Immunohistochemical expression of GLUT1 and its correlation with unfavorable histology and TP53 codon 72 polymorphism in Wilms tumors.

Abstract excerpt

Reprogramming of energy metabolism, such as increased glycolysis, is a hallmark of cancer cells. One mechanism by which cancer cells fuel glycolysis is through increased uptake of glucose across cell membranes via the glucose transporter GLUT1. One of the transcriptional repressors of GLUT1 is wild-type TP53, and cancer-associated loss of function mutations within the DNA-binding domain of TP53 impairs the...

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