Hello, I'm a student from Korea who just started the first year of a graduate school... and I have a question about angiogenic switch.
I read an article published on Cell and it said a mutant Kras driven lung adenoma progressed into adenocarcinoma after myc activation.
What I thought at first was, the adenocarcinoma would show highly vascularized status because it is more malignant and angiogenic than the adenoma. But the endothelial cell area (CD31+) decreased even though binding of VEGF-VEGFR2 increased. How come?
And is it possible for the adenocarcinoma to become normoxic though vessels are leaky? I thought leaky vessels are not able to carry oxygen evenly...