Abstract
Morris IV et al. adapted a mouse model of human pancreatic ductal adenocarcinoma and found that p53-dependent metabolic changes restrain tumour progression through α-ketoglutarate accumulation and promotion of a premalignant cell fate.
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Paper version not known
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
