vivo

TL;DR: A drug-inducible small guide RNA (sgRNA) vector system allowing for ubiquitous and efficient gene deletion in murine and human cells mediates the efficient, temporally controlled deletion of MCL-1 in human Burkitt lymphoma cell lines that require this anti-apoptotic BCL-2 protein for sustained survival and growth.
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BH3-Mimetic Drugs: Blazing the Trail for New Cancer Medicines.

TL;DR: The BCL-2 inhibitor venetoclax has been approved for treatment of refractory chronic lymphocytic leukemia and this drug and inhibitors of pro-survival MCL-1 and B CL-XL are being tested in diverse malignancies.
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Epstein–Barr virus–associated Burkitt lymphomagenesis selects for downregulation of the nuclear antigen EBNA2

TL;DR: A subset of BL tumors in which the Latency III-associated EBNA promoter Wp is active and most EBNAs are expressed, but where a gene deletion has specifically abrogated the expression of EBNA2 is identified, implying that BL can be selected from a Latencies III progenitor and that the principal selection pressure is for downregulation of the c-Myc antagonist EBNA 2.