Activation of the tumour suppressor p53 upon cellular stress can induce a number of different cellular processes?The diverse actions of these processes are critical for the protective function of p53 in preventing the...Activation of the tumour suppressor p53 upon cellular stress can induce a number of different cellular processes?The diverse actions of these processes are critical for the protective function of p53 in preventing the development of cancer.However,it is still not fully understood which process(es)activated by p53 is/are critical for tumour suppression and how this might differ depending on the type of cells undergoing neoplastic transformstion and the nature of the drivers of oncogenesis.Moreover,it is not clear why upon activation of p53 some cells undergo cell cycle arrest and senescence whereas others die by apoptosis.Here we discuss some of the cellular processes that are crucial for p53-mediated tumour suppression and the factors that could impact cell fate upon p53 activation.Finally,we describe therapies aimed either at activating wild-type p53 or at changing the behaviour of mutant p53 to unleash tumour growth suppressive processes for therapeutic benefit in malignant disease.展开更多
Forty years have passed since the groundbreaking achievement of cloning T-cell receptor genes [1, 2]. The rich narrative that sets the stage for this significant event is incredibly striking, and its profound legacy i...Forty years have passed since the groundbreaking achievement of cloning T-cell receptor genes [1, 2]. The rich narrative that sets the stage for this significant event is incredibly striking, and its profound legacy in contemporary immunology and medical science is truly remarkable.展开更多
文摘Activation of the tumour suppressor p53 upon cellular stress can induce a number of different cellular processes?The diverse actions of these processes are critical for the protective function of p53 in preventing the development of cancer.However,it is still not fully understood which process(es)activated by p53 is/are critical for tumour suppression and how this might differ depending on the type of cells undergoing neoplastic transformstion and the nature of the drivers of oncogenesis.Moreover,it is not clear why upon activation of p53 some cells undergo cell cycle arrest and senescence whereas others die by apoptosis.Here we discuss some of the cellular processes that are crucial for p53-mediated tumour suppression and the factors that could impact cell fate upon p53 activation.Finally,we describe therapies aimed either at activating wild-type p53 or at changing the behaviour of mutant p53 to unleash tumour growth suppressive processes for therapeutic benefit in malignant disease.
文摘Forty years have passed since the groundbreaking achievement of cloning T-cell receptor genes [1, 2]. The rich narrative that sets the stage for this significant event is incredibly striking, and its profound legacy in contemporary immunology and medical science is truly remarkable.
