NBME 11 VEGF question

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LuckiestOne

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65 yr old man undergoes operation to remove an abd mass,histological examination shows,large number of blood vessels,further analysis shows increased VEGF in tumor, which of the following stimulated the production of vegf in the tumor?

increased endostatin
decreased endostatin
increased pco2
decreased pco2
increased po2
decreased po2
increased thrombospondin
decreased thrombospondin

I feel like multiple choices can be answers here.. Obviously decreased pO2 causes increased VEGF via same mechanism in macular degeneration of high altitude acclimatization, but why can't "decreased endostatin" or "decreased thrombospondin" be answer as well?

Endostatin and thrombospondin are both VEGF inhibitors, sometimes expressed in tumors to produce angiogenic effect.

Thanks in advance.

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Not sure about the answer, but there is actually an NBME 11 thread buried somewhere in this forum (check a few pages back), and lots of people have posted answers/explanations to some of the tougher questions. Check it out and see if you can find your answers there.
 
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I'm gonna go with hypoxia, so upon further research and one slide from a Genetics lecture many moons ago, I found out that Hypoxia -> increased HIF -> increased VEGF. HIF is easily degradable in high O2 and is a transcription factor that responds to low O2.

Note that HIF also induces glycolytic enzymes.
 
I'm gonna go with hypoxia, so upon further research and one slide from a Genetics lecture many moons ago, I found out that Hypoxia -> increased HIF -> increased VEGF. HIF is easily degradable in high O2 and is a transcription factor that responds to low O2.

Note that HIF also induces glycolytic enzymes.

Thanks for your input. I understand why hypoxia would be correct, I am just confused why low endostatin/thrombospondin wouldn't be correct answer as well since those are specifically VEGF inhibitors lacking in many vascularized tumors,
 
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