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个人简介
He generated and characterised the NUP98-HOXD13 mouse model of myelodysplasia, the first mouse model of this disease and still one of the best and most-used around the world.
Dr Slape's research career has had two primary objectives: to understand the mechanisms of transformation of chronic pre-leukemia conditions to acute leukemia, and to investigate the disease stem cells in pre-leukemia conditions to find therapeutic targets for both phases of haematological disease. The NUP98-HOXD13 transgenic mouse is an ideal model toward both ends; the mice have symptoms of MDS from birth, but only progress to acute myeloid leukemia (AML) after six months, and are therefore an ideal model to study the molecular events necessary to drive transformation from chronic to acute disease, or to study aberrantly self-renewing stem cells in isolation, prior to transformation.
Towards the first objective, Dr Slape has performed and published studies identifying spontaneous drivers of this transformation to disease, and also artificially driving transformation using a retroviral mutagenesis screen to identify induced oncogenic gene expression events. His apoptosis work has resulted in the paradigm-shifting discovery that apoptosis drives transformation of the disease to acute leukemia, where it has hitherto been thought of as a protective mechanism against cancer. Aspects of the second objective run throughout work directed at the first, but have come to the fore in his current work targeting disease stem cell interactions with their modified environment, and the role this plays in promoting their self-renewal. The current work aims to disrupt these interactions to evict the stem cells from the niche, assisting existing therapies to eradicate disease.
Dr Slape's research career has had two primary objectives: to understand the mechanisms of transformation of chronic pre-leukemia conditions to acute leukemia, and to investigate the disease stem cells in pre-leukemia conditions to find therapeutic targets for both phases of haematological disease. The NUP98-HOXD13 transgenic mouse is an ideal model toward both ends; the mice have symptoms of MDS from birth, but only progress to acute myeloid leukemia (AML) after six months, and are therefore an ideal model to study the molecular events necessary to drive transformation from chronic to acute disease, or to study aberrantly self-renewing stem cells in isolation, prior to transformation.
Towards the first objective, Dr Slape has performed and published studies identifying spontaneous drivers of this transformation to disease, and also artificially driving transformation using a retroviral mutagenesis screen to identify induced oncogenic gene expression events. His apoptosis work has resulted in the paradigm-shifting discovery that apoptosis drives transformation of the disease to acute leukemia, where it has hitherto been thought of as a protective mechanism against cancer. Aspects of the second objective run throughout work directed at the first, but have come to the fore in his current work targeting disease stem cell interactions with their modified environment, and the role this plays in promoting their self-renewal. The current work aims to disrupt these interactions to evict the stem cells from the niche, assisting existing therapies to eradicate disease.
研究兴趣
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bioRxiv (Cold Spring Harbor Laboratory) (2020)
Benjamin J Shields,Christopher I Slape, Ngoc Phuoc An Vo,Jacob T. Jackson,Adriana Pliego-Zamora,Hansini Ranasinghe, Wei Shi, David J Curtis,Matthew P McCormack
semanticscholar(2019)
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